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Two Eurofins DiscoverX scientists on physiological relevance, the GPCRs that refuse to work, and why obesity biology brought the field back. << Back to podcast list Strategic Partner(s) Jane Lamerdin and Gaurav Agrawal: Building GPCR Assays That Reflect Real Biology GPCRs spent years in the background while pharmacology chased other targets. Obesity and GLP-1 biology changed that, and the largest target class is once again at the front of drug discovery. In this conversation, two Eurofins DiscoverX scientists reflect on what nearly three decades of building GPCR assays has taught them about what a trustworthy assay actually requires. The recurring theme is physiological relevance. Overexpressing a receptor produces a big, convenient signal, but it distorts the pharmacology and drifts away from what happens in a real cell. Lamerdin and Agrawal explain why the field, and increasingly regulators, now expect assays built closer to native expression, and why that raises the technical bar considerably. Along the way they discuss the receptors that simply refuse to yield an assay, from adhesion GPCRs to orphans trapped in the endoplasmic reticulum, and the long road from a discovery-grade assay to one robust enough for potency and lot release. For Agrawal it is personal: he spent his PhD on four GPCRs and now stewards 289, carrying those early lessons into every assay his team validates. About the Guests Jane Lamerdin is VP of R&D at Eurofins DiscoverX, where she oversees development of novel cell-based assays and tools for both portfolio expansion and client-focused projects. She brings more than twenty years of industry experience across diverse cell-based assays, supporting client drug discovery campaigns, method development, and qualification of assays for late-stage biologics. Her background spans high-throughput, molecular, and systems biology research, which lets her speak to what an assay needs at every stage of a program. Gaurav Agrawal earned his PhD in cell and molecular biology from the Indian Institute of Science, studying how GPCRs activate. During his postdoc at UC San Diego, he discovered a novel intracellular trafficking pathway essential for organelle biogenesis. At Eurofins DiscoverX, Agrawal leads market development for the cell-based assay portfolio and supports method transfers to CROs and CDMOs for biologics and biosimilars, keeping him in close contact with the scientists running these assays day to day. Scientific Themes of the Conversation Physiological relevance versus overexpression as the standard for a credible cell-based assay The company's arc from cyclic AMP screening into arrestin and internalization biology The obesity and GLP-1 resurgence that returned GPCRs to the front of drug discovery De-orphanizing GPCRs, including receptors stuck in the endoplasmic reticulum Moving a single GPCR assay from discovery through potency testing and lot release Community and client feedback as the real engine of new product development Key Insights from the Conversation Overexpression buys signal at the cost of truth. A single receptor can trigger a large, amplified cyclic AMP response, which makes overexpression assays convenient but unrepresentative. The easy readout drifts away from the biology researchers actually want to measure. Physiological relevance is now an expectation, not a preference. Regulators have begun telling companies directly that assays need to reflect near-primary expression levels. That raises the technical bar, since detecting such low expression pushes the limits of available methods. One assay is not one assay. A cell line that is excellent for discovery screening can be unsuitable for potency and lot release, where plate-to-plate, analyst-to-analyst, and year-to-year consistency become non-negotiable. Bridging that gap takes months of hardening work. Failure is documented, not buried. Decades of careful record-keeping on assays that never worked, from adhesion GPCRs to certain photoreceptor-like targets, let the team avoid reinventing dead ends and focus energy where progress is still possible. GPCRs never left; the attention did. For years the field's spotlight drifted to checkpoints and T-cell receptors. The obesity and type 2 diabetes wave brought GPCRs back to the front seat, and with it a fresh round of questions about how these receptors actually work. Scientists first, vendor second. The guests frame their work as talking to peers who understand the same pains, not selling a catalog. The support inbox and community collaborations feed directly back into what gets built next. Episode Timeline Timestamps were generated using AI for readability. 00:00 Meet the Eurofins DiscoverX scientists 03:20 From four receptors to 289: Agrawal's path into GPCRs 07:00 The Human Genome Project to pharmacology: Lamerdin's route 10:40 Why the largest target class still surprises them 21:40 How DiscoverX began, from cyclic AMP to arrestin 33:20 The assays that refused to work 36:30 De-orphanizing GPCRs stuck in the ER 46:40 Obesity, GLP-1, and the return of GPCRs 47:40 Physiological relevance as the real bottleneck 53:40 One message: scientists first Selected Quotes GPCRs are back. I'm very glad they're back in the front seat. Overexpression assays are not physiologically relevant. I like to call myself a jack of all trades, maybe master of none, but enough to be dangerous. You will not be disappointed to talk science about GPCRs when you reach out to us, and we love to talk to you. Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Pierre Eftekhari About Dr. Pierre Eftekhari "Clinical physiologist and biologist , with more than 25 years of experience in drug development. have been engaged in GPCR cellular and clinical pharmacology as scientist or PI in neonatal lupus, Cardiomyopathy, hypertension, chagas disease. I have participated and initiated methodologies for development of pharmacologically active anti-GPCR antibodies like agonist, antagonist, inverse agonist or blocker. During my Scholar period I have published or contributed in 38 published scientific work mainly in the field of immunology and pharmacology of GPCR. The majority of my research is concentrated on rhodopsin family with a few works on metabotropic receptor. Since the creation of Inoviem scientific in Nov. 2011 by myself we have been regularly working with GPCRs for our pharma and biotech clients. The latter mainly in target deconvolution and patient stratification." Dr. Pierre Eftekhari on the web Inoviem Scientific ResearchGate LinkedIn Twitter Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Neil Grimsey About Dr. Neil Grimsey " During my postdoctoral studies at USCD, I discovered a novel GPCR-dependent atypical kinase activation mechanism that drives vascular edema and inflammation. These studies shaped my future goals as an Assistant Professor in the College of Pharmacy at the University of Georgia Athens. My group studies the spatiotemporal dynamics of atypical inflammation and the control of disease progression. We have developed an array of fluorescent biosensors to map kinase activity in living cells and are exploring innovative techniques to delineate the molecular dynamics of atypical p38 and suppress kinase activation. To further define the role of atypical p38 signaling responses we are studying how atypical p38 controls the onset and pathogenesis of acute lung injury, retinal vasculopathies, and infections. " Dr. Neil Grimsey on the web LinkedIn University of Georgia Google Scholar X (Twitter) Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Aylin Hanyaloglu About Dr. Aylin Hanyaloglu Dr. Aylin Hanyaloglu has been a Principal Investigator at Imperial College London since 2007. She received her BSc in Human Biology from King’s College London in 1997, and while her Ph.D. commenced at the MRC Human Reproductive Sciences Centre, Edinburgh, a move to Perth, Australia resulted in her Ph.D. in Molecular Endocrinology being awarded in 2002 with Distinction from the University of Western Australia. Dr. Hanyaloglu undertook her postdoctoral training at the University of California, San Francisco with Professor Mark von Zastrow where she identified novel core cellular machinery critical for G protein-coupled receptor trafficking and signaling. Her research focuses on understanding the fundamental cell biological mechanisms regulating GPCR activity, including spatial control of GPCR signaling and receptor crosstalk, and applying these mechanisms for distinct GPCRs in diverse physiological and pathophysiological systems, with particular focus on women's health, pregnancy, and nutrient sensing in the gut. Her work is currently funded by Biotechnology and Biological Sciences Research Council (BBSRC), Diabetes UK, Wellcome Trust, and the Medical Research Council. Dr. Aylin Hanyaloglu on the web LinkedIn Researchgate Twitter Imperial College London Elsevier Loop Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Nyla Naim, Dr. Michael Lemieux & Dr. Jason Nasse About Dr. Nyla Naim Nyla is a Senior Scientist on the Scientific Support Team at Addgene . She received her Ph.D. at the University of Pittsburgh and continued her postdoctoral research at the University of Vermont studying cellular signaling, biosensors, and optogenetics. Nyla supports biomedical research by connecting researchers with resources and promoting reproducible science. Dr. Nyla Naim on the web LinkedIn Dr. GPCR Ecosystem About Dr. Michael Lemieux ''My name is Michael (Mike) Lemieux and I am a Connecticut native. I completed my Ph.D. in molecular and cell biology at UConn and then joined Addgene as a Quality Control Scientist in 2015. Since then I transitioned into a Scientific Support role to leverage my passion for helping people! Beyond my interest in science, I am a strong advocate for graduate education reform and I love to write.'' Dr. Michael Lemieux on the web Addgene Blog Dr. GPCR Ecosystem About Dr. Jason Nasse Dr. Jason Nasse is a senior scientist at Addgene specializing in the use of AAV viral vectors. He obtained his Ph.D. in Neuroscience from Ohio State University focusing on synaptic plasticity and adrenergic receptor modulation of both pre-and postsynaptic properties. By taking a very non-traditional path to obtain a Ph.D. Dr. Nasse has had the opportunity to experience how science is performed across different sectors and around the country. Prior to his role at Addgene, Jason held roles in academia, big pharma, and non-profit research organizations. Dr. Jason Nasse on the web LinkedIn Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Benjamin Myers About Dr. Benjamin Myers Ben Myers is an assistant professor at the University of Utah School of Medicine in Salt Lake City, UT, and an investigator with the Huntsman Cancer Institute. Ben’s research focuses on Smoothened and other class F GPCRs which play essential roles in embryonic development and in cancer. His group studies the unusual signaling mechanisms employed by these atypical 7-transmembrane receptors, combining biochemical and structural approaches with cell biology and in vivo models. These studies have revealed new and unexpected ways for membrane lipids to regulate GPCR activity and for GPCRs to control intracellular kinases. More recently, Ben’s lab has begun studying GPCR signaling pathways that operate within the primary cilium, a tiny antenna-shaped structure at the cell surface with critical links to development, physiology, and disease. Ben studied developmental and cancer signaling as a postdoctoral fellow with Philip Beachy at Stanford University. Prior to that, Ben received his Ph.D. from UCSF in 2008, where he worked with David Julius on the structure, function, and physiology of ion channels and GPCRs in the nervous system. Dr. Benjamin Myers on the web Website Twitter Pubmed University of Utah Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Sri Kosuri About Dr. Sri Kosuri Sri is a biologist that has helped build technologies, labs, and companies in synthetic biology, functional genomics, and bioinformatics over the last 20 years. He is passionate about developing more rational ways to understand and engineer biology. Sri is a co-founder at Octant and an Associate Professor at UCLA in the Chemistry and Biochemistry Department. His lab has worked on building large-scale ways of empirically exploring questions in protein biochemistry, human genetic variation, gene regulation, chemical biology, synthetic biology, and functional genomics. Sri previously worked at the Wyss Institute and Harvard, where he built numerous technologies in gene synthesis, DNA information storage, gene editing, and large-scale multiplexed assays. He helped build Gen9, a gene synthesis company, as a member of the SAB and was the first employee of Joule Unlimited, an engineered algal biofuel company. He is a Searle Scholar (2015), NIH New Innovator (2014), and received his ScD in Biological Engineering at MIT and BS in Bioengineering at UC Berkeley. Sri is originally from New Jersey, Philadelphia, and Kansas and was born in North Carolina. He enjoys eating, getting outdoors, and traveling with his wife and two children. Dr. Sri Kosuri on the web Octant Kosuri Lab Twitter LinkedIn Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Rosie Dawaliby About Dr. Rosie Dawaliby "I’m an expert in early-stage drug discovery, targeting membrane proteins, especially GPCR. I have 10 years of experience in the development and management of R&D projects and teams in the field of pharmacology, in prestigious academic laboratories as well as in biopharmaceutical companies in Europe and the United States. I hold a Ph.D. in Life Sciences from the University of Lausanne, Switzerland, Department of Biochemistry (2005-2009), where I started working on membranes and membrane protein biochemistry by studying membrane fusion and autophagy in yeast and mammalian cells. I have developed my expertise in the field of pharmacology and biochemistry of GPCR and the crucial role of the lipidic environment on their structure and function during my post-doctoral work (2010-2015). This joint project between prof. Brian Kobilka's lab at Stanford University and the SFMB laboratory at the Université Libre de Bruxelles (ULB) resulted in the first systematic study of phospholipid's effect on GPCR conformation and function. In 2016, I joined a company that specialized in therapeutic candidate discovery targeting GPCR ( Confo Therapeutics ) as a team and project leader for antibody discovery for metabolic and inflammatory diseases. I developed G.CLIPS biotech's innovative technology as a synthesis of the different knowledge, experiences, and know-how from the different stages of my career. Before founding G.CLIPS biotech in June 2020. And since then, my incredible adventure as CEO of this fast-growing company started and is continuing." Dr. Rosie Dawaliby on the web LinkedIn Dr. GPCR Ecosystem G.CLIPS Biotech on the web Website LinkedIn Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

Chris Tate co-founded Heptares after reading one paper on a Friday afternoon. This conversation covers thermostabilization, cryoEM, and GPCR structural biology. << Back to podcast list Strategic Partner(s) Chris Tate: Thermostabilizing GPCRs for Structural Biology For most of the 1990s and early 2000s, GPCR structural biology was not a biology problem - it was a stability problem. Receptors that fell apart in any useful detergent could not be crystallized, and without crystals, there were no structures. Chris Tate spent years working on membrane proteins that were simply too unstable to study by crystallography, and the question of how to solve that became the organizing problem of his career. The answer came from an unexpected source: a paper on thermostabilization of an unrelated membrane protein, read on a Friday afternoon in the library. That insight led to a systematic mutation screen, a 21-degree improvement in receptor thermostability, and eventually the co-founding of Heptares - a company now running over 250 GPCR structures and six clinical candidates. This conversation covers how thermostabilization changed what was structurally possible, how cryoEM then redrew the map again, and what the first solved Class D GPCR dimer reveals about receptor architecture at its most unexpected. ABOUT THE GUEST Chris Tate is a group leader at the MRC Laboratory of Molecular Biology in Cambridge, UK, where his research focuses on the structural and biochemical study of membrane proteins, with particular emphasis on GPCRs. His work developed the thermostabilization platform - a systematic approach to engineering receptor stability for structural biology - that enabled the first high-resolution crystal structures of multiple GPCRs in defined conformational states. He co-founded Heptares (now Sosei Heptares) in 2007, a company that has since produced over 250 GPCR structures and advanced six candidates into clinical trials. His current structural work extends to Class D GPCRs, including the recently solved first dimer architecture in this receptor family. SCIENTIFIC THEMES OF THE CONVERSATION Membrane protein instability as the overlooked bottleneck in GPCR structural biology The thermostabilization platform - from concept to systematic mutation screen From academic discovery to co-founding Heptares: decision, funding, and growth CryoEM and the conformational states that crystallography could never access Class D GPCR architecture - what a dimer with no prior blueprint looks like What remains unsolved: why drug discovery still fails in late-stage clinical trials KEY INSIGHTS FROM THE CONVERSATION Stability, not biology, was the bottleneck The reason GPCR structures took so long was not scientific complexity - it was that the receptors destroyed themselves in every detergent needed for crystallography. Tate's work reframed the problem: before asking what a receptor does, you first have to ask whether it can survive the conditions required to study it. A Friday afternoon and a paper on an unrelated protein The thermostabilization insight did not come from the lab. It came from Tate's habit of spending Friday afternoons in the library reading outside his immediate field. A 1999 paper on thermostability of diacylglycerol kinase - a protein with no connection to GPCRs - produced a light-bulb recognition that reshaped his entire research direction. 21 degrees changed what was chemically possible Thermostabilizing the beta-adrenergic receptor by 21 degrees Celsius was not a marginal improvement. It meant the receptor could survive in harsh short-chain detergents that had previously killed it instantly - including SDS. That stability was what made crystallization tractable and what became the foundation of Heptares. CryoEM opened conformational space that crystallography had locked out The arrestin-coupled state of a GPCR - a structure that required the agonist-bound receptor to be held in its active conformation - could never have come from crystallography. CryoEM removed that constraint, and Tate argues the field is still at the beginning of what this means: inactive-state structures, full conformational sets, and throughputs that were previously inconceivable. A Class D GPCR dimer with no prior blueprint The first solved structure of a Class D GPCR - a yeast receptor from family D - turned out to be a dimer, with an architecture that breaks the rules of class A receptor biology. The dimer interface sits on helix 1, involves a domain-swapped N-terminus and helix 7, is twice the area of the G protein coupling interface, and positions helix 4 over 20 angstroms from where it appears in any known class A receptor. A PhD student solved it in under two years. Drug discovery's real bottleneck is not structural Tate is direct about where the field now stands: accumulating GPCR structures is no longer the limiting step in drug discovery. The harder problem is understanding the human body well enough to predict why a compound that works in vitro fails in Phase 2 or Phase 3 - and solving that will require tools and systems that structural biology alone cannot provide. Science requires a skin like a rhino Tate's advice to young scientists is not procedural - it is temperamental. Science is brutal, things fail for months, and the only way through is genuine passion for being in the lab. He still asks every candidate who wants to join his group one question: do you know, in chemical terms, how a miniprep kit works? The answer reveals whether someone is curious about science or merely using it. EPISODE TIMELINE Timestamps are AI-generated from the transcript and may vary slightly from the final edited audio. 01:35 Meet Tate - membrane protein biochemist, MRC LMB 02:12 Career origin: from calcium ATPase to bacterial transporters 13:52 Path into GPCRs - instability as the bottleneck nobody was solving 17:00 The Friday afternoon library paper that changed GPCR structural biology 24:21 Thermostabilizing the beta receptor by 21 degrees - in any detergent, including SDS 25:56 Co-founding Heptares - the canteen conversation and the venture capital meeting 32:02 Raising £21M during the 2009 financial crisis 37:43 The cryoEM revolution - why the arrestin-coupled structure could never have come from a crystal 45:17 Unpublished: a Class D GPCR dimer - one PhD student, 18 months, a Nature paper 49:05 Advice for young scientists: what it actually takes to survive science 54:35 The curiosity test: do you know how your miniprep kit works? 58:34 Three aha moments - a diffraction pattern, a thermostabilization screen, and a synchrotron SELECTED QUOTES "None of my best ideas have ever arisen from being in the lab. Never. Because when you're in the lab, you're thinking about what's in front of you." "I don't think ever in my life I will ever write an application and just produce so much more than what I wrote in the original application." "Science is brutal. It is absolutely brutal. Things don't work for months. You have to be robust, you have to have a skin like a rhino sometimes." "When you see the GPCR field, all you see is this accelerating number of structures and information, and that is just going to get faster and faster. And I think that is now the minor part." About this episode Dr. Chris Tate obtained his Ph.D. from the University of Bristol in 1989 and then moved to the University of Cambridge (Dept. of Biochemistry) to work on bacterial sugar transporters. After obtaining a research fellowship at Girton College (Cambridge) he moved to the LMB in 1992 to work in Richard Henderson's group on the serotonin transporter. Chris also worked on the E. coli multidrug transporter EmrE and obtained both 2D and 3D crystals as well as a 3D structure using cryo-EM. In 2005 he started working on the development of conformational thermostabilization of GPCRs, which resulted in the structure of the β1-adrenoceptor. Subsequent work has focused on understanding the molecular basis of GPCR pharmacology through structure determination of the β1-adrenoceptor and adenosine A2A receptor in multiple different conformations bound to ligands of different efficacy. In 2016 mini-G proteins were developed as a tool for the structure determination of GPCRs in the fully active state. Structures have been determined by X-ray crystallography of receptors coupled to either mini-Gs or mini-Go, and also by electron cryo-microscopy of receptors coupled to mini G protein bound to βγ subunits. Recent work includes the first structure determination of a GPCR bound to a biased agonist and coupled to arrestin and also the first structure of a Class D receptor. Join me to learn more about Chris’s work and his role in founding Heptares which was later acquired by Sosei and became Sosei Heptares . Dr. Chris Tate on the web LinkedIn ResearchGate Pubmed Google Scholar Sosei Heptares Wikipedia MRC Laboratory of Molecular Biology Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

In this short resilience conversation, Dr. Graciela Pineyro shares what a forced lab shutdown taught her about prioritization, remote lab meetings, and running a research program across closed borders. << Back to podcast list Strategic Partner(s) Graciela Pineyro: Resilience, Lab Life, and the Zoom Effect Research doesn't pause neatly. In March 2020, Dr. Graciela Pineyro — a principal investigator at CHU Sainte-Justine in Montreal studying GPCR signaling — watched her lab close from one day to the next. This short resilience conversation, part of a Dr. GPCR Podcast series capturing the realities of scientific life, returns to Dr. Pineyro several months into the shutdown to hear what she learned. The discussion moves across three overlapping questions: how a forced pause reshapes scientific prioritization, how remote lab meetings alter who speaks up and why, and what it costs a scientist personally to keep a lab running across a closed international border. For Dr. Pineyro, whose husband remained in Uruguay for the duration of the shutdown, the scientific work and the human cost were never separate conversations. What emerges is a quiet argument that the structural shifts the pandemic forced — project planning in self-contained blocks, flatter meeting dynamics, planned reflection time — may deserve to survive the return to the bench. About the Guest Dr. Graciela Pineyro is a principal investigator at CHU Sainte-Justine in Montreal, where her research group works on GPCR signaling. She is a returning guest of the Dr. GPCR Podcast; her earlier episode covers her scientific profile in depth, including her research trajectory, laboratory focus, and contributions to the field. This resilience conversation captures her voice not as a researcher presenting results, but as a PI speaking candidly about how her program is navigating a moment no one planned for. Scientific Themes of the Conversation Forced pause as a prioritization tool — How closure reveals what a lab would otherwise never stop to question. The democratizing effect of remote meetings — Why some lab members speak more freely from home than they ever did in person. Experimental planning under uncertainty — Structuring projects into self-contained blocks so a lab can survive iterative shutdowns. The personal geography of modern science — What it costs a scientist when the research program and the family are in different countries. Civic responsibility in returning to the bench — Deconfining a research center slowly, with planning for possible return to closure. Key Insights from the Conversation The pause was never just a pause. Dr. Pineyro frames the shutdown not as lost time but as a rare moment of recul — the French word for a step back that allows for perspective. She talks about finally being able to ask which projects deserved to be finished first, second, third. The question was always there; the pause was what forced it to be answered. Zoom did not flatten the lab. It flattened the hierarchy of who gets heard. The most striking observation in the conversation: lab members who rarely spoke up during in-person meetings began contributing more on Zoom. Dr. Pineyro notes she isn't sure why — something about speaking from home, something about reduced interpersonal threat. But the finding is sharp enough to take seriously when in-person dynamics return. Planning in blocks is a form of resilience. The lab restructured projects into discrete, self-contained units — each one designed so that if the research center closed again, the team would still have something to analyze, something to write. This is operational wisdom that long outlives the pandemic. The personal cost doesn't stay outside the lab. Dr. Pineyro speaks openly about her husband being stuck in Uruguay since March, missing their planned reunion, hoping for Christmas. She does not separate this from the scientific conversation — and the listener shouldn't either. Running a lab during the pandemic was rarely just a scientific problem. Returning to the bench is a decision, not a default. The research center was deconfining at 20% capacity the week of the recording. Dr. Pineyro frames reopening as something her team is taking "civically with responsibility and a grain of salt" — acknowledging that back-and-forth closures may be the new baseline. That framing, made months before it became the standard narrative, is worth noticing. Some pandemic-era practices deserve to survive. The implicit argument threaded through the whole conversation: the structural shifts forced by the shutdown — planned reflection, remote meeting inclusion, block-based project design — may be worth keeping. Not because the pandemic was good for science, but because normal lab life had quietly suppressed some of the things the pause made visible. Episode Timeline Timestamps were generated using AI for readability. 00:00 Introduction and 2020 Summit announcement 01:45 Welcoming a returning guest 02:02 How COVID reshaped the lab and the personal cost 03:30 Using forced pause for prioritization 04:10 Planning experiments in self-contained blocks 04:47 The Zoom effect — quieter voices speaking up 05:49 Closing reflections 06:01 Outro Selected Quotes "One day we were doing experiments, and the next we had to close. We have to go back now and start from scratch." "Zoom democratizes the world. People that usually do not speak so much in the lab meetings were speaking a little bit more through Zoom." "We are sort of thinking in advancing our projects in sort of blocks, closing some questions very tightly. So if we are sent back home, at least we have something to work on." "We are all prepared to take this civically with responsibility and also with a grain of salt, knowing that we might have to be going back and forth for a while before everything goes back to normal." About this episode: Dr. Graciela Pineyro is a professor of pharmacology at the department of pharmacology and physiology of the University of Montreal. She has done extensive work on the molecular pharmacology of opioid receptors and is currently focusing on the pharmacology of cannabinoids in the context of pain. We chatted about how the current pandemic has affected her personally and professionally. Dr. Graciela Pineyro on the web Dr. Graciela Pineyro on LinkedIn Dr. Graciela Pineyro - University of Montreal Dr. Graciela Pineyro - CHU Ste-Justine Research Centre Pineyro Lab Publications on Google Scholar Pineyro Lab on Pubmed Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

A conversation with Charlotte Crauwels exploring computational protein design, hybrid GPCR constructs, and how computational pipelines can accelerate GPCR signaling research and drug discovery. << Back to podcast list Strategic Partner(s) Charlotte Crauwels: Designing Hybrid GPCRs with Computational Protein Engineering Scientific Abstract G protein–coupled receptors (GPCRs) are among the most extensively studied protein families in pharmacology and drug discovery, yet many receptors remain poorly characterized or “orphan,” lacking known endogenous ligands. In this conversation, Charlotte Crauwels discusses her work developing computational strategies to support the design of hybrid or chimeric GPCRs. Charlotte Crauwels’ research focuses on building computational pipelines that guide the rational design of GPCR chimeras by combining structural elements from well-characterized receptors with poorly understood ones. These hybrid receptors enable researchers to probe receptor signaling, investigate G protein coupling preferences, and explore structural determinants of receptor activation. By evaluating large numbers of candidate constructs in silico , computational screening can help prioritize experimental designs before testing in the laboratory. The discussion also explores the broader relationship between experimental and computational research in GPCR biology. Ms. Crauwels emphasizes the critical role of well-annotated experimental data for training predictive models and highlights the importance of collaboration between bench scientists and computational researchers. Listeners gain insight into how computational protein design can accelerate receptor signaling research and contribute to new approaches for GPCR discovery and pharmacological characterization. About the Guest Charlotte Crauwels is a computational scientist specializing in protein design and GPCR biology. She conducted her PhD at the Vrije Universiteit Brussel in the research group of Dr. Wim Vranken, focusing on computational approaches for GPCR engineering. Her research centers on developing computational pipelines that guide the design of hybrid or chimeric GPCR constructs to study receptor signaling and structural determinants of receptor activation. Her work integrates bioinformatics, protein modeling, and experimental collaboration to support GPCR discovery and functional characterization. Scientific Themes of the Conversation Computational protein design for GPCR engineering Hybrid and chimeric GPCR constructs Experimental–computational feedback loops in receptor biology Data quality and annotation in computational pharmacology Deorphanization strategies for poorly characterized GPCRs Structural determinants of GPCR signaling pathways Key Insights from the Conversation Experimental Data Drives Computational Discovery Computational models are fundamentally dependent on high-quality experimental data. Charlotte Crauwels emphasizes that predictive models are only as reliable as the datasets used to train them, highlighting the importance of properly annotated experimental datasets in GPCR pharmacology. Computational Tools Help Guide Experimental Design Rather than replacing experiments, computational approaches provide guidance. In Ms. Crauwels’ work, computational pipelines rank potential GPCR chimera designs, helping experimental scientists prioritize which constructs to test first in the lab. Hybrid GPCRs Provide Insight into Orphan Receptors Chimeric GPCR constructs combine components from well-characterized receptors with poorly understood receptors. This strategy can reveal signaling pathways or structural features of orphan GPCRs that cannot easily be studied otherwise. Collaboration Between Bench and Computational Scientists Is Essential Computational researchers depend on experimental validation, while experimental scientists benefit from predictive models that help narrow down possible hypotheses. Successful GPCR research increasingly depends on close collaboration between these two domains. Communication Challenges Between Research Disciplines Computational and experimental scientists often use different terminology and assumptions. Dr. Crauwels describes how misunderstandings can arise from differences in language, experimental details, or sequence definitions—highlighting the need for clear communication in interdisciplinary projects. Data Transparency Enables Better Models Publishing negative results and detailed experimental metadata can significantly improve computational models. Even unsuccessful experiments can contain valuable information for machine learning or predictive modeling. GPCR Biology Continues to Produce “Gotcha Moments” Despite decades of research, GPCRs remain complex and surprising. Dr. Crauwels notes that researchers often experience unexpected results that challenge assumptions about receptor signaling and structural behavior. Episode Timeline 00:00 — Introduction Introduction of Dr. Crauwels and her PhD work in computational GPCR research. 02:20 — Scientific Path Into Computational Biology How bioengineering and bioinformatics led Dr. Crauwels toward computational protein design. 09:15 — The Role of Computational Science in GPCR Research The relationship between experimental data and computational modeling. 16:00 — Collaboration Between Experimental and Computational Scientists Why feedback loops between lab work and computational analysis are critical. 26:30 — Designing Hybrid GPCR Constructs The concept of chimeric GPCRs and how they can be used to study receptor signaling. 30:00 — Building a Computational Pipeline for Chimera Design Using in silico modeling to rank candidate receptor designs before laboratory testing. 36:30 — GPCR ChimeraDB and Data Challenges The challenge of collecting standardized data on chimeric GPCR experiments. 41:30 — “Gotcha Moments” in GPCR Research Why GPCRs continue to surprise even experienced researchers. 43:50 — Advice for Young Computational Scientists The importance of collaboration, conferences, and stepping outside research silos. 48:20 — Career Reflections and What Comes Next Thoughts on the transition after a PhD and continuing research in GPCR biology. Selected Quotes “Computational work allows you to look at data from a different perspective and identify patterns that would be difficult to see experimentally.” “Garbage in, garbage out—computational models depend entirely on the quality of experimental data.” “Hybrid GPCRs allow us to use what we already know about one receptor to understand another that is poorly characterized.” “Every time you think you understand GPCRs, they surprise you again.” Full Transcript (Formatted for readability — original transcript preserved) Yamina Berchiche: Hello everyone. This is Yamina from Dr. GPCR, and today I'm very excited to have with me Charlotte Crauwels. Charlotte is finishing up her PhD, and we’ve been trying to sit down and have this conversation for quite some time. Charlotte, welcome to the podcast. Charlotte Crauwels: Thank you for having me. Yamina Berchiche: Why don't we start by you introducing yourself and telling us about what you're working on right now? Charlotte Crauwels: So as you mentioned, I’m a final-year PhD student at the Vrije Universiteit Brussel in Belgium. I work in the group of Dr. Wim Vranken. I would define myself as a computational protein designer focusing on GPCRs. Looking back, my path to this work was not very linear. I wasn’t originally planning to do a PhD, and I wasn’t planning to work on GPCRs either. I studied bioengineering in Brussels, and during my master’s I was introduced to bioinformatics. I discovered that I really enjoyed working with data and computational tools. For my master’s thesis, I studied antibodies and nanobodies and how they bind to their antigens. That experience convinced me that research might be something I wanted to pursue. At that time, I wasn’t sure what career direction I wanted, so I started contacting computational research groups in Belgium. Eventually, I connected with my current supervisor and began developing GPCR-related research projects. And by coincidence, I ended up working on GPCRs—and I’m actually very happy that I did. Yamina Berchiche: Looking back at your PhD trajectory, what originally drew you to computational research? Charlotte Crauwels: I think it was the idea that we now have enormous amounts of biological data available. We have powerful computational tools that allow us to explore biological systems in ways that were not possible before. So my motivation was really the idea of engineering life—using data and computational methods to understand biological systems and potentially optimize them. Yamina Berchiche: Computational scientists are not always well represented in GPCR discussions. How do you see the role of computational approaches in GPCR biology? Charlotte Crauwels: I think computational scientists are very dependent on experimental work. We don't generate the original data ourselves—we analyze and build models based on experimental data. That means the quality of computational work depends heavily on the quality of the underlying experimental datasets. People often say “garbage in, garbage out.” If the experimental data is poorly annotated or incomplete, the computational predictions will not be reliable. This is why sharing experimental data—and annotating it well—is so important. Yamina Berchiche: You also mentioned the importance of collaboration between experimental and computational researchers. Charlotte Crauwels: Yes, absolutely. I always encourage computational scientists to find experimental collaborators. When you collaborate across disciplines, you create a feedback loop. Computational models generate predictions, experimentalists test them, and the new data helps refine the models. It also makes research more dynamic and motivating. You feel that your work contributes directly to someone else’s experiments. Yamina Berchiche: Let’s talk about your PhD project. What was the core idea behind your research? Charlotte Crauwels: The goal of my PhD was to develop a computational pipeline that supports the design of hybrid—or chimeric—GPCRs. A hybrid GPCR is a receptor constructed by combining elements from two different receptors. Typically, you take a well-characterized GPCR and combine it with a poorly characterized receptor. For example, you might take the extracellular and transmembrane domains of the beta-2 adrenergic receptor and combine them with intracellular loops from an orphan GPCR. This allows researchers to activate the receptor using a known ligand while observing the signaling behavior of the poorly characterized receptor. Yamina Berchiche: So you can essentially probe the signaling pathways of receptors that are otherwise difficult to study. Charlotte Crauwels: Exactly. These hybrid constructs allow researchers to investigate signaling pathways, structural determinants of receptor activation, and even help resolve receptor structures. But designing these hybrids is difficult. Some receptor combinations work very well, while others fail—even when the receptors are very similar. My work focuses on building a computational framework that generates many possible hybrid designs and evaluates them in silico. The system ranks candidate constructs and suggests the most promising ones for experimental testing. Yamina Berchiche: That seems much more efficient than testing dozens of constructs experimentally. Charlotte Crauwels: Yes, that’s the idea. My goal is simply to provide a tool that helps experimental scientists prioritize which constructs to test first. Yamina Berchiche: You also built a database during your PhD. Charlotte Crauwels: Yes. One of the challenges I faced early in my PhD was collecting data on previously published chimeric GPCR constructs. The terminology used in the literature is inconsistent. Some papers call them hybrid receptors, others call them chimeric receptors, and sometimes they’re just described as constructs. It took over a year to gather and curate the data. We eventually created a publicly available database called GPCR ChimeraDB , which collects known hybrid GPCR designs and links them to structural and sequence information. Yamina Berchiche: Let’s switch to a more personal question. What advice would you give to scientists entering computational GPCR research? Charlotte Crauwels: First, dare to ask. People are often more willing to help than we think. Ask to attend conferences, ask for collaborations, ask questions. Second, don’t stay in your bubble. Computational scientists can easily become isolated. It’s important to attend workshops, meet experimental scientists, and keep the broader research context in mind. Yamina Berchiche: Final question. What comes next after your PhD? Charlotte Crauwels: I’m not completely sure yet. But I would be very happy if I can continue working on GPCRs in some way. I feel like I’m just starting to understand how research works. After several years of learning and making mistakes, you finally feel ready to take on bigger questions. So whether it’s in academia or industry, I hope to continue doing research related to GPCR biology. Yamina Berchiche: Charlotte, thank you so much for joining the podcast. It was a pleasure speaking with you. Charlotte Crauwels: Thank you. It was very fun. Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. 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<< Back to podcast list Strategic Partner(s) Vaithish Velazhahan About Vaithish Velazhahan Vaithish obtained dual bachelor’s degrees with honors in Medical Biochemistry and Microbiology from Kansas State University, USA. His undergraduate thesis work on studying the biochemical mechanisms of flavonoids in cancer using nuclear magnetic resonance spectroscopy (NMR) led to a Barry M. Goldwater Scholarship. He then received a prestigious Gates Cambridge Scholarship to study for a Ph.D. at the MRC Laboratory of Molecular Biology and the University of Cambridge, where he is currently a final year Ph.D. candidate. His Ph.D. work has been focused on understanding the structure and activation of Class D fungal GPCRs. He has developed novel tools and methodologies to study fungal GPCRs which allowed the determination of the first structures of the prototypical fungal GPCR Ste2. This work has led to two first-authored manuscripts published in the journal Nature. Vaithish has been recognized with the MRC LMB's Max Perutz Prize for outstanding Ph.D. work and has been elected a Research Fellow at Gonville and Caius College, which is one of the most prestigious positions at the University of Cambridge. Vaithish Velazhahan on the web Twitter GatesCambridge PubMed Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

When his lab closed in 2020, Dr. Paul Insel turned dry-lab science into a reframing of COVID-19 pathobiology as a GPCR signaling imbalance — and a figure in The Economist. << Back to podcast list Strategic Partner(s) Paul Insel: Rethinking COVID-19 Pathobiology Through GPCR Signaling In the spring and summer of 2020, pharmacologist Dr. Paul Insel did something unusual for a working lab scientist: he stopped pipetting, and started writing. With his UC San Diego postdoc Krishna Sriram, he reread the literature on ACE inhibitors and angiotensin receptor blockers in the context of severe acute respiratory illness and concluded — against a swell of clinical panic — that the case for their danger in COVID-19 didn't hold up. What came next was a series of papers reframing severe COVID-19 as a disease of signaling imbalance: an overdrive of AT1R activation by angiotensin II, paired with a loss of ACE2-generated angiotensin 1-7. The therapeutic logic that follows is less about attacking the virus and more about rebalancing a GPCR-driven system that the infection has thrown off-axis. A figure from that British Journal of Pharmacology paper was later redrawn by The Economist for a general-audience article on COVID pathobiology — an unexpected crossover for work that began as armchair science during a lockdown walk. This conversation matters to Dr. Insel personally because he is, in his own words, a vulnerable patient — immunosuppressed, older, asthmatic — and what he's describing is not abstract. It's what he would want a physician to understand if he were the one in the hospital bed. About the Guest Dr. Paul Insel is Distinguished Professor of Pharmacology and Medicine at UC San Diego, where he also co-directs the MD-PhD program. His research career has centered on GPCR signaling — with particularly deep work on beta-adrenergic receptors, cyclic AMP regulation, and receptor biology across tissue systems. Beyond the lab, he has been a long-standing contributor to the Goodman & Gilman textbook of pharmacology and is writing its next chapter on angiotensin signaling and angiotensin drugs. He is also involved nationally in MD-PhD program leadership. Scientific Themes of the Conversation The angiotensin imbalance hypothesis of COVID-19 pathobiology — AT1R overdrive versus ACE2/Ang 1-7 insufficiency Drug repurposing as a pandemic strategy — from ACE inhibitors and ARBs to PAR1 and PAR4 antagonists The "gas pedals and brakes" philosophy of cell signaling and pharmacology Dry-lab pharmacology and what becomes possible when wet-lab work stops GPCR density and tissue-specific therapeutic opportunity — type II pneumocytes, beta-2 receptors, and the asthma parallel The ethics of acting on conviction — off-label drug use during a pandemic Key Insights from the Conversation The ACE inhibitor scare was built on a bogus reading of the literature. Early in the pandemic, senior clinicians were stopping their own ACE inhibitors and ARBs based on hypothesis-driven fears of worse outcomes. Dr. Insel and Krishna Sriram went to the primary data and concluded the claim was not supported. The review was accepted at Clinical Pharmacology and Therapeutics within weeks. Severe COVID-19 may be a story of signaling imbalance, not just viral damage. The British Journal of Pharmacology paper reframes pathobiology as an imbalance between AT1R activation and ACE2-generated angiotensin 1-7. If the virus disrupts one arm of this receptor-peptide system, the therapeutic question stops being "what do we add?" and becomes "what do we rebalance?" Biology runs on opposing forces, and good pharmacology learns to see them. Kinases and phosphatases. Cyclases and phosphodiesterases. ACE1 and ACE2. Dr. Insel returns repeatedly to his "gas pedals and brakes" frame — a lens that has quietly shaped how he reads both disease mechanism and drug targets across a long career. The lung's beta-2 story has been sitting in plain sight for fifty years. Type II pneumocytes carry the highest beta-2 receptor density in the body. Long-acting beta-agonists paired with glucocorticoids have been the mainstay of asthma treatment for decades. The connection to acute respiratory distress syndrome — and to the mechanism through which dexamethasone actually works — is, in his reading, underdiscussed rather than speculative. "Don't just do something. Stand there." A clinical mentor's line that became the frame for the lockdown months. Four papers in roughly two months — what Dr. Insel calls armchair science. Not casual, not opinion-writing; dry-lab pharmacology done with the same seriousness as bench work, just with different tools. A figure can travel further than the paper it came from. The schematic from the BJP paper was redrawn by The Economist, with attribution, for a general-audience article on COVID pathobiology. Dr. Insel notes wryly that it's the only paper his family has ever really responded to. The ethics of acting on conviction is its own paper. Midway through writing the angiotensin work, Dr. Insel realized no one had written criteria for how to decide about off-label use of a drug during a pandemic — when mechanism is compelling, safety is reasonable, and trial evidence isn't there yet. He is writing that paper with an ethicist and a law-school colleague. It is exactly the kind of work a pharmacologist does when the lab is closed. Episode Timeline Timestamps were generated using AI for readability. 00:00 Opening and 2020 Summit context 01:45 Dry-lab science — how the work shifted when the wet lab closed 02:37 Rereading the ACE inhibitor scare — and the BJP paper that followed 07:40 Expanding the hypothesis — PAR1, PAR4, and upstream pathobiology 11:00 Gas pedals and brakes — biology's architecture of opposing forces 14:00 Type II pneumocytes, beta-2 density, and the asthma parallel 22:40 The ethics of off-label drug use during a pandemic 25:00 Genetic determinants of severity — ACE1 isoforms and population data 28:40 Vaccine development speed and public trust 33:40 Staying sane — pickleball, walking, and community Selected Quotes "Don't just do something. Stand there. That's sort of what we've been doing. And I think we've made some contributions that are pretty interesting. I really want to do something to help people. That's what this is all about, really." — Dr. Paul Insel "Almost most biological systems are all about gas pedals and brakes. We have kinases and phosphatases. We have cyclases that make cyclic AMP and phosphodiesterases that degrade it. Nature has built in these systems consistently." — Dr. Paul Insel "If you would have told me three months ago that I was going to end up having a figure in The Economist — forget about one of the science journals — in The Economist…" — Dr. Paul Insel "It's still about GPCRs." — Dr. Paul Insel About this episode Dr. Paul Insel is currently a Distinguished Professor of Pharmacology and the University of California San Diego. Paul thinks broadly about science and has been actively publishing papers about his ideas on how COVID symptoms could be treated while we wait for a vaccine, particularly about ACE2 and angiotensin. For the past 30 years, he has been the Director of MD/Ph.D. training program at UCSD and has served as Editor or Senior Editor of numerous scientific journals, including but not limited to the Journal of Clinical Investigation, Molecular Pharmacology, British Journal of Pharmacology, and American Journal of Physiology-Cell Physiology. Dr. Paul Insel on the web Insel Laboratory Institute of Engineering in Medicine UC San Diego UCSD Profiles Google PubMed Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. 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<< Back to podcast list Strategic Partner(s) Nicole Perry-Hauser About Nicole (Nicki) Perry-Hauser I am a postdoctoral research fellow endeavoring to build a productive, independent scientific research career in adhesion G protein-coupled receptor (aGPCR) biology. My long-term research interests involve resolving signaling pathways downstream of aGPCRs and establishing how/if these receptors’ adhesive properties influence signaling events, and in turn, whether signaling impacts synapse formation and neuronal wiring. Mutations in aGPCRs have been linked to various neuropsychiatric phenotypes, and my work will provide a basis for understanding aGPCR biology in the nervous system. Nicole (Nicki) Perry-Hauser on the web LinkedIn Research Gate Pubmed Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

Explore how GPCR signaling shapes mosquito feeding and mating behaviors with Dr. Laura Duvall. Insights for GPCR researchers and functional assay innovators. << Back to podcast list Strategic Partner(s) Why Mosquitoes Hunt You: GPCR Control of Blood Feeding and Mating Scientific Abstract A female mosquito that has just fed on human blood stops seeking humans for three to four days while she digests that meal and develops eggs. Laura Duvall's lab has traced this suppression to a specific neuropeptide Y family receptor, one she first identified as a postdoctoral fellow and has since found expressed almost exclusively in an unexpected tissue, the mosquito rectum. Her group works at the intersection of neuropeptide signaling, behavioral genetics, and vector biology in Aedes aegypti, the species responsible for transmitting Zika, dengue, and chikungunya. This conversation traces her path from circadian rhythm research in Drosophila to mosquito behavior, and lays out why a receptor built to regulate host seeking and mating might offer a way to interrupt pathogen transmission at its source rather than treating each disease separately. What pulls Duvall back to this receptor personally is its apparent conservation: the same NPY family receptor she found in mosquito gut tissue has a close relative in the human colon, doing a job no one has fully worked out yet. About Laura Duvall runs a research lab in the Department of Biological Sciences at Columbia University, where her group studies how mosquitoes regulate innate behaviors, primarily blood feeding and mating. She trained in neuroscience during her PhD, characterizing how pigment dispersing factor and related GPCRs coordinate circadian clock cells in the Drosophila brain, then moved into mosquito research as a postdoctoral fellow with Leslie Vosshall at Rockefeller University. Her lab uses CRISPR based gene editing, automated behavioral assays, and video tracking to study neuropeptide Y family receptors in Aedes aegypti, with a particular focus on host seeking suppression and female mating receptivity. Scientific Themes of the Conversation - Neuropeptide Y family receptors as conserved regulators of feeding and reproductive behavior - Host seeking suppression in blood fed females as a druggable behavioral switch - Cross species pharmacological crosstalk between human and mosquito receptors - Unexpected receptor localization outside canonical neuronal tissue - Automated, experimenter free behavioral assays as a response to human bias in the data - Vector behavior disruption as an alternative to pathogen specific therapeutics Key Insights from the Conversation A single gene deletion reopened a closed behavioral window. Duvall's lab used CRISPR to mutate the receptor she had identified as important for host seeking suppression. Blood fed females that should have lost interest in humans for several days continued seeking hosts anyway. Watching one gene override such a strong, evolutionarily tuned behavioral drive was, in her words, almost magical. A neuropeptide receptor turned up in a tissue no one expected. When the lab went looking for where this NPY family receptor was expressed, they assumed brain tissue. Instead, expression was almost exclusive to the mosquito rectum, a structure Duvall says she did not know existed as a distinct entity until the result came back. The rectal finding stopped looking strange once the mammalian literature caught up. Humans and other mammals have NPY2 receptors in the colon, and non-neuronal excitable cells there are known to synthesize and release neurotransmitters. Work on neuropod and enterochromaffin cells in mammals has become a guide for what Duvall's lab looks for next in the mosquito gut. Removing the experimenter from the room removed a source of bias. Duvall's team built an automated system to deliver host associated cues to mosquitoes around the clock, including at 4am and in darkness, specifically because a human presence, and even which human is present, measurably skews mosquito attraction data. Baseline attractiveness to mosquitoes is real, stable, and not about soap. Referencing work from a former labmate, Duvall described how a person's attractiveness to mosquitoes stays consistent over time regardless of shampoo or soap, which is why her lab has to control carefully for who serves as the human stimulus in an assay. One receptor sits at the intersection of two very different behaviors. The same NPY family Duvall calls her favorite includes a receptor in the female mosquito that detects a male derived signal after mating and suppresses her receptivity to mate again, sometimes for the rest of her life. Disrupting it experimentally can leave females able to mate with multiple males. Disrupting one behavior could interrupt transmission of several diseases at once. Because Aedes aegypti transmits Zika, dengue, and chikungunya through the same host seeking behavior, Duvall argues that turning off attraction to humans at the level of the receptor could block all of these pathogens at their point of transmission, rather than requiring a therapeutic for each one. Episode Timeline - Growing up in rural North Carolina, where the path to science ran through a work study job in a lab - Choosing neuroscience and circadian rhythms as a graduate research focus - Studying pigment dispersing factor signaling in Drosophila clock cells, and a first entry point into GPCRs - An interview that turned into a mosquito postdoc with Leslie Vosshall - Identifying a neuropeptide Y family receptor important for blood feeding regulation - A CRISPR edit that reopened host seeking behavior in blood fed females - What CRISPR based mosquito gene editing looks like in practice, from guide design to the olfactometer assay - Moving to automated, video tracked behavioral assays to remove human bias from the data - Finding the receptor expressed almost exclusively in the mosquito rectum, and its parallel in the human colon - Disrupting host seeking behavior as a way to block transmission of Zika, dengue, and chikungunya - Building a mosquito research facility from scratch, and what day to day lab life looks like - The receptor behind mating suppression in female mosquitoes, and its favorite status in the lab Timestamps were generated using AI for readability. Selected Quotes "This mutant mosquito disrupting a single gene and changing this incredibly strong behavioral drive was something that was almost magical." "It's a neuropeptide receptor, but in fact it seems to be expressed exclusively in the mosquito rectum. A tissue that I did not know existed until we got this result." "There's nothing more satisfying than just sticking your arm in a tube and seeing if you can get them to turn down their attraction to your arm." "In some ways my view of neuroscience and signaling between the brain and the body is relatively narrow. It's really important to have these sensors everywhere in the system." Guest Links - LinkedIn: https://www.linkedin.com/in/laura-duvall-28a03485/ - Google Scholar: https://scholar.google.com/citations?user=Vk3KGSoAAAAJ&hl=en - Lab: https://www.duvalllab.com/ Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Annabelle Milner About Annabelle Milner Annabelle completed her undergraduate degree in Biomedical Sciences at the University of Bath. As part of the degree, she undertook a 1-year research-based placement at the Charles Perkins Centre in Sydney, investigating the effects of dietary carbohydrates on metabolic health with Dr. Jibran Wali. From here, she returned to the UK. She began her Ph.D. at Imperial College London with Prof Aylin Hanyaloglu, Prof Gary Frost, and Dr. Alastair Brown (Sosei Heptares), where she is currently a final year Ph.D. student. Annabelle’s Ph.D. work focuses on microbial-derived metabolites that signal through GPCRs expressed in the GI. In particular, she is looking at L- and D-lactate-activated HCAR1 signaling. She presented her Ph.D. work at the Society of Endocrinology Conference 2022 and was awarded the best oral poster prize. Outside the lab, she enjoys baking and swimming and has recently taken up paddle boarding. Annabelle Milner on the web Linkedin Researchgate Pubmed Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Tanishka S. Saraf About Tanishka S. Saraf " My research focuses on evaluating and targeting serotonin 1A receptors for therapeutic outcomes for Fragile X Syndrome. During my PhD, I learnt radioligand binding assays, behavioral assays, autoradiography, stereotaxic surgeries, electroencephalography, immunohistochemistry, mouse colony management and breeding. I would like to keep working in the central nervous system disorders realm to understand the neurobiology of neuropsychiatric disorders and to develop safe and effective treatments. " Tanishka S. Saraf on the web FRAXA Research Foundation Google Scholar ResearchGate LinkedIn Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Stephen Ferguson About Dr. Stephen Ferguson Dr. Stephen Ferguson is a Professor in the Department of Cellular and Molecular Medicine at the University of Ottawa. He did B.Sc. in biology at McGill University and received his Ph.D. under the mentorship of Dr. Brian Collier in the Department of Pharmacology and Therapeutics at McGill University (1994). He did his postdoctoral training with Dr. Marc G. Caron at Duke University (1994-1997), where he and his colleagues investigated the role of G protein-coupled receptor kinases and beta-arrestin in regulating G protein-coupled receptor endocytosis, trafficking, and signaling. He has held four Canada Research Chairs since 2001 and was previously a Heart and Stroke Foundation of Canada MacDonald Scholar (1998-2003) and Heart and Stroke Foundation of Ontario Career Investigator (2003-2016). He was a recipient of Canada's Top 40 under 40 award in 2004 and received Queen Elizabeth II, Diamond Jubilee Medal, in 2012. He has also received both Junior (2001) and Senior (2005) investigator awards from the Pharmacological Society of Canada. Most recently, in 2021, he was elected as a Fellow of the Canadian Academy of Health Science (FCAHS). His research career has focused on the investigation of the regulation of G protein-coupled receptors signaling mechanisms in health and disease. He currently holds multiple research grants from the Canadian Institutes of Health Research (CIHR) for his research investigating the role of metabotropic glutamate receptor signaling in Huntington’s and Alzheimer’s disease. Dr. Stephen Ferguson on the web Carlton University Canada Research Chairs Twitter ResearchGate LinkedIn Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

Jacob Lee and Jin Cho, co-founders of GeneMode, on the ten billion dollars American labs waste every year — and why rebuilding research software from scratch is the most direct path to faster cures. << Back to podcast list Strategic Partner(s) Jacob Lee and Jin Cho: Rebuilding the Software Layer Under Modern Research Most scientific research still runs on infrastructure built for a different century. Spreadsheets lock when two people open them. Freezer inventories live in a senior postdoc's head. An estimated ten billion dollars is spent every year in the United States rebuying reagents already sitting on a shelf nobody could find. In this conversation, Jacob Lee and Jin Cho — co-founders of GeneMode — describe what they saw when they looked at that infrastructure as outsiders and as scientists at once. Lee is a bioengineer whose first year of graduate school was defined by scheduling thirty-minute appointments on a senior postdoc's calendar just to access the lab's inventory software, and that experience is what turned frustration into a company. Cho came from engineering software for military drones at General Atomics, and was stunned when he saw what his friend's lab was paying for a tool that looked straight out of Windows XP. They talk about the slow architecture of drug discovery, the compounding cost of irreproducibility, and why rebuilding the tools scientists use every day is, for them, the most direct path to getting cures to patients faster. About the Guests Jacob Lee is the CEO and co-founder of GeneMode. He trained as a bioengineer and worked as a research scientist in stem cell and cancer labs before founding the company. His frustrations as a first-year graduate student navigating inaccessible lab software became the seed for GeneMode. He leads the company's product vision, focused on inventory, experiment management, and research reproducibility. Jin Cho is the CTO and co-founder of GeneMode. Trained in electrical and computer engineering, he began his career at General Atomics building software for military drones before reuniting with his high-school friend Lee to rebuild research tools from the ground up. At GeneMode he leads the engineering team and the platform's weekly release cycle. Scientific Themes of the Conversation The cost of irreproducibility — waste, delay, and the compounding friction of bad tools Access asymmetry in research — who gets to use the lab's software, and who waits Research software as infrastructure — why tools built for scientists behave differently than tools adapted to them The drug discovery timeline — preclinical, clinical, and regulatory phases, and where software actually matters Collaboration in shared labs — real-time editing, shared freezers, and the Excel-lock problem Lab automation and the hidden operating cost of being a scientist Key Insights from the Conversation Ten billion dollars vanishes every year into duplicate reagent orders. Lee describes an estimate that American labs spend roughly ten billion dollars annually on reagents they already own but can't locate. The cost isn't just money — it's the erosion of reproducibility that follows from not knowing what's in the freezer. Access to the lab's tools is often rationed by seniority. In Lee's first graduate lab, only the principal investigator and a senior postdoc had logins for the expensive inventory software. As a student, he scheduled thirty-minute appointments on a postdoc's calendar to learn how to use a tool the lab had already paid thousands of dollars for. Excel is the default research tool because no one built a better one for scientists. The co-founders argue that most lab software wasn't built for scientists — it was built for general business use and retrofitted. That explains the locked files, the manual re-entry, the outdated look, and the poor fit with how research actually moves. Lab infrastructure is the hidden variable in drug discovery timelines. COVID-era conversations about why vaccines take eighteen months tend to focus on the clinical and regulatory phases. Lee reframes the question toward the preclinical phase, where data management and reproducibility quietly compound every delay downstream. Private and shared workspaces both matter, even in collaborative labs. Cho and Lee describe designing for the reality of shared benchwork: most labs want everything visible to everyone, but individual scientists still need space for protocols-in-progress or personal collections they're not ready to publish internally. Fast release cycles are a signal of infrastructure maturity. Cho describes shipping updates weekly, prioritizing customer-reported bugs and feature requests with a design-to-test-to-ship loop that most scientific software vendors don't attempt. That cadence is itself a philosophical statement about who the tool serves. A ninth-grade English class is an unlikely origin for scientific infrastructure. The GeneMode story starts with two teenagers in the same high-school classroom, different majors, different career paths, and a late-night message asking whether lab software could be hacked together in a weekend. The answer turned out to be no — but the question turned into a company. Episode Timeline Timestamps were generated using AI for readability. 00:00 Summit week welcome and episode introduction 01:34 Meeting the co-founders — CEO Lee and CTO Cho 03:11 From stem cell research to bioengineering frustration 04:03 The ninth-grade English class where the story starts 04:59 Seeing Windows XP-era software inside a modern lab 07:01 What GeneMode actually does that Excel can't 10:15 Onboarding a ten-person lab onto one shared platform 12:18 Ten billion dollars in wasted reagents 16:13 What's coming next — tools across the experimental lifecycle 18:32 Algorithms that predict when reagents will run out 22:43 A weekly release cycle built around user feedback 24:13 Why vaccines still take eighteen months Selected Quotes "A lot of the problems that we're solving is around data sharing for scientists — by having inventory, experiment management, applications, and data all in one collaborative workspace." — Jacob Lee "It looks like software that was built a couple of decades ago. And what surprised me even more was his lab was paying thousands of dollars for this legacy-looking software. I was mind-blown." — Jin Cho "In a lab of ten people, only the principal investigator and a very senior postdoc had access to the software. And as a student, I had to actually schedule times on my postdoc's calendar in thirty-minute segments just to learn how to use that tool." — Jacob Lee "The end goal is really much bigger than helping scientists manage their research projects or inventory. Our mission is to make that research repeatable and reproducible so that we can get those cures faster." — Jacob Lee About this episode In this special episode of the Dr.GPCR podcast , I sat down with the co-founders of Genemod . Jacob Lee and Jin Choe met in ninth grade in English class and have been friends since. Although both went to the same college, Jacob and Jin choose different career paths. One day as they were catching up, Jacob shared his struggles of managing samples and an incredible amount of data and projects in the lab with Jin. Our of this need Genemod was born. Today, Genemod has built a freezer management tool and a project management tool where scientists can manage their reagents, samples, and projects on one intuitive platform. The team is planning on building even more tools that will make Genemod the go-to platform for all research scientists to make research more efficient. Genemode on the web Website Jacob Lee on LinkedIn Jacob Lee on Dr. GPCR Ecosystem Jin Choe on LinkedIn Jin Choe on Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Silvia Sposini About Dr. Silvia Sposini " I'm originally from Rome, Italy, where I studied Biological Sciences as a BSc student. I moved to London as a short experience (3 months) during my MSc but I ended up staying for a full year and and a PhD! During my time in London I investigated regulatory mechanisms of GPCR action, namely dimerization and membrane trafficking, in Dr Aylin Hanyaloglu 's lab at Imperial College London. In 2018 I got married and moved to France, to join the Interdisciplinary Institute for Neurosciences in Bordeaux. Still working on GPCR trafficking but this time in neurons. In 2021 I became mum of a gorgeous baby girl, Elena. I am currently funded by a postdoctoral fellowship from Wellcome Trust, working on a collaborative project (Dr Hanyaloglu's lab at ICL + Dr Perrais' lab at IINS) focused on understanding the interplay between GPCR signalling and trafficking in neurons using microscopy and proteomics based techniques. " Dr. Silvia Sposini on the web Bordeaux Neurocampus LinkedIn ResearchGate X (Twitter) Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Jean Martin Beaulieu About Dr. Jean Martin Beaulieu Dr. Beaulieu received a Ph.D. in Neurological Sciences from McGill University and completed his post-doctoral training at Duke University. Prior to his recruitment Dr. Beaulieu was an associate professor and Canada Research Chair (Tier2) in the Department of Psychiatry and Neuroscience at Laval University. Dr. Beaulieu’s research is aimed at understanding how cellular and molecular mechanisms regulated by psychoactive drugs intersect with genetic risk factors for mental illnesses such as schizophrenia, depression, and bipolar disorder. Dr. Beaulieu has pioneered work establishing a role for Beta-arrestin signaling in the brain in vivo and has established its importance in D2 dopamine receptors (D2R) functions. These receptors belong to the super-family of G-protein coupled receptors (GPCR), the major molecular target for drug development. In particular, D2R is the main pharmacological target of antipsychotic drugs prescribed for schizophrenia and bipolar disorders. Work by the Beaulieu Lab has demonstrated that mood stabilizer drugs (e.g. lithium) used for bipolar disorder therapy target signaling mechanisms regulated by dopamine receptors, thus providing a framework to understand how different drug classes can engage overlapping cellular mechanisms to exert their action. The Beaulieu group is presently investigating how cell surface express proteins can act as allosteric modulators of D2R signaling and explores the potential usefulness of beta-arrestins for the development of new pharmaceutical agents. Translational validation is important to validate findings obtained from experimental models research and bridge the gap between bench and bedside. Working in collaboration with geneticists, the Beaulieu-Lab has identified interactions between cellular mechanisms engaged by D2R and psychiatric drugs with genetic risk factors implicated in schizophrenia by large whole-genome association studies (GWAS) in humans. These investigations have led to the identification of an RNA binding protein (FXR1P) involved in the regulation of protein synthesis as a potential downstream effector of the action of mood stabilizers and other psychoactive drugs. In addition to basic research, the Beaulieu group is also actively implicated in translational research and industry collaboration to develop new drugs and drug development technology. Dr. Jean Martin Beaulieu on the web University of Toronto Google Scholar LinkedIn ResearchGate Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Simone Prömel & Dr. Ines Liebscher About Dr. Simone Prömel Simone Prömel is currently a professor of cell biology at the Heinrich Heine University Düsseldorf, Germany. Being a biochemist by training, she completed her Ph.D. at the Institute of Biochemistry at the University of Oxford, UK. During this time, she discovered her love for Adhesion GPCRs and started delineating the molecular mechanisms of the Adhesion GPCR Latrophilin-1. These extraordinary receptors, about which there was not much known other than that they are huge and somehow play important roles in health and disease, fascinated her so much that she continued working on them when she started her own lab at Leipzig University. There she focused on the different modes of action of Adhesion GPCRs and found that they do not only mediate classical G protein signals into cells but can also communicate solely via their N termini. Today, she and her team are working on the questions of how Adhesion GPCRs integrate the different signals on a molecular level and how these are translated into physiological functions in various model organisms. Together with Ines Liebscher, Simone is leading an EU-funded COST Network on Adhesion GPCRs: CA18240 Adher´n Rise. Dr. Simone Prömel on the web Prömel Lab Pubmed Researchgate Twitter Dr. GPCR Ecosystem About Dr. Ines Liebscher Dr. Liebscher is a Professor at the Rudolf Schönheimer Institute of Biochemistry at the Medical Faculty of the Leipzig University. During her medical studies in Leipzig, she had her first encounter with an orphan GPCR as the subject of her MD thesis. Being faced with the vast unknown biochemical and pharmacological territory that would be helpful to study orphan receptors she enrolled in the MD/Ph.D. program of Leipzig University. Her postdoctoral work leads her to investigate a whole family of orphan receptors: adhesion GPCRs. With the little knowledge on these receptors available, there were multiple questions to tackle. Starting with proving and characterizing G-protein coupling, Ines spends several years studying the activation mechanism of adhesion GPCRs. In collaboration with great fellow adhesion GPCR scientists around the globe she established a tethered agonist -extracellular matrix- mechano-activation- activation scenario that forms the basis for her current projects that focus on the structural and physiological implications of these findings. Together with Simone Prömel, Ines is leading a COST Network on adhesion GPCRs: CA18240 Adher'nRise. Dr. Ines Liebscher on the web Website LinkedIn Researchgate Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

Randy Hall on the receptor tail the field ignored, the adhesion GPCR experiment that did the opposite of what he expected, and writing Lefkowitz's memoir. << Back to podcast list Strategic Partner(s) Randy Hall: Adhesion GPCRs and the Tail Nobody Wanted SCIENTIFIC ABSTRACT Most of what the field now takes for granted about the C terminus of a GPCR was, in the mid 1990s, considered uninteresting. Randy Hall arrived in Bob Lefkowitz's lab from a background in ionotropic glutamate receptors, noticed that the beta adrenergic receptors carried short motifs resembling the ones that recruit scaffold proteins to NMDA receptors, and asked what bound there. He was told the answer was nothing. At the time, the lab chasing the first GPCR crystal structure was cutting the tail off entirely. What he found reframed how the field explains why closely related receptor subtypes produce different effects on cell physiology. This conversation follows that thread into adhesion GPCRs, a subfamily of 33 human receptors with enormous extracellular N termini that cleave themselves and then stay together. Hall describes the experiment designed to kill receptor signaling that instead amplified it, the tethered agonist model his lab proposed in 2011, and why a family once dismissed as undruggable now looks like a serious therapeutic frontier. He also explains how he came to write the memoir of his mentor, a project he pitched three times over fifteen years before the answer was yes. ABOUT RANDY Randy Hall is Professor of Pharmacology and Chemical Biology at Emory University School of Medicine, where he has run his lab since 1999. He trained with Gary Lynch at UC Irvine on ionotropic glutamate receptors, then with Thomas Soderling at the Vollum Institute on receptor trafficking and phosphorylation, before joining Bob Lefkowitz's lab at Duke to work on adrenergic receptor regulation. His lab uses proteomic and interaction screening approaches to map the proteins that bind GPCR intracellular tails, and has published on receptors from the adrenergic, purinergic, glutamatergic, GABAergic and adhesion subfamilies. Recent work centers on GPR37 and GPR37L1 and on the adhesion receptors BAI1, BAI2 and GPR56, with a particular focus on disease associated mutations that disturb receptor signaling or trafficking. He is a Fellow of the AAAS and coauthor, with Bob Lefkowitz, of the 2021 memoir A Funny Thing Happened on the Way to Stockholm. SCIENTIFIC THEMES OF THE CONVERSATION - Why the GPCR C terminus turned out to determine subtype specific function - Adhesion GPCRs: self cleaving receptors, huge N termini, and the tethered agonist model - Constitutive activity as a disease mechanism, from the alpha 1 receptor to BAI2 - Orphan receptors and where the next generation of GPCR drugs will come from - In silico screening, and what human plus machine collaboration means for drug discovery - Problem selection: how young scientists choose what to spend years on - Writing a scientific memoir, and why honesty is the load bearing part KEY INSIGHTS FROM THE CONVERSATION Changing subfields is when discovery happens Hall deliberately chose a second postdoc in a different receptor family rather than extending his graduate work. He argues that staying close to a hot topic feels safe but narrows a scientist's development, and that the moment you carry one field's questions into another is often the most productive window of a career. His own case is the evidence: NMDA receptor scaffolding logic applied to beta adrenergic receptors. The tail everyone was discarding When Hall asked what the C termini of the beta adrenergic receptors did, the lab's answer was that they could be removed with G protein coupling intact. The structural effort underway at the time simply deleted them. That consensus is precisely why he went looking, and the distinct binding partners he found for beta 1 and beta 2 offered an explanation for how two subtypes coupling to the same G protein can have opposite effects on cell physiology. Skepticism first, then a crowded field The early data drew hard questions at Gordon conferences from senior figures who were not convinced. Within a few years, dozens of labs were running similar studies across every GPCR subfamily. Hall describes the real measure of acceptance as the moment other groups start doing the experiments themselves. The experiment that did the opposite Predicting that an endogenous ligand acted on the large N terminus of GPR56, his lab truncated it, expecting a dead receptor. Signaling increased massively instead, and the same held for BAI1. That inversion became the basis for the model his lab proposed in 2011, in which removing or reconfiguring the N terminus unveils a cryptic tethered agonist, and it has since been reproduced across the family by other groups. From undruggable to promising Drug development veterans long treated large adhesive proteins as poor targets because their interaction interfaces are too big to disrupt with small molecules. Hall's counterpoint is that adhesion GPCRs are not only adhesive proteins, they are also GPCRs, with a seven transmembrane pocket. Screening work has since produced agonists and antagonists, and the first cryo EM structure of an adhesion GPCR, GPR97, showed glucocorticoid binding, raising the possibility that steroid activation of G protein pathways has been hiding in this family. When receptors are tuned and mutations detune them The BAI2 mutation Hall's lab linked to a neurodegenerative condition sits on the C terminus and makes the receptor constitutively overactive, pointing back to the protein interactions he has studied since the 1990s. He traces the concept to basic work by Susanna Cotecchia on the alpha 1 receptor in the early 1990s, research with no clinical intent that became the template for explaining a long list of human diseases. Choose important problems, not easy ones Hall's advice to junior scientists is that trivial questions are not measurably easier to solve than important ones, so the years spent are better invested in something that matters. He recommends heading for subfields in turmoil, where there is disagreement and unsolved mystery, with the single constraint that the technology to answer the question must already exist. EPISODE TIMELINE Timestamps were generated using AI for readability. - 00:00 Opening announcements - 01:34 Introducing Randy Hall - 02:02 The Feynman book, and pitching a memoir to Bob Lefkowitz three times - 06:45 Deciding which stories survive, and finding a publisher who believed in science memoirs - 17:03 Nature walks, synaptic plasticity, and falling for the first event in cell signaling - 19:39 Switching subfields, and spotting a motif nobody was looking at - 23:51 Pushback at Gordon conferences, and what acceptance actually looks like - 26:34 Moving the lab toward orphan and adhesion GPCRs - 34:00 The truncation that was supposed to kill signaling - 37:34 Pulling the pin from the grenade: the tethered agonist model - 39:38 Are adhesion GPCRs druggable, and what GPR97 changed - 46:46 In silico screening, chess, and humans working alongside machines - 52:09 Disease mutations across the adhesion family - 1:00:41 Choosing important problems over easy ones - 1:07:10 Openings in the Hall lab SELECTED QUOTES "That was how lowly regarded the C terminus was. They were just throwing it in the trash." "Go for subfields where the seas are rough and the sky is dark and there are a lot of mysteries." "If you are surprised by the result of your own experiment, then probably other scientists will also be surprised." "There is no connection between the importance of a problem and how easy it is to solve." GUEST LINKS - Hall Lab: http://www.pharm.emory.edu/hall/index.html - LinkedIn: https://www.linkedin.com/in/randy-hall-79923839 - Google Scholar: https://scholar.google.com/citations?user=tfsXwHUAAAAJ&hl=en&oi=ao - ResearchGate: https://www.researchgate.net/profile/Randy-Hall - A Funny Thing Happened on the Way to Stockholm: https://www.simonandschuster.com/books/A-Funny-Thing-Happened-on-the-Way-to-Stockholm/Robert-J-Lefkowitz/9781643136387 - Dr. GPCR Ecosystem: https://www.ecosystem.drgpcr.com/search?q=Randy+Hall Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Inês Pinheiro, Monserrat Avila Zozaya & Yamina Berchiche About Inês Pinheiro PharmD by training and Ph.D. candidate in Hartley's lab at the University of Geneva. As a young researcher fascinated by chemokine receptors, molecular pharmacology, drug discovery, and immuno-oncology. Inês Pinheiro on the web LinkedIn University of Geneva Twitter Dr. GPCR Ecosystem About Monserrat Avila Zozaya I am a cell biologist interested in studying GPCRs, especially adhesion GPCRs. Motivated by my scientific passion, I recently started a postdoctoral fellowship to study the role of GPCRs in the mechanisms of pain and its comorbidities. Monserrat Avila Zozaya on the web Antony Boucard Lab Dr. GPCR Ecosystem About Yamina Berchiche Dr. Yamina A. Berchiche is the founder of Dr. GPCR, an ecosystem designed to bring together stakeholders interested in using G-Protein Coupled Receptors (GPCRs), that control virtually everything in the body, as drug targets. The mission of Dr. GPCR is to accelerate GPCR drug discovery by sharing the latest research and technology advances in the field and providing exposure to scientists through the Dr. GPCR podcast. Dr. Berchiche obtained her Master’s and Ph.D. in Biochemistry at the University of Montreal in Canada before training at The Rockefeller University in New York and the National Institutes of Health in Bethesda, Maryland. She developed expertise over the past two decades studying structure/function relationships of GPCRs using live-cell bioluminescence resonance energy transfer (BRET). Her work focused on chemokine receptors, members of the GPCR family that control cell movement in the body. Yamina Berchiche on the web Website LinkedIn Facebook Twitter ResearchGate PubMed Google Scholar Dr. GPCR Ecosystem Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. GPCR Board About Dr. Yamina Berchiche "Dr. Yamina A. Berchiche is the founder of Dr. GPCR, an ecosystem designed to bring together stakeholders interested in using G-Protein Coupled Receptors (GPCRs) that control virtually everything in the body as drug targets. The mission of Dr. GPCR is to accelerate GPCR drug discovery by sharing the latest research and technology advances in the field and providing exposure to scientists through the Dr. GPCR podcast. Dr. Berchiche obtained her Master’s and Ph.D. in Biochemistry at the University of Montreal in Canada before training at Rockefeller University in New York and the National Institutes of Health in Bethesda, Maryland. She developed expertise over the past two decades studying structure/function relationships of GPCRs using live-cell bioluminescence resonance energy transfer (BRET). Her work focused on chemokine receptors, members of the GPCR family that control cell movement in the body." Dr. Yamina Berchiche on the web Website LinkedIn Facebook Twitter ResearchGate PubMed Google Scholar Dr. GPCR About Dr. Maria Waldhoer "I am a pharmacologist with a ~30 years background in academia and industry, working both in big pharma and biotech settings. My experience in basic research at several universities worldwide and early R&D at Novo Nordisk A/S allowed me to shape a swiss start-up company from a scientifc idea to a thriving Biotech focusing on Systems Biology & AI to accelerate the quest for novel & safer drugs on GPCRs. After a well needed break from the grind, I am now a scientific/business consultant for clients both in Academia and in the Life sciences and Healthcare industry. I am a recent convert and strong advocate for integrating mindfulness and mental wellbeing into demanding work routines." Dr. Maria Waldhoer on the web LinkedIn T witter Pubmed Dr. GPCR About Dr. JoAnn Trejo "Dr. JoAnn Trejo earned her Ph.D. at UC San Diego. She completed her postdoctoral fellowship at UC San Francisco under the guidance of Professor Shaun Coughlin where she worked on the newly discovered protease-activated GPCRs. Dr. Trejo joined the faculty in the Department of Pharmacology at the University of North Carolina in 2000 and then moved to UC San Diego School Medicine, Department of Pharmacology in 2008, where she quickly rose through the ranks to tenured professor in 2012. In 2014, she was appointed Vice-Chair of the Department of Pharmacology. The long-term goal of Dr. Trejo’s research program is to gain a thorough and mechanistic understanding of processes that control cell signaling by protease-activated receptors (PARs) and the impact on vascular inflammation and cancer progression. PARs are GPCRs that are activated through an atypical irreversible proteolytic mechanism. The precise control of PAR signaling is critical for proper temporal and spatial dynamics of signaling and appropriate cellular responses. Discovering new aspects of PAR signaling is important for increasing the fundamental knowledge of GPCR biology and for the identification of drug targets and future drug development. Dr. Trejo’s research has focused on PAR1, which has important functions in hemostasis, thrombosis, inflammation, and cancer and is an important drug target. She has made numerous important discoveries related to the mechanisms that control PAR1 signaling and closely related family members and published extensively on this topic. Dr. Trejo has been continuously funded by the NIH for >20 years and was a recipient of the prestigious American Heart Association Established Investigator Award. Her laboratory is the recognized expert on protease-activated receptors, particularly PAR1, and over the years she has discovered novel aspects of GPCR biology, acquired critical expertise, and rigorous approaches to examine PAR1 function using human cultured cells and mouse models. Dr. Trejo has presented her studies at 52 national/international meetings and 66 academic seminars across the U.S." Dr. JoAnn Trejo on the web UC San Diego Trejo Lab Wikipedia LinkedIn Google Scholar Orcid Twitter UC San Diego School of Medicine Researchgate Dr. GPCR About Anne Marie Quinn "Anne Marie Quinn has a long and varied work experience in the biocomputing and bioinformatics fields. From 1987 to 1994, they were the Director of Biocomputing at The Salk Institute, where they managed institute-wide network and biocomputing services, served on the Steering Committee of the San Diego Supercomputer Center, and provided consultation for genetic sequence analysis, molecular modeling and database searching. In 1994, they became a Bioinformatics Scientist at CuraGen Corporation. From 1995 to 2002, they worked at Yale University School of Medicine as the Bioinformatics Core Facility Manager, where they managed a technical support team providing scientific data analysis and database development services, contributed analytic support resulting in authorship of numerous scientific publications and new funding, and developed and co-taught a new course in bioinformatics for graduate students. From 2002 to 2006, they were a Senior Application Scientist at Accelrys, where they were the technical point of contact for customers assessing features of software products for drug discovery and genomic analysis, delivered technical presentations and software demonstrations to prospective customers worldwide, and developed web-based case notes, marketing seminars and product literature for scientific software. Finally, since 2006, they have been the Chief Executive Officer at Montana Molecular, LLC. Anne Marie Quinn attended Yale University from 1998 to 2000, where they earned a Master of Public Health (MPH) degree in Biostatistics and Bioinformatics. Prior to that, they obtained a Bachelor of Arts (B.A.) degree from California State University, Long Beach in 1982." Anne Marie Quinn on the web Google Scholar The Org LinkedIn Twitter Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

Sokhom Pin shares how he built a biotech career around GPCRs, designed a custom PhD path, and led teams through empowerment and purpose. << Back to podcast list Strategic Partner(s) GPCR Pharmacology, Career Twists & Serendipity with Sokhom Pin From the Bench to the Boardroom Sokhom Pin’s story begins not with prestige or privilege but with grit and commitment. From his early work as a technician at Johns Hopkins Hospital to leading biology at Servo Therapeutics, Sokhom’s journey is rooted in practicality and purpose. He shares: "All my industry experience has been GPCR-focused." Starting at DuPont, then BMS, Novartis, and eventually founding in vitro pharmacology departments, Sokhom always stayed anchored to G protein-coupled receptors (GPCRs). Family First, Always The decision to shift from academia to industry wasn’t driven by disillusionment—it was about responsibility. “I had two kids and realized I just couldn’t support a family on a technician’s salary.” This pragmatic decision led him to high-throughput screening at DuPont, proving that scientific ambition doesn’t have to mean sacrificing personal commitments. Falling in Love with GPCRs GPCR pharmacology captured his scientific curiosity. Sokhom recalls how binding assays at BMS introduced him to the depth and complexity of receptor pharmacology: “It’s not just about IC50s. There’s allosterism, receptor desensitization… it opened a whole new world.” This moment became pivotal—transforming technical proficiency into passion. Designing a Non-Traditional PhD While working full-time, Sokhom architected a one-of-a-kind PhD program between BMS and UConn. “I had to find a way. I wanted a PhD, but I couldn’t quit my job.” Through strategic coordination, he executed a PhD entirely in the industry setting—efficient, targeted, and rooted in real-world projects like CGRP receptor antagonists. From Scientist to Leader At Alkermes, Sokhom took his first leadership role and finally experienced the power of empowerment . “That’s the moment that changed my entire career. I was trusted to build a team from scratch.” He focused on culture—ensuring passion and purpose drove performance. The Power of the Right Culture Whether it was Alkermes or Cerevel, Sokhom emphasized that team culture trumps individual genius . “It doesn’t matter how brilliant someone is—if they’re toxic, I don’t want them on the team.” He built what others called the “happiest team at Alkermes,” showing that joy and scientific rigor aren’t mutually exclusive. Network or Miss Out One powerful shift came when Sokhom leaned into networking—despite being an introvert. “I changed from being an extreme introvert to someone who thrives on connection.” His story underscores how something as simple as forwarding a resume or reaching out for coffee can change careers. The Lifecycle of GPCR Popularity Sokhom has witnessed the waves of scientific fashion: “There was a time GPCRs were hot, then ignored. Now they’re back.” His unwavering dedication through these cycles became an asset—many others shifted focus, leaving a smaller, highly skilled group of GPCR specialists. Lessons from Molecules and Mentors He draws inspiration from scientific complexity and colleagues like Arthur Christopoulos and Terry Kenakin. “What fascinates me is how the same molecule behaves differently depending on one amino acid.” He blends classical receptor pharmacology with biosensor technology, always adapting to new tools and insights. Don’t Let Weakness Define You The episode ends with a deeply human reflection: “Don’t let your weakness define your life. Overcome it. I used to sweat thinking about presentations. Now I love them.” Whether it’s networking, leadership, or technical mastery, Sokhom’s message is clear: keep evolving, and don’t settle. Key Takeaway Sokhom Pin's journey is a masterclass in scientific persistence , non-traditional success , and values-driven leadership . For any scientist navigating career uncertainty—his story is both roadmap and inspiration. About Sokhom Pin Sokhom Pin is a receptor pharmacologist with over 20 years of drug discovery research in the pharmaceutical industry, where he works mainly on GPCRs as therapeutic targets. He is passionate about mechanistic profiling of therapeutic molecules as well as drug discovery in general. Outside of science Sokhom enjoys outdoor activities such as hiking, boating, fishing, and biking. Sokhom Pin on the web LinkedIn Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

Join us in strengthening the global GPCR community. Your tax-deductible donation supports education, collaboration, and innovation. Dr GPCR is a 501(c)(3) non-profit. 501(c)(3) Non-Profit Help Us Build a Global Home for GPCR Science Your donation bridges the gap between academia and biotech — transforming knowledge into real-world impact, faster. Make a Contribution Secure via Wix Payments - Tax-deductible - One-time or recurring Where Your Donation Goes? Fueling Every Corner of the GPCR Ecosystem Every contribution directly supports the programs, tools, and gatherings that make this community thrive. 🎓 Dr. GPCR University Expanding cutting-edge educational programs — new lessons, interactive modules, and resources accessible to GPCR professionals everywhere. 💼 Job Board & Career Growth Helping researchers and biotech companies find the right opportunities to grow together through our community job board. 🤝 Retreats & Happy Hours Free and affordable gatherings that foster collaboration and mentorship across disciplines — connecting scientists, founders, and innovators. ⚙️ Community Infrastructure Maintaining and improving the tools, platforms, and systems that keep the Dr. GPCR Ecosystem open, reliable, and thriving. Choose Your Impact Every Gift Moves the Science Forward Whether it's keeping Happy Hours free or funding the next scholarship, your contribution makes a tangible difference. $25 Supporter Keeps Dr. GPCR Happy Hours and community events free or affordable worldwide. Donate $25 $1,000 Catalyst Funds scholarships, retreats, and mentorship opportunities for early-career GPCR researchers. Donate $1,000 Most Popular $250 Champion Expands University content with new lessons, updated materials, and interactive learning modules. Donate $250 $5,000+ Visionary Powers new educational initiatives and programs that shape the future of GPCR research. Donate $5,000 🎁 Give the Gift of Learning $500 Gift a Membership Donate a full year of Dr. GPCR University Premium to a colleague, mentee, or even yourself — the gift of cutting-edge GPCR education. Gift Premium Access ⭐ Full Partner Recognition $20,000+ Strategic Partner Recognized across Dr. GPCR channels — logo on our website, acknowledgment in podcasts, videos, and events, and a direct line to our leadership. Become a Partner Donate Frequency One time One time Monthly Monthly Yearly Yearly Amount $25 $25 $250 $250 $1,000 $1,000 $5,000 $5,000 Other Other 0/300 Comment (optional) Donate $25 Donor Recognition Your Generosity, Acknowledged We believe every contribution deserves recognition. ✉️ Personal Thank-You Every donor receives a personal thank-you email and tax receipt. 🎙️ Public Acknowledgment Selected donors are thanked in podcast intros, videos, and events. ⭐ Strategic Partner Status At $20K+, your logo is featured on our website and community pages, with acknowledgment across all Dr. GPCR channels. Frequently Asked Questions Common Questions Is my donation tax-deductible? Yes. Dr. GPCR is a registered 501(c)(3) non-profit organization. Contributions are tax-deductible to the extent permitted by law. Can I donate on behalf of a company? Yes — use the "Comment" section in the donation form to add the company name, and we'll provide an invoice/receipt. Can I set up a monthly donation? Absolutely. Monthly donations sustain long-term programs and can be changed at any time through the donation form. Will I be recognized publicly? Yes — we love thanking our donors through our channels and platform. You can also opt out if you prefer privacy. Help Us Close the Gap Between Academia and Biotech Together, we can accelerate GPCR discoveries and develop more effective drugs for everyone. Donate Now

<< Back to podcast list Strategic Partner(s) Anything BUT GPCRs with Dr. Mikel Garcia-Marcos About Dr. Mikel Garcia-Marcos "I was trained as a biochemist and molecular biologist during my Ph.D (2005) in Spain and Belgium, and subsequently as a cell biologist during my postdoc (2006-2011) with Dr. Marilyn Farquhar (UC, San Diego), a pioneer of modern Cell Biology. All my formal training was in the area of signal transduction, and I continued to work on this area since I established my own laboratory in the Department of Biochemistry at Boston University in 2012. My research aims to understand the mechanisms and consequences cell communication via heterotrimeric G-proteins (Gαβγ) because they represent major intracellular hubs of signaling with very direct biomedical relevance. To achieve this goal, we use a wide range of established approaches (biochemistry, cell biology, genetics) and experimental systems (purified proteins, cultured cells, model organisms) in combination with the development of novel tools (biosensors, chemogenetics, optogenetics). Our ongoing efforts have direct implications in cancer, embryonic development defects, and neurological disorders." AI Summary In the podcast episode "Anything but GPCRs" featuring Dr. Mikel Garcia-Marcos, the host Yamina explores Dr. Garcia-Marcos's academic journey, which spans training in Spain, Belgium, and a postdoctoral fellowship at UC San Diego, where he navigated a career focused on G protein-coupled receptors (GPCRs) while aiming to maintain broad scientific interests. Dr. Garcia-Marcos shares insights on transitioning from postdoctoral research to leading his own lab, addressing the challenges of applying for academic positions and the importance of networking, adaptability, and mentorship in fostering a collaborative research environment. The conversation further delves into the dynamics of managing a diverse team, emphasizing the role of personality assessments in enhancing team cohesion and performance. Dr. Garcia-Markos reflects on milestones in his research journey, reinforcing the passion that drives scientists in the GPCR field, and engages listeners to connect with the podcast for a richer community experience. Dr. Mikel Garcia-Marcos on the web Boston University LinkedIn Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>

<< Back to podcast list Strategic Partner(s) Dr. Gregory Tall About Dr. Gregory Tall " Dr. Gregory Tall earned his Ph.D. in Biomedical Sciences from U.T. Southwestern Medical Center with Bruce Horazdovsky, Ph.D. They worked on the interactome of yeast and mammalian Rab5 homologs including identification of Rab5 GEFs. In 2000, Dr. Tall moved upstairs to conduct his postdoctoral work on heterotrimeric G proteins and the novel interactor, Ric-8 with Alfred Gilman, M.D. Ph.D. In 2007, Dr. Tall joined the faculty in the Department of Pharmacology and Physiology at the University of Rochester Medical Center, there establishing his lab and major research directions. Dr. Tall moved to the University of Michigan in 2016 as an Associate Professor of Pharmacology and is a current active member of the department. The current goals of the Tall lab are to understand the basic mechanism by which Ric-8 proteins fold all heterotrimeric G protein alpha subunits, to exploit a Ric-8-based technology to purify recombinant G proteins and to use the G proteins in assays to explore the mechanisms of action of the 33-member adhesion GPCR family or Family B2 GPCRs. We found that adhesion GPCRs are activated by a tethered peptide agonist mechanism that differed from the common example known at the time, protease activated receptors (PARs). PARs have an N-terminal leader sequence that is clipped by exogenous proteases to reveal a new N-terminus that serves as the tethered agonist. Adhesion GPCRs pre-cleave themselves and the two resultant fragments of the receptor remain together to conceal the tethered peptide agonist. Mechanical dissociation of the two fragments aided by protein binding ligands and cell movement serves to decrypt the tethered agonist for binding to its orthosteric site. Our current goals are to explore this mechanism in detail and to understand how it may happen for the 33 adhesion GPCRs in complex physiological contexts…one being our discovery that GPR56 is the platelet receptor that senses collagen and shear force to initiate the platelet activation program. Dr. Tall has been continuously funded by the NIH since receiving an early RO1 award at Rochester. He has continued funding at Michigan through the MIRA R35 program. Dr. Tall has presented his work at 59 invited seminars including national and international meetings and academic departmental seminars. " Dr. Gregory Tall on the web The Tall Lab University of Michigan Google Scholar Twitter Dr. GPCR Unlock the Full Dr. GPCR Learning Ecosystem ✔ Full Masterclass library ✔ Terry's Pharmacology Corner ✔ Advanced GPCR courses ✔ Scientific discussions → Become Premium Upcoming Live Expert Sessions ➚ 🔒Explore the Full Masterclass ➚ Enjoying the Dr. GPCR Podcast? Leave a Review. Leave a quick review to help more scientists find the show—and help us keep improving every episode. It takes <60 seconds and makes a big difference. ★ Review on Apple Podcasts ★ Rate on Spotify ✉️ Send feedback to the team Thanks for listening to this podcast episode Follow us on your favorite Podcast Player << Previous Podcast Episode Next Podcast Episode >>