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Questions about how opioids impair breathing, why xylazine complicates interventions, and how receptor-level While writing a literature review on opioid and alcohol addiction susceptibility, something shifted. This approach makes her models not just rigorous, but translational—bridging the gap between receptor She is especially interested in mu-opioid receptor signaling  and how xylazine, as an alpha-2 adrenergic That personal loss transforms complex receptor pharmacology into something immediate and human.

Bigger Picture: GPCR Science Meets Public Health At its core, Catherine Demery’s research  is about receptors and signaling pathways—how mu-opioid  and alpha-2 adrenergic receptors  interact to disrupt breathing Fentanyl acts with devastating potency at the mu-opioid receptor , while xylazine exerts sedative effects Fentanyl, through the mu-opioid receptor, blunts the brainstem’s inspiratory drive so that each breath By displacing opioids from the mu-opioid receptor, it restores breathing within minutes.

There, she chose to write a review on genetic variation in susceptibility to alcoholism and opioid addiction—a Returning to the Opioid Questions That Mattered Now, as a PhD candidate in the Traynor and Anand labs at the University of Michigan, Catherine is focused on the mechanisms of opioid-induced respiratory "I've always been really passionate and somewhat sensitive to people who struggle with opioid abuse.

the University of Michigan, walks us through how positive allosteric modulators (PAMs) targeting the mu-opioid receptor could preserve pain relief while reducing the devastating side effects of traditional opioids .” – Ben Clements By combining chronic pain models with receptor-level pharmacology, Ben is bridging GPCR University today. _______________ Keyword Cloud: GPCR research community, GPCR drug discovery, mu-opioid receptor, positive allosteric modulators, GPCR training program, GPCR online course, GTPγS assay, chronic

October 2022 Coincident Regulation of PLCβ Signaling by Gq-Coupled and μOpioid Receptors Opposes Opioid The current frontline approach for pain-management is the use of opioid analgesics. The primary analgesic target of opioids is the μ-opioid receptor (MOR). found that MOR alone could not stimulate PLC, but rather required a coincident signal from a Gq coupled receptor could lead to identification of new non-MOR targets that would allow for lower dose utilization of opioid

August 2022 "Opioid receptors (ORs) represent one of the most significant groups of G-protein coupled receptor (GPCR) drug targets and also act as prototypical models for GPCR function.

Opioid receptors are G-protein-coupled receptors (GPCRs) part of cell signaling paths of direct interest to the opioid receptor, because opioid drugs typically have a protonated amino group that contributes to receptor binding, and the functioning of GPCRs may involve protonation change. In this review, we discuss the relationship between structure, function, and dynamics of opioid receptors from the perspective of the usefulness of computational studies to evaluate protonation-coupled opioid-receptor

September 2022 To probe the activation mechanism of the Delta opioid receptor by an agonist ADL5859 started from inactive conformation using molecular dynamic simulations "The δ-opioid receptor (DOR) is a critical While the receptor with the crystal ligand (i.e. antagonist naltrindole) maintained the inactive conformation in all three independent simulations, the receptor with ADL5859 was adopting toward the active conformation

September 2022 "Morphine, the most widely used analgesic, relieves severe pain by activating the μ-opioid receptor (MOR), whereas naloxone, with only slight structural changes compared to morphine, exhibits inhibitory effect, and is used to treat opioid abuse.

September 2022 Fentanyl activates ovarian cancer and alleviates chemotherapy-induced toxicity via opioid receptor-dependent activation of EGFR "Background Fentanyl is an opioid analgesic and is widely used

The company’s scientific approach relied on targeting GPCRs — specifically opioid receptors — using biased to bring a novel, safer class of pain therapeutics to patients — an urgent need in the midst of the opioid The company’s goal is to model receptor dynamics — including biased signaling — to predict drug behavior Superluminal is building systems that learn from receptor movement, conformational shifts, and complex By making receptor behavior computationally predictable, Ajay and his team are working to reduce the

The reagents are compatible with HTRF readers  and validated in GLP1R  and Mu opioid receptor (MOR)   partner content, we help scientists connect, collaborate, and innovate in the world of G protein-coupled receptors

and dynorphins, and four opioid receptors (ORs): μ-opioid receptor (MOR), κ-opioid receptor (KOR), δ-opioid Opioid receptors belong to class A of G protein-coupled receptors or GPCRs and signaled mainly through Morphine is an agonist of Mu opioid receptor (MOPR) and one of the objectives in the development of new A brief history of opiates, opioid peptides, and opioid receptors. Opioid Receptor-Mediated Regulation of Neurotransmission in the Brain.

controlling the trafficking of the receptor to the cell surface. In addition, VAMP2 can interact with other GPCRs, such as the beta-2 adrenergic receptor and the mu-opioid receptor (MOR) [1,6,7]. Conformational specificity of opioid receptors is determined by subcellular location irrespective of Phosphorylation state of muopioid receptor determines the alternative recycling of receptor via Rab4

Watch Episode 170 What We’re Missing in Pain Research In GPCR drug discovery, receptors typically steal These findings suggest a path forward that isn’t about blocking a single receptor but about rewiring Whether working on opioid withdrawal, addiction vulnerability, or chronic pain, GPCR-related signaling emerged as the core mediator  — demonstrating the reach of these signaling pathways beyond classical receptor pain. ___________ Keyword Cloud: RGS4 , GPCR data platform , GPCR training program , pain research , opioid

"Biased Signaling is Structurally Encoded As An Autoproteolysis Event in Adhesion G Protein-Coupled Receptor GPCR Activation and Signaling Atypical Chemokine Receptor 3 'Senses' CXC Chemokine Receptor 4 Activation GPCRs in Neuroscience Mu-opioid receptor selective superagonists produce prolonged respiratory depression A corazonin G protein-coupled receptor gene in the tick Ixodes scapularis yields two splice variants, each coding for a specific corazonin receptor.

of what’s inside this week’s Premium Edition: Industry insights:  Metabolic GPCRs in the spotlight; receptor

In this exclusive Expert Drug Hunter lesson, Terry Kenakin dismantles 100 years of receptor theory and Discover how receptors actually behave, how ligands uniquely sculpt their function, and how cryptic allosteric

all these situations, chemokines interact with seven-transmembrane chemokine-type G protein-coupled receptors (chemokine receptors, CKRs) and glycosaminoglycans (GAGs) to regulate the movement of leukocytes throughout In humans there are approximately 45 chemokines, 19 chemotactic or G-protein coupled chemokine receptors (CKRs) that signal via Gαi and 4 official atypical chemokine receptors (ACKRs) which engage in ligand CCR2 is an example of a dual-function receptor that directly regulates both cell migration and scavenging

It has been applied to different GPCR binding assays, such as CXCR4, opioid receptors, CCK1 and CCK2. Crystal Structure of the Human Cannabinoid Receptor CB1. Crystal Structure of the Human Cannabinoid Receptor CB2. Identification of Cannabinoid Receptor Subtype  Selective Ligands. Pyrazole Antagonists of the CB1 Receptor with Reduced Brain Penetration.

The bioactive lysophospholipid sphingosine-1-phosphate (S1P) acts via five different subtypes of S1P receptors Several S1PR therapeutic drugs have been developed to treat these diseases; however, they lack receptor In this article, we describe a 2.2 Å resolution room temperature crystal structure of the human S1P5 receptor demonstrates a unique ligand-binding mode, involving an allosteric sub-pocket, which clarifies the receptor

influence predominantly arises via engagement with the principal two G-protein-coupled cannabinoid receptors Earlier publications have indicated that expression of CB1 receptor mRNA and protein has been recognized The part played by CB1 receptor activation or inhibition with respect to these functions and relevant This can be deduced from the qRT-PCR assays; triggering CB1 receptors amplifies both NR4A1 and NR4A3 The impact of ACEA is inhibited by the selective CB1 receptor antagonist, rimonabant.

read our previous post, you probably know what CELT-335 is and its high affinity for the cannabinoid 1 receptor Introduction Cannabinoid receptors are GPCRs, and two main types exist, CB1R and CB2R. It has been proven that when different ligands bind to the receptors the effects are different depending The bias depends on the agonist’s structure as well as the state of the cannabinoid receptor (whether It binds to the receptor, which is labelled with Tb.

Yamina's Corner , our founder Yamina Berchiche works closely with organizations to help them navigate receptor Push the boundaries  of receptor pharmacology and its real-world applications. They’re already behind blockbuster drugs: GLP-1 receptor agonists  – reshaping obesity & type 2 diabetes Dopamine D2 receptor modulators  – transforming treatment for Parkinson’s & schizophrenia. Serotonin & dopamine receptor modulation  for neuropsychiatric disorders.

September 2022 "Serotonin receptor 5-HT2A and tropomyosin receptor kinase B (TrkB) strongly contribute decreased TrkB autophosphorylation, preventing its activation with agonist 7,8-DHF, even with low 5-HT2A receptor A blockade of 5-HT2A receptor with the preferential antagonist ketanserin prevented the receptor-mediated Our data reveal the functional role of 5-HT2A–TrkB receptor heterodimerization and suggest that the regulated

Chemokine receptors (CKRs) belong to a subfamily of G-protein-coupled receptors (GPCRs) and play a crucial chemokine system exhibits great versatility, with more than 50 chemokines interacting with over 20 receptors complexes and revealing the diverse and multifaceted nature of the chemokine receptor system. Currently, there are more than 40 available structures of chemokines and their receptors in the Protein This structural variation may explain why chemokine receptors typically recognize chemokines from only

October 2022 "The canonical model for G protein-coupled receptors (GPCRs) activation assumes that stimulation In this model, GPCR signaling is turned-off by receptor phosphorylation via GPCR kinases (GRKs) and subsequent recruitment of β-arrestins, resulting in receptor internalization into endosomes. Internalized receptors can then recycle back to the cell surface or be trafficked to lysosomes for degradation This is the case for the parathyroid hormone (PTH) type 1 receptor (PTHR), which engages on sustained

The chemokine receptor system is implicated in a wide range of inflammatory, autoimmune and infectious The involvement of chemokines and their receptors in several aspects of cancer biology, represents a This redundancy can be seen as problematic in drug discovery as blocking a single receptor might not Therefore, an alternative approach is to make use of chemokine receptors redundancy and the fact that Furthermore, both chemokines and receptors can homo- and hetero-oligomerize, impacting receptor/ligand-binding

Biased agonism is a phenomenon where different ligands acting on the same receptor trigger distinct signaling is gaining significant attention in drug discovery, especially in the context of G protein-coupled receptors (GPCRs) like the glucagon-like peptide-1 receptor (GLP-1R). Additionally, GLP-1R couple to G protein-coupled receptor kinases (GRKs) and recruit β-arrestins, adding For instance, the interaction of GLP-1 with ECL3, which leads to a tight conformation of the receptor's

Emerging evidence suggests adenosine G protein-coupled receptors (GPCRs) are promising therapeutic targets The adenosine A1 and A2A receptors are expressed in the human brain and have a proposed involvement in Targeting these receptors preclinically can mitigate pathogenic β-amyloid and tau neurotoxicity whilst accessible summary of the literature on Alzheimer's disease and the therapeutic potential of A1 and A2A receptors Although there are no available medicines targeting these receptors approved for treating dementia, we