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September 2022 PLC-IP3-ORAI pathway participates in the activation of the MRGPRB2 receptor in mouse peritoneal

Additionally, we detect a shortening of PC in PINK1-deficient human cellular and mouse models of familial

The mouse cytomegalovirus G protein-coupled receptor homolog, M33, coordinates key features of in vivo The mouse cytomegalovirus (MCMV) GPCR, M33, facilitates dendritic cell (DC)-dependent viremia, the extravasation The mouse CMV (MCMV) GPCR homolog, designated M33, is important for cell-associated virus spread and

Divergence, however, in the amino acid sequences of rodent and human PTH receptors (rat and mouse PTH1Rs potential uncertainty, we used a homologous recombination-based knockin (KI) approach to generate a mouse the human PTH1R replaces a segment (exon 4) of the murine PTH1R gene so that the human and not the mouse Expression is directed by the endogenous mouse promoter and hence occurs in all biologically relevant

A knock-in mouse expressing a non-cleavable GPR116 mutant phenocopies the pulmonary phenotype of GPR116 We further highlight residues in transmembrane 7 (TM7) that mediate stronger signaling in mouse versus

September 2022 β2-Adrenergic Receptor Expression and Intracellular Signaling in B Cells Are Highly Dynamic during Collagen-Induced Arthritis "The sympathetic nervous system (SNS) has either a pro-inflammatory or anti-inflammatory effect, depending on the stage of arthritis. In the past, treatment of arthritic B cells with a β2-adrenergic receptor (β2-ADR) agonist has been shown to attenuate arthritis. In this study, the expression and signaling of β2-ADR in B cells during collagen-induced arthritis (CIA) were investigated to provide an explanation of why only B cells from arthritic mice are able to improve CIA. Splenic B cells were isolated via magnetic-activated cell sorting (MACS). Adrenergic receptors on B cells and intracellular β2-ADR downstream molecules (G protein-coupled receptor kinase 2 (GRK-2), β-Arrestin 2, p38 MAPK, extracellular signal-regulated kinase 1/2 (ERK1/2) and cAMP response element-binding protein (CREB)) were analyzed at different time points in naïve and arthritic B cells with and without stimulation of β2-ADR agonist terbutaline by flow cytometry. β2-ADR-expressing B cells increase during CIA without a change in receptor density. Moreover, we observed a profound downregulation of GRK-2 shortly after induction of arthritis and an increase in β-Arrestin 2 only at late stage of arthritis. The second messengers studied (p38, ERK1/2 and CREB) followed a biphasic course, characterized by a reduction at onset and an increase in established arthritis. Stimulation of CIA B cells with the β-ADR agonist terbutaline increased pp38 MAPK independent of the timepoint, while pERK1/2 and pCREB were enhanced only in the late phase of arthritis. The phosphorylation of p38 MAPK, ERK1/2 and CREB in the late phase of arthritis was associated with increased IL-10 produced by B10 cells. The change of β2-ADR expression and signaling during sustained inflammation might be an integral part of the switch from pro- to anti-inflammatory action of sympathetic mechanisms in late arthritis." Read more at the source #DrGPCR #GPCR #IndustryNews

August 2022 "The calcium-permeable cation channel TRPM3 can be activated by heat and the endogenous steroid pregnenolone sulfate. TRPM3's best understood function is its role as a peripheral noxious heat sensor in mice. However, the channel is expressed in various tissues and cell types including neurons as well as glial and epithelial cells. TRPM3 expression patterns differ between species and change during development. Furthermore, a plethora of TRPM3 variants that result from alternative splicing have been identified and the majority of these isoforms are yet to be characterized. Moreover, the mechanisms underlying regulation of TRPM3 are largely unexplored. In addition, a micro-RNA gene (miR-204) is located within the TRPM3 gene. This complexity makes it difficult to obtain a clear picture of TRPM3 characteristics. However, a clear picture is needed to unravel TRPM3's full potential as experimental tool, diagnostic marker and therapeutic target. Therefore, the newest data related to TRPM3 have to be discussed and to be put in context as soon as possible to be up-to-date and to accelerate the translation from bench to bedside. The aim of this review is to highlight recent results and developments with particular focus on findings from studies involving ocular tissues and cells or peripheral neurons of rodents and humans." Read more at the source #DrGPCR #GPCR #IndustryNews

Moreover, through systematic survival analysis on OR genes, OR51E1 (mouse Olfr558) was identified as a potential biomarker of unfavorable overall survival, and OR2C1 (mouse Olfr15) was identified as a potential OR5D18 (mouse Olfr1155) was the most frequently mutated OR gene, and OR5AR1 (mouse Olfr1019) showed IDH

Here, we generated a G protein-biased GPR3 mouse model to investigate the physiological and pathophysiological and leads to a decrease in the area and compaction of amyloid plaques in the preclinical AppNL-G-F AD mouse

Xenograft mouse model was generated to investigate the in vivo efficacy of fentanyl.

“There was this very interesting phenotype the lab found where, as a mouse was starting to enter what

with the MRAP2 mutants R125H and R125C, which are found in human patients with extreme obesity, and mouse

Here, we characterize divergent signaling signatures in mouse astrocytes of the PFC and primary sensory

In a mouse model of contact hypersensitivity, β-arrestin-biased CXCR3-mediated inflammation is dependent

Mouse models have provided invaluable information on the roles for PKA subunits in brain and key metabolic

therapeutic effects of trehalose and saccharin on macrophage IL‐1β production and eosinophilia in the mouse

We generated mutant mouse lines lacking the entire Defensin (Def) gene cluster in keratinocytes or Mrgpra2a

The absence of VLGR1 in tissues and cells derived from VLGR1-deficient mouse models resulted in alterations

Using shRNA knockdown and CRISPR/Cas9 knockout cell lines, as well as mouse models, we confirmed the

CHO-K1 cells expressing the human β3 -AR, and 8 compounds were active in CHO-K1 cells expressing the mouse

pattern of cell expression has been directly challenged by a publication purporting ACKR1 expression in mouse

different antibodies, all raised against a peptide comprising the C-terminal residues 443-473 of the mouse

Here we tested the effects of DOI on head-twitch behavior (HTR) - a mouse behavioral proxy of human psychedelic

DREADD was expressed in hippocampal astrocytes of a lipopolysaccharide (LPS)-induced neuroinflammation mouse

S., Vojtek, M., Sousa, J. B., & Diniz, C. (2021). S., Sousa, J. B., Gonçalves, J., & Diniz, C. (2019).

of a biarylamine acting as agonist at human β3 adrenoceptors and exerting BRL37344-like effects on mouse

Target the µ-Opioid Receptor Design and Synthesis of Novel GPR139 Agonists with Therapeutic Effects in Mouse

In this study, we established an experimental Sjögren's syndrome (ESS) mouse model to elucidate the molecular

gene function analysis uncover GPR183 as a key mediator for methionine to stimulate milk synthesis in mouse

Arrb1 deficiency suppressed HBx-induced hepatocellular carcinogenesis in several mouse models.