proliferation in the progression of experimental pulmonary hypertension in rats Latrophilin-2 mediates fluid shear stress mechanotransduction at endothelial junctions GPCRs in Neuroscience Male-specific behavioral

The research of GPCRs in the cochlea is essential for the understanding of the cochlea development, hearing disorders, and the treatment for hearing loss. In addition, hearing loss can be caused by mutations of certain GPCRs, such as Vlgr1, Gpr156, S1P2, and And A1, A2A, and CB2 activation by agonists has protective functions on noise- or drug-induced hearing loss, and hearing protection."

August 2022 "Aims: The pathophysiological mechanism(s) underlying non-alcoholic fatty liver disease (NAFLD) have yet to be fully delineated and only a single drug, peroxisome proliferator-activated receptor (PPAR) α/γ agonist saroglitazar, has been approved. Here, we sought to investigate the role of Regulator of G Protein Signaling 7 (RGS7) in hyperlipidemia-dependent hepatic dysfunction. " Read more at the source #DrGPCR #GPCR #IndustryNews

Deficiency of β-arrestin2 alleviates apoptosis through GRP78-ATF6-CHOP signaling pathway in primary Sjögren's syndrome The etiology of primary Sjögren's syndrome (pSS) remains unknown, and there is no ideal drug for the specific treatment of pSS. β-arrestin2 is a key protein that mediates desensitization and internalization of G protein-coupled receptors (GPCRs) and it participates in inflammatory and immune responses that have been found to mediate apoptosis in autoimmune disease. In this study, we established an experimental Sjögren's syndrome (ESS) mouse model to elucidate the molecular mechanisms of β-arrestin2 in pSS. First, excessive activation of β-arrestin2 and GRP78-ATF6-CHOP apoptosis signaling were detected in specimens from pSS patients. In vivo, we found that inhibition of GRP78-ATF6-CHOP apoptosis signaling improved ESS symptoms, and the targeted deletion of β-arrestin2 significantly increased saliva flow, alleviated salivary gland indices, and improved tissue integrity in the ESS model by downregulating GRP78-ATF6-CHOP apoptosis signaling. In vitro, we used IFNα to stimulate human salivary gland epithelial cells (HSGECs), and the results showed that IFNα activated GRP78-ATF6-CHOP apoptosis signaling, decreased cell viability, and induced apoptosis, which were negatively regulated by the ERS inhibitor 4-PBA. In addition, β-arrestin2 depletion downregulated GRP78-ATF6-CHOP apoptosis signaling to alleviate cell apoptosis, and the effect depended on the interaction between GRP78 and β-arrestin2. In summary, our results suggest that excessive activation of GRP78-ATF6-CHOP apoptosis signaling is involved in the pathogenesis of pSS and that β-arrestin2 encourages inflammation-induced epithelial apoptosis through GRP78-ATF6-CHOP apoptosis signaling. This research further clarified the underlying role of β-arrestin2 and provided an experimental foundation for β-arrestin2 depletion in the treatment of the human autoimmune disorder pSS. Read full article

Kinase PTK2 and Integrin αIIbβ3 Signaling in Collagen- and GPVI-Dependent Thrombus Formation under Shear signaling receptors in collagen-dependent platelet aggregation and in arterial thrombus formation under shear The suppressive rather than activating effects of pGRP were confined to blood flow at a high shear rate Peptides did not influence GPVI-induced aggregation and Ca2+ signaling in the absence of shear. - and GPVI-dependent thrombus formation, which is modulated by GPR56 and exclusively at high shear.

Samples of synovial fluid and peripheral blood were analyzed for CD45+CD3+CD4+GPR15+ and CD45+CD3+CD8 Also, the frequency CD4+/CD8+ GPR15+ T lymphocytes are higher in synovial fluid of established RA patients

acids and cancer The path of GPR87: from a P2Y-like receptor to its role in cancer progression Ascitic Shear Stress Activates GPCRs and Downregulates Mucin 15 to Promote OvarianCancer Malignancy Bispecific antibodies

"Protecting neurons from death during oxidative and neuroexcitotoxic stress is key for preventing cognitive pCREB levels which prevented a decrease in pro-survival protein, BCL2, during H2O2-induced oxidative stress β-arrestin Knockout HEK293 cells showed that the NF-α1/CPE-5-HTR1E-mediated protection against oxidative stress human primary neurons diminished the NF-α1/CPE-mediated protection of these neurons against oxidative stress interacts with serotonin receptor 5-HTR1E to activate the β-arrestin/ERK/CREB/BCL2 pathway to mediate stress-induced

The pathogenesis of preeclampsia include poor placentation, uteroplacental malperfusion, oxidative stress , endoplasmic reticulum stress, dysregulated immune tolerance, vascular inflammation and endothelial

radical production, potentially protecting diabetes mellitus patients who are experiencing oxidative stress

transcriptional regulation, and more, PKA signaling regulates cellular metabolism and emotional and stress

The orphan receptor GPR97, activated by glucocorticoid stress hormones, is a prototypical aGPCR.

GPCR, hear anecdotes, and get important announcements. prototypical M2 muscarinic receptor localizes to the mitochondria and regulates cell respiration under stress

The adrenal gland plays an important role in the modulation of cardiac neurohormonal stress because it

Procrastination may seem tempting, but tackling your work incrementally will save time and reduce stress

implicated in Hc interaction with macrophages, including the ragulator complex (involved in nutrient stress

condition long-term GPCR activities associated with the regulation of protein expression patterns, cellular stress

airway contraction, melatonin significantly potentiated acetylcholine-stimulated [Ca2+]i increases, stress

diet-induced obesity GPCRs in Neuroscience The neuropeptide receptor npr-38 regulates avoidance and stress-induced

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Signaling GPR116 alleviates acetaminophen-induced liver injury in mice by inhibiting endoplasmic reticulum stress

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accumbens Understanding the Molecular Regulation of Serotonin Receptor 5-HTR1B-β-Arrestin1 Complex in Stress

GPCR-mediated calcium and cAMP signaling determines psychosocial stress susceptibility and resiliency

transcriptomic and serum metabolomic assessment reveals systemic implications of acute ozone-induced stress

of the histamine H1 receptor [Enhancement of mast cells activation by ATP via P2X4 receptor] Osmotic stress

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