August 2022 GPR3 expression in retinal ganglion cells contributes to neuron survival and accelerates GPR3 is unique in its ability to constitutively activate the Gαs protein without a ligand, which elevates Our earlier reports suggested that GPR3 enhances both neurite outgrowth and neuronal survival. GPR3 was relatively highly expressed in retinal ganglion cells (RGCs). Evaluation of the effect of GPR3 on axonal regeneration using GPR3 knockout mice revealed that GPR3 in

Our previous work demonstrated that GPR3-mediated β-arrestin signaling modulates amyloid-β (Aβ) generation in vitro and that Gpr3 deficiency ameliorates Aβ pathology in vivo. However, Gpr3-deficient mice display several adverse phenotypes, including elevated anxiety-like behavior consequences of selective elimination of GPR3-mediated β-arrestin signaling in vivo. In contrast to Gpr3-deficient mice, G protein-biased GPR3 mice do not display elevated anxiety levels

roles of focal adhesion kinase (protein tyrosine kinase 2, PTK2), the shear-dependent collagen receptor GPR56 peptides that interfered with integrin αIIb binding (pCIB and pCIBm) or mimicked the activation of GPR56 integrin αIIbβ3, and CIB1 in collagen- and GPVI-dependent thrombus formation, which is modulated by GPR56

< GPCR News < GPCRs in Oncology and Immunology GPR68-ATF4 signaling is a novel prosurvival pathway in Notably GPR68, an acid sensing GPCR, is upregulated in radioresistant GBM. Usage of Lorazepam, which has off target agonism of GPR68, is linked to worse clinical outcomes for a To determine GPR68 inhibition's mechanism of cell death we use DAVID pathway analysis of RNAseq. In this context, GPR68 suppresses ATF4, inhibition of GPR68 increases expression of ATF4 which leads

< GPCR News < GPCRs in Oncology and Immunology GPR56 signaling pathway network and its dynamics in the transition of glioblastoma Published date November 19, 2023 Abstract "G protein-coupled receptor 56 (GPR56 In our earlier study, we reported that GPR56 is expressed heterogeneously in glioblastoma (GBM) and is plausible cross-connectivity across different axes attributable to GPR56 function. GPR56 signaling and mesenchymal transition."

< GPCR News < GPCRs in Oncology and Immunology GPR4 in the pH-dependent migration of melanoma cells in Membrane-bound receptors, such as the proton-sensitive GPCR (pH-GPCR) GPR4, are considered as potential In this study, we investigated the pH-dependent migration of GPR4 wildtype/overexpressing SK-Mel-28 cells Migration of GPR4 overexpressing SK-Mel-28 cells was enhanced in a range of pH 6.5 - pH 7.5 as compared In Boyden chamber experiments, GPR4 overexpression only increased migration at pH 7.5 in a Matrigel-free