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

GPR39 is a GPCR which can interact with Zn and modulate the colonocytes' survival. The clinical significance of GPR39 in colon cancer has never been reported. Materials: In our study, we compared GPR39 expression between colon cancers and tumor-adjacent tissues The clinical significance of GPR39 was evaluated by analyzing the correlations with clinicopathological The prognostic significance of GPR39 was estimated with univariate and multivariate analyses.

SVEP1 regulates GPCR-mediated vasoconstriction via integrin α9β1 and α4β1 1.5 GPCRs in Neuroscience GPR3

< GPCR News < GPCRs in Oncology and Immunology G protein-coupled estrogen receptor (GPER)/GPR30 forms in MCF7 breast cancer cells Published date January 10, 2024 Abstract "G protein-coupled receptor 30 (GPR30 GPR30 constitutively and PDZ-dependently inhibits β1AR-mediated cAMP production. Deleting the GPR30 C-terminal PDZ motif (-SSAV) does not interfere with the receptor complex, indicating These results argue that GPR30 and β1AR form a PDZ-independent complex in MCF7 cells through which GPR30

We detected the expression of GPR37 in NSCLC tissues and cell lines. The study explored the influence of GPR37 on tumor cell proliferation. Furthermore, we examined the effects of GPR37 on tumor cell apoptosis and invasion. Most importantly, we investigated whether GPR37 affects cisplatin-induced drug resistance in NSCLC. Knockdown of GPR37 significantly inhibits the occurrence and development of NSCLC.