< GPCRs in Oncology and Immunology GPR176 Promotes Cancer Progression by Interacting with G Protein GNAS Mechanistically, the G protein GNAS is recruited intracellularly to transduce and amplify extracellular A homolog model tool confirmed that GPR176 recruits GNAS intracellularly via its transmembrane helix The GPR176/GNAS complex inhibits mitophagy via the cAMP/PKA/BNIP3L axis, thereby promoting the tumorigenesis

Targeted capture sequencing revealed GNAS as the only driver gene, as previously reported. ontology analysis was performed for differentially expressed proteins between wild-type and mutant GNAS The results suggested that GNAS mutations impact endocrinological features in acromegaly through GPCR These results identified a biological connection between GNAS mutations and the clinical and biochemical

of the bone is characterized by fibrotic, expansile bone lesions caused by activating mutations in GNAS fibrous dysplasia (FD) , osteoblasts , trabecular bone , G-protein coupled receptor signaling , GPCR , Gnas

< GPCR News < GPCRs in Oncology and Immunology Comparative Analysis of the GNAI Family Genes in Glioblastoma subunit 3 (GNAI3) and a poor prognosis. A single-cell analysis was used to assess GNAI3 expression in GBM. The results demonstrated that GNAI family genes, specifically GNAI3, were significantly associated with Our findings suggest that the GNAI3 gene holds potential as a prognostic biomarker for GBM.

understand the role of mesenchymal Gαq/11 in lung development, we generated constitutive (Pdgfrb-Cre+/-;Gnaqfl /fl;Gna11-/-) and inducible (Pdgfrb-Cre/ERT2+/-;Gnaqfl/fl;Gna11-/-) mesenchymal Gαq/11 deleted mice.