GPCRs in Oncology and Immunology GPR176 Promotes Cancer Progression by Interacting with G Protein GNAS

GPCRs in Cardiology, Endocrinology, and Taste Pathogenic variants of the GNAS gene introduce an abnormal

functional insight into the interaction of Clostridioides difficile toxin B and FZD7 Loss-of-function of GNAL

< 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