{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Choi KM"],"funding":["NHLBI NIH HHS","National Heart, Lung, and Blood Institute"],"pagination":["7759-7774"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8530868"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["236(11)"],"pubmed_abstract":["Yes-associated protein (YAP) and PDZ-binding motif (TAZ) have emerged as important regulators of pathologic fibroblast activation in fibrotic diseases. Agonism of Gαs-coupled G protein coupled receptors (GPCRs) provides an attractive approach to inhibit the nuclear localization and function of YAP and TAZ in fibroblasts that inhibits or reverses their pathological activation. Agonism of the dopamine D1 GPCR has proven effective in preclinical models of lung and liver fibrosis. However, the molecular mechanisms coupling GPCR agonism to YAP and TAZ inactivation in fibroblasts remain incompletely understood. Here, using human lung fibroblasts, we identify critical roles for the cAMP effectors EPAC1/2, the small GTPase RAP2c, and the serine/threonine kinase MAP4K7 as the essential elements in "],"journal":["Journal of cellular physiology"],"pubmed_title":["GPCR-mediated YAP/TAZ inactivation in fibroblasts via EPAC1/2, RAP2C, and MAP4K7."],"pmcid":["PMC8530868"],"funding_grant_id":["HL132256","R01 HL133320","R21 HL132256","T32 HL105355","HL105355","R01 HL092961","HL092961"],"pubmed_authors":["Aravamudhan A","Link PA","Tschumperlin DJ","Choi KM","Diaz Espinosa AM","Haak AJ","Wood DK","Cummins KA"],"additional_accession":[]},"is_claimable":false,"name":"GPCR-mediated YAP/TAZ inactivation in fibroblasts via EPAC1/2, RAP2C, and MAP4K7.","description":"Yes-associated protein (YAP) and PDZ-binding motif (TAZ) have emerged as important regulators of pathologic fibroblast activation in fibrotic diseases. Agonism of Gαs-coupled G protein coupled receptors (GPCRs) provides an attractive approach to inhibit the nuclear localization and function of YAP and TAZ in fibroblasts that inhibits or reverses their pathological activation. Agonism of the dopamine D1 GPCR has proven effective in preclinical models of lung and liver fibrosis. However, the molecular mechanisms coupling GPCR agonism to YAP and TAZ inactivation in fibroblasts remain incompletely understood. Here, using human lung fibroblasts, we identify critical roles for the cAMP effectors EPAC1/2, the small GTPase RAP2c, and the serine/threonine kinase MAP4K7 as the essential elements in ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2025-04-05T13:44:27.563Z","creation":"2025-04-05T13:44:27.563Z"},"accession":"S-EPMC8530868","cross_references":{"pubmed":["34046891"],"doi":["10.1002/jcp.30459"]}}