{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Franks NE"],"funding":["George M. O'Brien Michigan Kidney Translational Core Center","NCI NIH HHS","National Institutes of Health","George M. O'Brien Michigan Kidney Translational Core Center","NIH HHS"],"pagination":["dev203012"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11795293"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["151(24)"],"pubmed_abstract":["Growth arrest specific 1 (GAS1) is a key regulator of mammalian embryogenesis, best known for its role in hedgehog (HH) signaling, but with additional described roles in the FGF, RET, and NOTCH pathways. Previous work indicated a later role for GAS1 in kidney development through FGF pathway modulation. Here, we demonstrate that GAS1 is essential for both mesonephrogenesis and metanephrogenesis - most notably, Gas1 deletion in mice results in renal agenesis in a genetic background-dependent fashion. Mechanistically, GAS1 promotes mesonephrogenesis in a HH-dependent fashion, performing a unique co-receptor function, while promoting metanephrogenesis in a HH-independent fashion, acting as a putative secreted RET co-receptor. Our data indicate that Gas1 deletion leads to renal agenesis through"],"journal":["Development (Cambridge, England)"],"pubmed_title":["Hedgehog-dependent and hedgehog-independent roles for growth arrest specific 1 in mammalian kidney morphogenesis."],"pmcid":["PMC11795293"],"funding_grant_id":["R01 CA275182"],"pubmed_authors":["Franks NE","Allen BL"],"additional_accession":[]},"is_claimable":false,"name":"Hedgehog-dependent and hedgehog-independent roles for growth arrest specific 1 in mammalian kidney morphogenesis.","description":"Growth arrest specific 1 (GAS1) is a key regulator of mammalian embryogenesis, best known for its role in hedgehog (HH) signaling, but with additional described roles in the FGF, RET, and NOTCH pathways. Previous work indicated a later role for GAS1 in kidney development through FGF pathway modulation. Here, we demonstrate that GAS1 is essential for both mesonephrogenesis and metanephrogenesis - most notably, Gas1 deletion in mice results in renal agenesis in a genetic background-dependent fashion. Mechanistically, GAS1 promotes mesonephrogenesis in a HH-dependent fashion, performing a unique co-receptor function, while promoting metanephrogenesis in a HH-independent fashion, acting as a putative secreted RET co-receptor. Our data indicate that Gas1 deletion leads to renal agenesis through","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2026-06-07T05:08:10.487Z","creation":"2026-06-07T03:07:13.222Z"},"accession":"S-EPMC11795293","cross_references":{"pubmed":["39629522"],"doi":["10.1242/dev.203012"]}}