{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Clayton SW"],"funding":["National Institutes of Health","NIAMS NIH HHS","NIH HHS"],"pagination":["21364"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7721728"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_abstract":["Previously, we showed that embryonic deletion of TGF-β type 2 receptor in mouse sclerotome resulted in defects in fibrous connective tissues in the spine. Here we investigated how TGF-β regulates expression of fibrous markers: Scleraxis, Fibromodulin and Adamtsl2. We showed that TGF-β stimulated expression of Scleraxis mRNA by 2 h and Fibromodulin and Adamtsl2 mRNAs by 8 h of treatment. Regulation of Scleraxis by TGF-β did not require new protein synthesis; however, protein synthesis was required for expression of Fibromodulin and Adamtsl2 indicating the necessity of an intermediate. We subsequently showed Scleraxis was a potential intermediate for TGF-β-regulated expression of Fibromodulin and Adamtsl2. The canonical effector Smad3 was not necessary for TGF-β-mediated regulation of Sclera"],"journal":["Scientific reports"],"pubmed_title":["Canonical and noncanonical TGF-β signaling regulate fibrous tissue differentiation in the axial skeleton."],"pmcid":["PMC7721728"],"funding_grant_id":["R56 AR053860","T32 AR069516","R01 AR053860"],"pubmed_authors":["Ban GI","Liu C","Serra R","Clayton SW"],"additional_accession":[]},"is_claimable":false,"name":"Canonical and noncanonical TGF-β signaling regulate fibrous tissue differentiation in the axial skeleton.","description":"Previously, we showed that embryonic deletion of TGF-β type 2 receptor in mouse sclerotome resulted in defects in fibrous connective tissues in the spine. Here we investigated how TGF-β regulates expression of fibrous markers: Scleraxis, Fibromodulin and Adamtsl2. We showed that TGF-β stimulated expression of Scleraxis mRNA by 2 h and Fibromodulin and Adamtsl2 mRNAs by 8 h of treatment. Regulation of Scleraxis by TGF-β did not require new protein synthesis; however, protein synthesis was required for expression of Fibromodulin and Adamtsl2 indicating the necessity of an intermediate. We subsequently showed Scleraxis was a potential intermediate for TGF-β-regulated expression of Fibromodulin and Adamtsl2. The canonical effector Smad3 was not necessary for TGF-β-mediated regulation of Sclera","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Dec","modification":"2025-04-19T06:54:51.841Z","creation":"2025-04-19T06:54:51.841Z"},"accession":"S-EPMC7721728","cross_references":{"pubmed":["33288795"],"doi":["10.1038/s41598-020-78206-4"]}}