<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Han B</submitter><funding>Canadian Institutes of Health Research</funding><pagination>4597-611</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4119410</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(17)</volume><pubmed_abstract>Transforming growth factor beta-induced (TGFBI/βIG-H3), also known as βig-H3, is a protein inducible by TGFβ1 and secreted by many cell types. It binds to collagen, forms part of the extracellular matrix and interacts with integrins on the cell surface. Recombinant TGFBI and transgenic TGFBI overexpression can promote both islet survival and function. In this study, we generated TGFBI KO mice and further assessed TGFBI function and signaling pathways in islets. Islets from KO mice were of normal size and quantity, and these animals were normoglycemic. However, KO islet survival and function was compromised in vitro. In vivo, KO donor islets became inferior to wild-type donor islets in achieving normoglycemia when transplanted into KO diabetic recipients. TGFBI KO mice were more prone to st</pubmed_abstract><journal>Human molecular genetics</journal><pubmed_title>TGFBI (βIG-H3) is a diabetes-risk gene based on mouse and human genetic studies.</pubmed_title><pmcid>PMC4119410</pmcid><funding_grant_id>MOP123389</funding_grant_id><funding_grant_id>MOP57697</funding_grant_id><pubmed_authors>Raelson J</pubmed_authors><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Han B</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Tremblay J</pubmed_authors><pubmed_authors>Luo H</pubmed_authors><pubmed_authors>Hu B</pubmed_authors><pubmed_authors>Qi S</pubmed_authors></additional><is_claimable>false</is_claimable><name>TGFBI (βIG-H3) is a diabetes-risk gene based on mouse and human genetic studies.</name><description>Transforming growth factor beta-induced (TGFBI/βIG-H3), also known as βig-H3, is a protein inducible by TGFβ1 and secreted by many cell types. It binds to collagen, forms part of the extracellular matrix and interacts with integrins on the cell surface. Recombinant TGFBI and transgenic TGFBI overexpression can promote both islet survival and function. In this study, we generated TGFBI KO mice and further assessed TGFBI function and signaling pathways in islets. Islets from KO mice were of normal size and quantity, and these animals were normoglycemic. However, KO islet survival and function was compromised in vitro. In vivo, KO donor islets became inferior to wild-type donor islets in achieving normoglycemia when transplanted into KO diabetic recipients. TGFBI KO mice were more prone to st</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Sep</publication><modification>2026-04-30T01:11:31.559Z</modification><creation>2026-04-07T15:43:12.578Z</creation></dates><accession>S-EPMC4119410</accession><cross_references><pubmed>24728038</pubmed><doi>10.1093/hmg/ddu173</doi></cross_references></HashMap>