ArticleHuman molecular genetics2014
TGFBI (βIG-H3) is a diabetes-risk gene based on mouse and human genetic studies.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Biochemically Constrained Multi-Omics Integration Reveals Protein-Metabolite Dependencies Across Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of COL5A1 and TGFBI as key basement membrane genes and their molecular mechanisms in gestational diabetes mellitus.Medicine · 2026Article
- Characterisation of airway inflammation and proteomes associated with cystic fibrosis-related diabetes.ERJ open research · 2025Article
- Design of a single particle-interferometric reflectance imaging sensor adipo-chip for obesity biomarker screening.Scientific reports · 2025Article
- Shared molecular mechanisms between type 2 diabetes and thyroid cancer: integrated bioinformatics insights for prognostic biomarker discovery.Endocrine connections · 2025Article
- Targeted serum proteomics of longitudinal samples from newly diagnosed youth with type 1 diabetes affirms markers of disease.Diabetologia · 2025Article
- Oxymatrine impedes Alzheimer's progression via the attenuation of hypercholesterolemia and fibrosis.Metabolic brain disease · 2025Article
- Identification of potential drug targets for insomnia by Mendelian randomization analysis based on plasma proteomics.Frontiers in neurology · 2024Article
- Targeted serum proteomics of longitudinal samples from newly diagnosed youth with type 1 diabetes distinguishes markers of disease and C-peptide trajectory.Diabetologia · 2023Article
- Type II Diabetes Mellitus Causes Extracellular Matrix Alterations in the Posterior Cornea That Increase Graft Thickness and Rigidity.Investigative ophthalmology & visual science · 2023Article
- Human umbilical cord mesenchymal stem cell-derived TGFBI attenuates streptozotocin-induced type 1 diabetes mellitus by inhibiting T-cell proliferation.Human cell · 2023Article
- Bioinformatics-based analysis of the roles of basement membrane-related gene AGRN in systemic lupus erythematosus and pan-cancer development.Frontiers in immunology · 2023Article
- Persistent coxsackievirus B1 infection triggers extensive changes in the transcriptome of human pancreatic ductal cells.iScience · 2022Article
- Construction of a novel miRNA regulatory network and identification of target genes in gestational diabetes mellitus by integrated analysis.Frontiers in genetics · 2022Article
- Potential underlying genetic associations between keratoconus and diabetes mellitus.Advances in ophthalmology practice and research · 2021Article
- Functions of Matricellular Proteins in Dental Tissues and Their Emerging Roles in Orofacial Tissue Development, Maintenance, and Disease.International journal of molecular sciences · 2021Review
- Vesicles Shed by Pathological Murine Adipocytes Spread Pathology: Characterization and Functional Role of Insulin Resistant/Hypertrophied Adiposomes.International journal of molecular sciences · 2020Article
- Article
- BIGH3 Promotes Osteolytic Lesions in Renal Cell Carcinoma Bone Metastasis by Inhibiting Osteoblast Differentiation.Neoplasia (New York, N.Y.) · 2018Article
- Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits.Nature genetics · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
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 straptozotocin-induced diabetes than the wild-type counterpart. Phosphoprotein array analysis established that AKT1S1, a molecule linking the AKT and mTORC1 signaling pathways, was modulated by TGFBI in islets. Phosphorylation of four molecules in the AKT and mTORC1 signaling pathway, i.e. AKT, AKT1S1, RPS6 and EIF4EBP1, was upregulated in islets upon TGFBI stimulation. Suppression of AKT activity by a chemical inhibitor, or knockdown of AKT1S1, RPS6 and EIF4EBP1 expression by small interfering RNA, modulated islet survival, proving the relevance of these molecules in TGFBI-triggered signaling. Human genetic studies revealed that in the TGFBI gene and its vicinity, three single-nucleotide polymorphisms were significantly associated with type 1 diabetes risks, and one with type 2 diabetes risks. Our study suggests that TGFBI is a potential risk gene for human diabetes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.