ArticleThe Journal of biological chemistry2008
BAT3 interacts with transforming growth factor-beta (TGF-beta) receptors and enhances TGF-beta1-induced type I collagen expression in mesangial cells.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- FOSL2 activates TGF-β1-mediated GLUT1/mTOR signaling to promote diabetic kidney disease.Journal of diabetes investigation · 2025Article
- The chromatin remodeling protein BRG1 regulates HSC-myofibroblast differentiation and liver fibrosis.Cell death & disease · 2023Article
- Introducing Molecular Chaperones into the Causality and Prospective Management of Autoimmune Hepatitis.Digestive diseases and sciences · 2023Review
- Expression Analysis ofBiology · 2021Article
- Signaling Receptors for TGF-β Family Members.Cold Spring Harbor perspectives in biology · 2016Review
- BAG-6, a jack of all trades in health and disease.Cellular and molecular life sciences : CMLS · 2014Review
- A soluble fragment of the tumor antigen BCL2-associated athanogene 6 (BAG-6) is essential and sufficient for inhibition of NKp30 receptor-dependent cytotoxicity of natural killer cells.The Journal of biological chemistry · 2013Article
- Bat3 promotes T cell responses and autoimmunity by repressing Tim-3–mediated cell death and exhaustion.Nature medicine · 2012Article
- Post-translational regulation of TGF-β receptor and Smad signaling.FEBS letters · 2012Review
- Bat3 facilitates H3K79 dimethylation by DOT1L and promotes DNA damage-induced 53BP1 foci at G1/G2 cell-cycle phases.The EMBO journal · 2012Article
- BAT3 regulates Mycobacterium tuberculosis protein ESAT-6-mediated apoptosis of macrophages.PloS one · 2012Article
- HLA-B-associated transcript 3 (Bat3/Scythe) negatively regulates Smad phosphorylation in BMP signaling.Cell death & disease · 2011Article
- Human lymphocyte antigen B-associated transcript 2, 3, and 5 polymorphisms and haplotypes are associated with susceptibility of Kawasaki disease and coronary artery aneurysm.Journal of clinical laboratory analysis · 2010Article
- Bile-induced genes in Clonorchis sinensis metacercariae.Parasitology research · 2008Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Transforming growth factor-beta1 (TGF-beta1) plays essential roles in a wide array of cellular processes, such as in development and the pathogenesis of tissue fibrosis, including that associated with progressive kidney diseases. Tight regulation of its signaling pathways is critical, and proteins that associate with the TGF-beta receptors may exert positive or negative regulatory effects on TGF-beta signaling. In the present study we employed a yeast-based two-hybrid screening system to identify BAT3 (HLA-B-associated transcript 3) as a TGF-beta receptor-interacting protein. Analysis of endogenously expressed BAT3 in various tissues including the kidney reveals the existence of approximately 140-kDa full-length protein as well as truncated forms of BAT3 whose expression is developmentally regulated. Endogenous BAT3 protein interacts with TGF-beta receptors type I and type II in renal mesangial cells. Functional assays show that expression of full-length BAT3 results in enhancement of TGF-beta1-stimulated transcriptional activation of p3TP-Lux reporter, and these effects require the presence of functional TGF-beta signaling receptors as demonstrated in R-1B and DR-26 mutant cells. Moreover, expression of full-length BAT3, but not C-terminal truncated mutant of BAT3, enhanced TGF-beta1-induced type I collagen expression in mesangial cells, whereas knock down of BAT3 protein expression by small interfering RNA suppressed the expression of type I collagen induced by TGF-beta1. Our findings suggest that BAT3, a TGF-beta receptor-interacting protein, is capable of modulating TGF-beta signaling and acts as a positive regulator of TGF-beta1 stimulation of type I collagen expression in mesangial cells.
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