Smad3-mSin3A-HDAC1 Complex is Required for TGF-β1-Induced Transcriptional Inhibition of PPARγ in Mouse Cardiac Fibroblasts
Author(s) -
Kaizheng Gong,
Mingxing Chen,
Rujun Li,
Yanghong He,
Huajiang Zhu,
Dan Yao,
Suzanne Oparil,
Zhengang Zhang
Publication year - 2016
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000453149
Subject(s) - chromatin immunoprecipitation , microbiology and biotechnology , transfection , transcription factor , peroxisome proliferator activated receptor , biology , smad , promoter , hdac1 , transcription (linguistics) , gene silencing , transcriptional regulation , luciferase , reporter gene , signal transduction , gene expression , gene , histone , biochemistry , histone deacetylase , linguistics , philosophy
We have recently demonstrated that activated transforming growth factor-β (TGF-β) signaling suppresses myocardial peroxisome proliferator-activated receptor γ (PPARγ) expression in the pressure overloaded heart. In this study, we aim to further define the molecular mechanisms that underlie TGF-β-induced PPARγ transcriptional inhibition.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom