Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive HF
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Cardiofibroblast, Fibroblast
DISEASE(S): Myocardial Ischemia
SUBMITTER: Natalie Landry
LAB HEAD: Ian M. C. Dixon
PROVIDER: PXD018246 | Pride | 2021-09-09
REPOSITORIES: Pride
Action | DRS | |||
---|---|---|---|---|
GPM10000002938-ControlH1.xls | Xls | |||
GPM10000002938.mgf | Mgf | |||
GPM10000002938.xml | Xml | |||
GPM10000002939-ControlH2.xls | Xls | |||
GPM10000002939.mgf | Mgf |
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Basic research in cardiology 20210413 1
We have previously shown that overexpression of SKI, an endogenous TGF-β<sub>1</sub> repressor, deactivates the pro-fibrotic myofibroblast phenotype in the heart. We now show that SKI also functions independently of SMAD/TGF-β signaling, by activating the Hippo tumor-suppressor pathway and inhibiting the Transcriptional co-Activator with PDZ-binding motif (TAZ or WWTR1). The mechanism(s) by which SKI targets TAZ to inhibit cardiac fibroblast activation and fibrogenesis remain undefined. A rat mo ...[more]