Proteomics

Dataset Information

0

Human Cardiac Fibroblast BioID2 Interactome for SKI and TAZ(WWTR1)


ABSTRACT: We used adenoviral-mediated overexpression of MYC-BioID2, MYC-BioID2-SKI, MYC-BioID2-WWTR1 (TAZ) in human primary cardiac fibroblasts to elucidate the interaction between SKI and the Hippo signaling pathway. Original data is also available on the Global Proteome Machine (http://hs2.proteome.ca/tandem/thegpm_tandem.html). Datasets are identified as follows: GPM10000002938 and 2939 are untreated negative control cell lysates; GPM10000002941 and 2942 are "empty" MYC-BioID2 vector; GPM10000002943 and 2944 are MYC-BioID2-SKI; and GPM10000002944 and 2945 are MYC-BioID2-WWTR1(TAZ).

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

Dataset's files

Source:
Action DRS
GPM10000002938-ControlH1.xls Xls
GPM10000002938.mgf Mgf
GPM10000002938.xml Xml
GPM10000002939-ControlH2.xls Xls
GPM10000002939.mgf Mgf
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Publications


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]

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