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The steroid receptor coactivator, GRIP-1, is necessary for MEF-2C-dependent gene expression and skeletal muscle differentiation

Article Abstract:

Steroid receptor coactivator (SRC) GRIP-1 is required for skeletal muscle differentiation and MEF-2C-dependent gene expression. The functional role of one SRC, GRIP-1, in muscle differentiation, a good model for analysis of the determining events in the cell's decision to differentiate or divide has been studied. It was seen that the MRNA encoding GRIP-1 is expressed in proliferating myoblasts and post-mitotic differentiated myotubes, and that protein levels increase in differentiation. This is the first study to attribute a function of the amino-terminal bHLH-PAS SRC region.

Author: Chen, Shen Liang, Dowhan, Dennis H., Hosking, Brett M., Muscat, George E.O.
Publisher: Cold Spring Harbor Laboratory Press
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1999
Australia, Striated muscle, Gene expression

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The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-beta-induced transcriptional activation

Article Abstract:

Smads control transcription of certain genes in response to TGF-beta receptor activation, but the processes of the transcription are not clearly understood. The TGF-beta-inducible Smad3 uses Smad4/DPC4, tumor suppressor, and CBP/p300 as transcription coactivators. They associate with Smad3, responding to TGF-beta. The coactivator functions and the physical interactions of CBP/p300 and smad4 with Smad3 make a model for the induction of gene expression responding to TFG-beta possible.

Author: Derynck, Rik, Zhang, Ying, Feng, Xin-Hua, Wu, Rui-Yun
Publisher: Cold Spring Harbor Laboratory Press
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
Genetic regulation, Tumor suppressor genes

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TGF-beta inhibits muscle differentiation through functional repression of myogenic transcription factors by Smad3

Article Abstract:

TGF-beta has been found to hold back muscle differentiation via functionally repressing myogenic transcription factors with Smad3. Smad3 acts downstream of TGF-beta to repress the MyoD family of bHLH factors, but Smad2 does not. Altered Smad3 signaling affects differentiation of cultured myoblasts and response to TGF-beta.

Author: Liu, Dong, Black, Brian L., Derynck, Rik
Publisher: Cold Spring Harbor Laboratory Press
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2001
Statistical Data Included

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Subjects list: Research, United States, Physiological aspects, Genetic aspects, Proteins, Cytochemistry, Cell differentiation, Cell receptors, Myogenesis, Genetic transcription, Transcription (Genetics)
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