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rdf:type |
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lifeskim:mentions |
umls-concept:C0007589,
umls-concept:C0013714,
umls-concept:C0018270,
umls-concept:C0040690,
umls-concept:C0205245,
umls-concept:C0205615,
umls-concept:C0332256,
umls-concept:C0439536,
umls-concept:C0596981,
umls-concept:C0597357,
umls-concept:C2752630
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pubmed:issue |
14
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pubmed:dateCreated |
1990-6-13
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pubmed:abstractText |
Transforming growth factor-beta (TGF-beta) has been shown to block the morphological and molecular events associated with myoblast differentiation. During fusion of C2 myoblasts, TGF-beta receptors are down-regulated, and muscle-specific genes become refractory to the inhibitory effects of TGF-beta. To define further the mechanisms that modulate TGF-beta receptor expression during myogenesis, we have developed culture conditions that support the differentiation of C2 cells in the absence of fusion and have examined the expression of functional TGF-beta receptors in biochemically differentiated mononucleated myocytes. Exposure of C2 myoblasts to growth factor-deficient medium containing 1.4 mM [ethylenebis(oxyethylenenitrilo)]tetraacetic acid (EGTA) leads to withdrawal from the cell cycle and high level expression of muscle-specific mRNAs and proteins. Under these conditions, TGF-beta receptors fail to be down-regulated, and the differentiation program remains sensitive to repression by TGF-beta. These studies demonstrate that EGTA uncouples muscle-specific gene expression from fusion in C2 cells and that in the absence of fusion, C2 myocytes retain a functional TGF-beta signaling system.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Creatine Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Cross-Linking Reagents,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholinergic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/Succinimides,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Troponin,
http://linkedlifedata.com/resource/pubmed/chemical/Troponin T,
http://linkedlifedata.com/resource/pubmed/chemical/disuccinimidyl suberate
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
265
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7914-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2159464-Animals,
pubmed-meshheading:2159464-Cell Differentiation,
pubmed-meshheading:2159464-Cell Line,
pubmed-meshheading:2159464-Creatine Kinase,
pubmed-meshheading:2159464-Cross-Linking Reagents,
pubmed-meshheading:2159464-Down-Regulation,
pubmed-meshheading:2159464-Egtazic Acid,
pubmed-meshheading:2159464-Gene Expression,
pubmed-meshheading:2159464-Mice,
pubmed-meshheading:2159464-Molecular Weight,
pubmed-meshheading:2159464-Muscles,
pubmed-meshheading:2159464-RNA, Messenger,
pubmed-meshheading:2159464-Receptors, Cell Surface,
pubmed-meshheading:2159464-Receptors, Cholinergic,
pubmed-meshheading:2159464-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:2159464-Succinimides,
pubmed-meshheading:2159464-Transforming Growth Factors,
pubmed-meshheading:2159464-Troponin,
pubmed-meshheading:2159464-Troponin T
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pubmed:year |
1990
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pubmed:articleTitle |
Functional receptors for transforming growth factor-beta are retained by biochemically differentiated C2 myocytes in growth factor-deficient medium containing EGTA but down-regulated during terminal differentiation.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, University of Texas M. D. Anderson Cancer Center, Houston 77030.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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