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| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0596981 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0007589 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0013714 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0205615 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C2752630 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0332256 | lld:lifeskim |
| pubmed-article:2159464 | lifeskim:mentions | umls-concept:C0439536 | lld:lifeskim |
| pubmed-article:2159464 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:2159464 | pubmed:dateCreated | 1990-6-13 | lld:pubmed |
| pubmed-article:2159464 | 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. | lld:pubmed |
| pubmed-article:2159464 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2159464 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2159464 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2159464 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2159464 | pubmed:month | May | lld:pubmed |
| pubmed-article:2159464 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:2159464 | pubmed:author | pubmed-author:ElyBB | lld:pubmed |
| pubmed-article:2159464 | pubmed:author | pubmed-author:OlsonE NEN | lld:pubmed |
| pubmed-article:2159464 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2159464 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:2159464 | pubmed:volume | 265 | lld:pubmed |
| pubmed-article:2159464 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2159464 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2159464 | pubmed:pagination | 7914-9 | lld:pubmed |
| pubmed-article:2159464 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:2159464 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2159464 | 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. | lld:pubmed |
| pubmed-article:2159464 | pubmed:affiliation | Department of Biochemistry and Molecular Biology, University of Texas M. D. Anderson Cancer Center, Houston 77030. | lld:pubmed |
| pubmed-article:2159464 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2159464 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2159464 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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