Source:http://linkedlifedata.com/resource/pubmed/id/21156935
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
152
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pubmed:dateCreated |
2010-12-15
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pubmed:abstractText |
In the field of molecular oncology, the Myc basic helix-loop-helix family of transcription factors has been extensively studied. The Myc proto-oncogene c-Myc binds DNA, activates or represses gene transcription, and consequently affects cellular proliferation. However, emerging evidence presents the existence of c-Myc variants that lack transcriptional activity. A cytoplasmic variant of c-Myc called "Myc-nick," which arises from calpain-mediated cleavage of c-Myc, assists in stable microtubule assembly. Furthermore, Myc-nick promotes MyoD-mediated myogenic differentiation, thus antagonizing its precursor. These results provide exciting new opportunities in formulating molecular approaches for treatment of cancer and in our understanding of cell differentiation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1937-9145
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
pe49
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pubmed:dateRevised |
2011-9-14
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pubmed:meshHeading | |
pubmed:year |
2010
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pubmed:articleTitle |
Myc-nick: the force behind c-Myc.
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pubmed:affiliation |
Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article
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