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rdf:type |
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lifeskim:mentions |
umls-concept:C0010531,
umls-concept:C0017337,
umls-concept:C0086661,
umls-concept:C0162493,
umls-concept:C0330390,
umls-concept:C0439851,
umls-concept:C0600499,
umls-concept:C1515877,
umls-concept:C1552596,
umls-concept:C1879547,
umls-concept:C1947931
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pubmed:issue |
51
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pubmed:dateCreated |
2002-11-6
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pubmed:abstractText |
The c-MYC proto-oncogene encodes a ubiquitous transcription factor involved in the control of cell growth and differentiation and broadly implicated in tumorigenesis. Understanding the function of c-MYC and its role in cancer depends upon the identification of c-MYC target genes. Here we show that c-MYC induces the activity of Protein Kinase A (PKA), a key effector of cAMP-mediated signal transduction, by inducing the transcription of the gene encoding the PKA catalytic subunit beta (PKA-Cbeta). c-MYC-mediated induction of PKA-Cbeta gene transcription occurs in multiple tissues, is independent of cell proliferation and is mediated by direct binding of c-MYC to the PKA-Cbeta gene promoter sequences. Constitutive expression of PKA-Cbeta in Rat1A cells induces their transformation, and c-MYC-induced transformation can be reverted by pharmacological inhibition of PKA, suggesting that up-regulation of PKA is critical for c-MYC-associated tumorigenesis. These results indicate that, by activating PKA, c-MYC can provide endogenous activation of the cAMP signal transduction pathway independently of extracellular signals.
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
7
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7872-82
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12420224-Animals,
pubmed-meshheading:12420224-B-Lymphocytes,
pubmed-meshheading:12420224-Cell Division,
pubmed-meshheading:12420224-Cell Line, Transformed,
pubmed-meshheading:12420224-Cell Transformation, Neoplastic,
pubmed-meshheading:12420224-Cyclic AMP,
pubmed-meshheading:12420224-Cyclic AMP-Dependent Protein Kinase Catalytic Subunits,
pubmed-meshheading:12420224-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:12420224-Enzyme Induction,
pubmed-meshheading:12420224-Fibroblasts,
pubmed-meshheading:12420224-Gene Expression Regulation,
pubmed-meshheading:12420224-Genes, Reporter,
pubmed-meshheading:12420224-Humans,
pubmed-meshheading:12420224-Isoenzymes,
pubmed-meshheading:12420224-Luciferases,
pubmed-meshheading:12420224-Mice,
pubmed-meshheading:12420224-Mice, Transgenic,
pubmed-meshheading:12420224-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:12420224-Organ Specificity,
pubmed-meshheading:12420224-Promoter Regions, Genetic,
pubmed-meshheading:12420224-Proto-Oncogene Proteins c-myc,
pubmed-meshheading:12420224-Rats,
pubmed-meshheading:12420224-Recombinant Fusion Proteins,
pubmed-meshheading:12420224-Second Messenger Systems,
pubmed-meshheading:12420224-Transcription, Genetic
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pubmed:year |
2002
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pubmed:articleTitle |
c-MYC activates protein kinase A (PKA) by direct transcriptional activation of the PKA catalytic subunit beta (PKA-Cbeta) gene.
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pubmed:affiliation |
Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
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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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