Source:http://linkedlifedata.com/resource/pubmed/id/17616678
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
13
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pubmed:dateCreated |
2007-7-9
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pubmed:abstractText |
Signal transducers and activators of transcription 3 (STAT3) was originally identified as a transcription factor that mediates cytokine-induced responses. In these pathways, Janus-activated kinase (JAK)-induced transient tyrosine phosphorylation of STAT3 promotes gene expression in response to a number of cytokines, which is inhibited by feedback mechanisms. A number of studies have shown that STAT3 is constitutively activated in human cancer cells, leading to cell proliferation. It is unclear, apart from a chronic tyrosyl phosphorylation of STAT3, what mechanisms contribute to the STAT3 deregulation in tumors. Earlier, we have isolated a novel growth inhibitory gene product, gene associated with retinoid-IFN-induced mortality 19 (GRIM-19), using a genetic approach. GRIM-19 is an IFN/retinoic acid-regulated growth suppressor. Subsequent analyses have shown that GRIM-19 binds to STAT3 and prevents interleukin-6-induced transcription of cellular genes. However, its effects on a constitutively active STAT3 and cellular transformation are unknown. In this study, we show that GRIM-19 suppresses constitutive STAT3-induced cellular transformation in vitro and in vivo by down-regulating the expression of a number of cellular genes involved in cell proliferation and apoptosis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/GRIM19 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/NADH, NADPH Oxidoreductases,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0008-5472
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
67
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6212-20
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:17616678-Animals,
pubmed-meshheading:17616678-Apoptosis,
pubmed-meshheading:17616678-Apoptosis Regulatory Proteins,
pubmed-meshheading:17616678-Cell Death,
pubmed-meshheading:17616678-Cell Proliferation,
pubmed-meshheading:17616678-Cell Transformation, Neoplastic,
pubmed-meshheading:17616678-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:17616678-Humans,
pubmed-meshheading:17616678-Interleukin-6,
pubmed-meshheading:17616678-Mice,
pubmed-meshheading:17616678-NADH, NADPH Oxidoreductases,
pubmed-meshheading:17616678-Phosphorylation,
pubmed-meshheading:17616678-Rats,
pubmed-meshheading:17616678-STAT3 Transcription Factor,
pubmed-meshheading:17616678-Transcription, Genetic,
pubmed-meshheading:17616678-Tretinoin
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pubmed:year |
2007
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pubmed:articleTitle |
Tumor-suppressive activity of the cell death activator GRIM-19 on a constitutively active signal transducer and activator of transcription 3.
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pubmed:affiliation |
Department of Microbiology and Immunology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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