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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0031727,
umls-concept:C0035820,
umls-concept:C0040648,
umls-concept:C0205430,
umls-concept:C0330390,
umls-concept:C0851827,
umls-concept:C0871261,
umls-concept:C1552644,
umls-concept:C1701901,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1823153,
umls-concept:C1881379,
umls-concept:C1998811,
umls-concept:C2349976,
umls-concept:C2911692
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pubmed:issue |
26
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pubmed:dateCreated |
2005-6-27
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pubmed:abstractText |
Transcription factor CCAAT/enhancer-binding protein-beta (C/EBP-beta) regulates a variety of cellular functions in response to exogenous stimuli. We have reported earlier that C/EBP-beta induces gene transcription through a novel interferon (IFN)-response element called gamma-IFN-activated transcriptional element. We show here that IFN-gamma-induced, C/EBP-beta/gamma-IFN-activated transcriptional element-dependent gene expression is regulated by mixed lineage kinases (MLKs), members of the mitogen-activated protein kinase kinase kinase family. MLK3 appears to activate C/EBP-beta in response to IFN-gamma by a mechanism involving decreased phosphorylation of a specific phosphoacceptor residue, Ser(64), within the transactivation domain. Decreased phosphorylation of Ser(64) was independent of IFN-gamma-stimulated ERK1/2 activation and did not require the ERK phosphorylation site Thr(189) located in regulatory domain 2 of C/EBP-beta. Together these studies provide the first evidence that MLK3 is involved in IFN-gamma signaling and identify a novel mechanism of transcriptional activation by IFN-gamma.
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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 |
Jul
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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 |
1
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pubmed:volume |
280
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
24462-71
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15878863-Animals,
pubmed-meshheading:15878863-Binding Sites,
pubmed-meshheading:15878863-Blotting, Western,
pubmed-meshheading:15878863-CCAAT-Enhancer-Binding Protein-beta,
pubmed-meshheading:15878863-Cell Line,
pubmed-meshheading:15878863-Chromatin Immunoprecipitation,
pubmed-meshheading:15878863-Enzyme Activation,
pubmed-meshheading:15878863-Gene Expression Regulation,
pubmed-meshheading:15878863-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:15878863-Green Fluorescent Proteins,
pubmed-meshheading:15878863-Interferon-gamma,
pubmed-meshheading:15878863-MAP Kinase Kinase Kinases,
pubmed-meshheading:15878863-Macrophages,
pubmed-meshheading:15878863-Mice,
pubmed-meshheading:15878863-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:15878863-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:15878863-Models, Biological,
pubmed-meshheading:15878863-Models, Genetic,
pubmed-meshheading:15878863-Mutation,
pubmed-meshheading:15878863-Phosphorylation,
pubmed-meshheading:15878863-Plasmids,
pubmed-meshheading:15878863-Protein Structure, Tertiary,
pubmed-meshheading:15878863-RNA, Small Interfering,
pubmed-meshheading:15878863-Serine,
pubmed-meshheading:15878863-Signal Transduction,
pubmed-meshheading:15878863-Time Factors,
pubmed-meshheading:15878863-Transcription, Genetic,
pubmed-meshheading:15878863-Transcriptional Activation,
pubmed-meshheading:15878863-Transfection
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pubmed:year |
2005
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pubmed:articleTitle |
A role for mixed lineage kinases in regulating transcription factor CCAAT/enhancer-binding protein-{beta}-dependent gene expression in response to interferon-{gamma}.
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pubmed:affiliation |
Greenebaum Cancer Center, Department of Microbiology and Immunology, University of Maryland School of Medicine, Balltimore, MD 21201, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, N.I.H., Extramural
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