| pubmed-article:15284232 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15284232 | lifeskim:mentions | umls-concept:C1335872 | lld:lifeskim |
| pubmed-article:15284232 | lifeskim:mentions | umls-concept:C1367307 | lld:lifeskim |
| pubmed-article:15284232 | lifeskim:mentions | umls-concept:C2247949 | lld:lifeskim |
| pubmed-article:15284232 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15284232 | lifeskim:mentions | umls-concept:C1523987 | lld:lifeskim |
| pubmed-article:15284232 | pubmed:issue | 40 | lld:pubmed |
| pubmed-article:15284232 | pubmed:dateCreated | 2004-9-27 | lld:pubmed |
| pubmed-article:15284232 | pubmed:abstractText | Interferon-gamma (IFNgamma) is a pluripotent cytokine whose major biological effects are mediated through a pathway in which STAT1 is the predominant and essential transcription factor. STAT3 can also be activated weakly by IFNgamma, but the mechanism of activation and function of STAT3 as a part of the interferon response are not known. Here we show that STAT3 activation is much stronger and more prolonged in STAT1-null mouse embryo fibroblasts than in wild-type cells. In response to IFNgamma, SRC-family kinases are required to activate STAT3 (but not STAT1) through tyrosine phosphorylation, whereas the receptor-bound kinases JAK1 and JAK2 are required to activate both STATs. Tyrosine 419 of the IFNgamma receptor subunit 1 (IFNGR1) is required to activate both STATs, suggesting that STAT1 and STAT3 compete with each other for the same receptor phosphotyrosine motif. Activated STAT3 can replace STAT1 in STAT1-null cells to drive the transcription of certain genes, for example, socs-3 and c/ebpdelta, which have gamma-activated sequence motifs in their promoters. Work from Ian Kerr's laboratory reveals that the gp130-linked interleukin-6 receptor, which usually activates STAT3 predominantly, activates STAT1 efficiently when STAT3 is absent. Because STAT1 and STAT3 have opposing biological effects (STAT3 is an oncogene, and STAT1 is a tumor suppressor), the reciprocal activation of these two transcription factors in response to IFNgamma or interleukin-6 suggests that their relative abundance, which may vary substantially in different normal cell types, under different conditions or in tumors is likely to have a major impact on how cells behave in response to different cytokines. | lld:pubmed |
| pubmed-article:15284232 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15284232 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15284232 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15284232 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15284232 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:15284232 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:15284232 | pubmed:author | pubmed-author:StarkGeorge... | lld:pubmed |
| pubmed-article:15284232 | pubmed:author | pubmed-author:QingYulanY | lld:pubmed |
| pubmed-article:15284232 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15284232 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:15284232 | pubmed:volume | 279 | lld:pubmed |
| pubmed-article:15284232 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15284232 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15284232 | pubmed:pagination | 41679-85 | lld:pubmed |
| pubmed-article:15284232 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:15284232 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15284232 | pubmed:articleTitle | Alternative activation of STAT1 and STAT3 in response to interferon-gamma. | lld:pubmed |
| pubmed-article:15284232 | pubmed:affiliation | Department of Molecular Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. | lld:pubmed |
| pubmed-article:15284232 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15284232 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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