| pubmed-article:11853668 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11853668 | lifeskim:mentions | umls-concept:C2004454 | lld:lifeskim |
| pubmed-article:11853668 | lifeskim:mentions | umls-concept:C0547070 | lld:lifeskim |
| pubmed-article:11853668 | lifeskim:mentions | umls-concept:C0036981 | lld:lifeskim |
| pubmed-article:11853668 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:11853668 | lifeskim:mentions | umls-concept:C0205369 | lld:lifeskim |
| pubmed-article:11853668 | lifeskim:mentions | umls-concept:C0449774 | lld:lifeskim |
| pubmed-article:11853668 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:11853668 | pubmed:dateCreated | 2002-2-20 | lld:pubmed |
| pubmed-article:11853668 | pubmed:abstractText | Alternative splicing of the gene for Stat3, a transcription factor activated by the IL-6 family of cytokines, produces two isoforms: Stat3alpha and a dominant-negative variant, Stat3beta. Stat3beta-deficient mice were generated by gene targeting. Despite intact expression and phosphorylation of Stat3alpha, overall Stat3 activity was impaired in Stat3beta(-/-) cells. Global comparison of transcription in Stat3beta(+/+) and Stat3beta(-/-) cells revealed stable differences. Stat3beta-deficient mice exhibit diminished recovery from endotoxic shock and hyperresponsiveness of a subset of endotoxin-inducible genes in liver. The hepatic response to endotoxin in wild-type mice is accompanied by a transient increase in the ratio of Stat3beta to Stat3alpha. These findings indicate a critical role for Stat3beta in the control of systemic inflammation. | lld:pubmed |
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| pubmed-article:11853668 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11853668 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11853668 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11853668 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11853668 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:11853668 | pubmed:author | pubmed-author:YooJoo-YeonJY | lld:pubmed |
| pubmed-article:11853668 | pubmed:author | pubmed-author:HusoDavid LDL | lld:pubmed |
| pubmed-article:11853668 | pubmed:author | pubmed-author:NathansDaniel... | lld:pubmed |
| pubmed-article:11853668 | pubmed:author | pubmed-author:DesiderioStep... | lld:pubmed |
| pubmed-article:11853668 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11853668 | pubmed:day | 8 | lld:pubmed |
| pubmed-article:11853668 | pubmed:volume | 108 | lld:pubmed |
| pubmed-article:11853668 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11853668 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11853668 | pubmed:pagination | 331-44 | lld:pubmed |
| pubmed-article:11853668 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11853668 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11853668 | pubmed:articleTitle | Specific ablation of Stat3beta distorts the pattern of Stat3-responsive gene expression and impairs recovery from endotoxic shock. | lld:pubmed |
| pubmed-article:11853668 | pubmed:affiliation | Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Baltimore, MD, USA. | lld:pubmed |
| pubmed-article:11853668 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11853668 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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