pubmed-article:12208853 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C0037663 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C1426207 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C0086222 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C1551336 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C0205460 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C1705733 | lld:lifeskim |
pubmed-article:12208853 | lifeskim:mentions | umls-concept:C2003905 | lld:lifeskim |
pubmed-article:12208853 | pubmed:issue | 43 | lld:pubmed |
pubmed-article:12208853 | pubmed:dateCreated | 2002-10-25 | lld:pubmed |
pubmed-article:12208853 | pubmed:abstractText | Suppressor of cytokine signaling (SOCS)-2 is a member of a family of intracellular proteins implicated in the negative regulation of cytokine signaling. The generation of SOCS-2-deficient mice, which grow to one and a half times the size of their wild-type littermates, suggests that SOCS-2 may attenuate growth hormone (GH) signaling. In vitro studies indicate that, while SOCS-2 can inhibit GH action at low concentrations, at higher concentrations it may potentiate signaling. To determine whether a similar enhancement of signaling is observed in vivo or alternatively whether increased SOCS-2 levels repress growth in vivo, we generated and analyzed transgenic mice that overexpress SOCS-2 from a human ubiquitin C promoter. These mice are not growth-deficient and are, in fact, significantly larger than wild-type mice. The overexpressed SOCS-2 was found to bind to endogenous GH receptors in a number of mouse organs, while phosphopeptide binding studies with recombinant SOCS-2 defined phosphorylated tyrosine 595 on the GH receptor as the site of interaction. Together, the data implicate SOCS-2 as having dual effects on GH signaling in vivo. | lld:pubmed |
pubmed-article:12208853 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12208853 | pubmed:language | eng | lld:pubmed |
pubmed-article:12208853 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12208853 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12208853 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12208853 | pubmed:month | Oct | lld:pubmed |
pubmed-article:12208853 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:12208853 | pubmed:author | pubmed-author:MetcalfDonald... | lld:pubmed |
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pubmed-article:12208853 | pubmed:author | pubmed-author:ThausAnne LAL | lld:pubmed |
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pubmed-article:12208853 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12208853 | pubmed:day | 25 | lld:pubmed |
pubmed-article:12208853 | pubmed:volume | 277 | lld:pubmed |
pubmed-article:12208853 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12208853 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12208853 | pubmed:pagination | 40181-4 | lld:pubmed |
pubmed-article:12208853 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:12208853 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12208853 | pubmed:articleTitle | Biological evidence that SOCS-2 can act either as an enhancer or suppressor of growth hormone signaling. | lld:pubmed |
pubmed-article:12208853 | pubmed:affiliation | Walter and Eliza Hall Institute of Medical Research and the Cooperative Research for Cellular Growth Factors, PO Royal Melbourne Hospital, VIC 3050, Australia. greenhalgh@wehi.edu.au | lld:pubmed |
pubmed-article:12208853 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12208853 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12208853 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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