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| pubmed-article:11970899 | lifeskim:mentions | umls-concept:C0028754 | lld:lifeskim |
| pubmed-article:11970899 | lifeskim:mentions | umls-concept:C0299583 | lld:lifeskim |
| pubmed-article:11970899 | lifeskim:mentions | umls-concept:C0908145 | lld:lifeskim |
| pubmed-article:11970899 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
| pubmed-article:11970899 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:11970899 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:11970899 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:11970899 | pubmed:dateCreated | 2002-4-23 | lld:pubmed |
| pubmed-article:11970899 | pubmed:abstractText | Common obesity is primarily characterized by resistance to the actions of the hormone leptin. Mice deficient in protein tyrosine phosphatase 1B (PTP1B) are resistant to diabetes and diet-induced obesity, prompting us to further define the relationship between PTP1B and leptin in modulating obesity. Leptin-deficient (Lep(ob/ob)) mice lacking PTP1B exhibit an attenuated weight gain, a decrease in adipose tissue, and an increase in resting metabolic rate. Furthermore, PTP1B-deficient mice show an enhanced response toward leptin-mediated weight loss and suppression of feeding. Hypothalami from these mice also display markedly increased leptin-induced Stat3 phosphorylation. Finally, substrate-trapping experiments demonstrate that leptin-activated Jak2, but not Stat3 or the leptin receptor, is a substrate of PTP1B. These results suggest that PTP1B negatively regulates leptin signaling, and provide one mechanism by which it may regulate obesity. | lld:pubmed |
| pubmed-article:11970899 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11970899 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11970899 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11970899 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11970899 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11970899 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:11970899 | pubmed:issn | 1534-5807 | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:TremblayMiche... | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:McGladeC... | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:KennedyBrian... | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:ChengAlanA | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:SimoncicPaul... | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:Lee-LoyAilsaA | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:UetaniNorikoN | lld:pubmed |
| pubmed-article:11970899 | pubmed:author | pubmed-author:ChaubeyVikas... | lld:pubmed |
| pubmed-article:11970899 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11970899 | pubmed:volume | 2 | lld:pubmed |
| pubmed-article:11970899 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11970899 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11970899 | pubmed:pagination | 497-503 | lld:pubmed |
| pubmed-article:11970899 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11970899 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11970899 | pubmed:articleTitle | Attenuation of leptin action and regulation of obesity by protein tyrosine phosphatase 1B. | lld:pubmed |
| pubmed-article:11970899 | pubmed:affiliation | McGill Cancer Center, McGill University, H3G 1Y6, Montreal, Quebec, Canada. | lld:pubmed |
| pubmed-article:11970899 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11970899 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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