| pubmed-article:19074988 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C0014239 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C0948265 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C0085536 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C0332161 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C1335281 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C1709439 | lld:lifeskim |
| pubmed-article:19074988 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:19074988 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19074988 | pubmed:dateCreated | 2009-2-27 | lld:pubmed |
| pubmed-article:19074988 | pubmed:abstractText | The protein tyrosine phosphatase PTP1B is a negative regulator of insulin signaling; consequently, mice deficient in PTP1B are hypersensitive to insulin. Because PTP1B(-/-) mice have diminished fat stores, the extent to which PTP1B directly regulates glucose homeostasis is unclear. Previously, we showed that brain-specific PTP1B(-/-) mice are protected against high-fat diet-induced obesity and glucose intolerance, whereas muscle-specific PTP1B(-/-) mice have increased insulin sensitivity independent of changes in adiposity. Here we studied the role of liver PTP1B in glucose homeostasis and lipid metabolism. | lld:pubmed |
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| pubmed-article:19074988 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19074988 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19074988 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:19074988 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19074988 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:19074988 | pubmed:issn | 1939-327X | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:KahnBarbara... | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:NeelBenjamin... | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:KimJason KJK | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:DelibegovicMi... | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:ChoYou-ReeYR | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:HongEun-Gyoun... | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:BenceKendra... | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:ZimmerDerekD | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:KauffmanCaitl... | lld:pubmed |
| pubmed-article:19074988 | pubmed:author | pubmed-author:RakKimberlyK | lld:pubmed |
| pubmed-article:19074988 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19074988 | pubmed:volume | 58 | lld:pubmed |
| pubmed-article:19074988 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19074988 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19074988 | pubmed:pagination | 590-9 | lld:pubmed |
| pubmed-article:19074988 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:19074988 | pubmed:meshHeading | pubmed-meshheading:19074988... | lld:pubmed |
| pubmed-article:19074988 | pubmed:meshHeading | pubmed-meshheading:19074988... | lld:pubmed |
| pubmed-article:19074988 | pubmed:meshHeading | pubmed-meshheading:19074988... | lld:pubmed |
| pubmed-article:19074988 | pubmed:meshHeading | pubmed-meshheading:19074988... | lld:pubmed |
