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| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C0878544 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C1150553 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C1418905 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C1418898 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C1325180 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C1325181 | lld:lifeskim |
| pubmed-article:16275868 | lifeskim:mentions | umls-concept:C1879648 | lld:lifeskim |
| pubmed-article:16275868 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:16275868 | pubmed:dateCreated | 2005-11-15 | lld:pubmed |
| pubmed-article:16275868 | pubmed:abstractText | AMP-activated protein kinase (AMPK) regulatory gamma2 subunit (PRKAG2) mutations cause a human cardiomyopathy with cardiac hypertrophy, preexcitation, and glycogen deposition. PRKAG2 cardiomyopathy is recapitulated in transgenic mice overexpressing mutant PRKAG2 N488I in the heart (TGgamma2N488I). AMPK is a heterotrimeric kinase consisting of 1 catalytic (alpha) and 2 regulatory (beta and gamma) subunits. Two alpha-subunit isoforms, alpha1 and alpha2, are expressed in the heart; however, the contribution of AMPK utilization of these subunits to PRKAG2 cardiomyopathy is unknown. Mice overexpressing a dominant-negative alpha2 subunit of AMPK (TGalpha2DN) provide a tool for selectively inhibiting alpha2, but not alpha1, subunit-associated AMPK activity. | lld:pubmed |
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| pubmed-article:16275868 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16275868 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16275868 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16275868 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:16275868 | pubmed:issn | 1524-4539 | lld:pubmed |
| pubmed-article:16275868 | pubmed:author | pubmed-author:SeidmanJ GJG | lld:pubmed |
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| pubmed-article:16275868 | pubmed:issnType | Electronic | lld:pubmed |
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| pubmed-article:16275868 | pubmed:volume | 112 | lld:pubmed |
| pubmed-article:16275868 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16275868 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16275868 | pubmed:pagination | 3140-8 | lld:pubmed |
| pubmed-article:16275868 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16275868 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16275868 | pubmed:articleTitle | Increased alpha2 subunit-associated AMPK activity and PRKAG2 cardiomyopathy. | lld:pubmed |
| pubmed-article:16275868 | pubmed:affiliation | Department of Genetics, Harvard Medical School, Howard Hughes Medical Institute, Boston, MA, USA. | lld:pubmed |
| pubmed-article:16275868 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16275868 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:16275868 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16275868 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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