| pubmed-article:18037896 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18037896 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:18037896 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:18037896 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:18037896 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:18037896 | pubmed:dateCreated | 2007-12-7 | lld:pubmed |
| pubmed-article:18037896 | pubmed:abstractText | The serine-threonine kinases Pim-1 and Akt regulate cellular proliferation and survival. Although Akt is known to be a crucial signaling protein in the myocardium, the role of Pim-1 has been overlooked. Pim-1 expression in the myocardium of mice decreased during postnatal development, re-emerged after acute pathological injury in mice and was increased in failing hearts of both mice and humans. Cardioprotective stimuli associated with Akt activation induced Pim-1 expression, but compensatory increases in Akt abundance and phosphorylation after pathological injury by infarction or pressure overload did not protect the myocardium in Pim-1-deficient mice. Transgenic expression of Pim-1 in the myocardium protected mice from infarction injury, and Pim-1 expression inhibited cardiomyocyte apoptosis with concomitant increases in Bcl-2 and Bcl-X(L) protein levels, as well as in Bad phosphorylation levels. Relative to nontransgenic controls, calcium dynamics were significantly enhanced in Pim-1-overexpressing transgenic hearts, associated with increased expression of SERCA2a, and were depressed in Pim-1-deficient hearts. Collectively, these data suggest that Pim-1 is a crucial facet of cardioprotection downstream of Akt. | lld:pubmed |
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| pubmed-article:18037896 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18037896 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18037896 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18037896 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:18037896 | pubmed:issn | 1546-170X | lld:pubmed |
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| pubmed-article:18037896 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18037896 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:18037896 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18037896 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18037896 | pubmed:pagination | 1467-75 | lld:pubmed |
| pubmed-article:18037896 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:18037896 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:18037896 | pubmed:articleTitle | Pim-1 regulates cardiomyocyte survival downstream of Akt. | lld:pubmed |
| pubmed-article:18037896 | pubmed:affiliation | San Diego State University Heart Institute, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA. | lld:pubmed |
| pubmed-article:18037896 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18037896 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18037896 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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