| pubmed-article:20203306 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20203306 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:20203306 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:20203306 | lifeskim:mentions | umls-concept:C0072476 | lld:lifeskim |
| pubmed-article:20203306 | lifeskim:mentions | umls-concept:C1947912 | lld:lifeskim |
| pubmed-article:20203306 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:20203306 | pubmed:dateCreated | 2010-4-16 | lld:pubmed |
| pubmed-article:20203306 | pubmed:abstractText | Cardioprotective signaling mediates antiapoptotic actions through multiple mechanisms including maintenance of mitochondrial integrity. Pim-1 kinase is an essential downstream effector of AKT-mediated cardioprotection but the mechanistic basis for maintenance of mitochondrial integrity by Pim-1 remains unexplored. This study details antiapoptotic actions responsible for enhanced cell survival in cardiomyocytes with elevated Pim-1 activity. | lld:pubmed |
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| pubmed-article:20203306 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:20203306 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20203306 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20203306 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20203306 | pubmed:issn | 1524-4571 | lld:pubmed |
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