Linked Life Data

18784362

Source:http://linkedlifedata.com/resource/pubmed/id/18784362

Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:18784362rdf:typepubmed:Citationlld:pubmed
pubmed-article:18784362lifeskim:mentionsumls-concept:C1522564lld:lifeskim
pubmed-article:18784362lifeskim:mentionsumls-concept:C0020564lld:lifeskim
pubmed-article:18784362lifeskim:mentionsumls-concept:C0072476lld:lifeskim
pubmed-article:18784362lifeskim:mentionsumls-concept:C0033095lld:lifeskim
pubmed-article:18784362lifeskim:mentionsumls-concept:C0152058lld:lifeskim
pubmed-article:18784362lifeskim:mentionsumls-concept:C1521733lld:lifeskim
pubmed-article:18784362lifeskim:mentionsumls-concept:C1879746lld:lifeskim
pubmed-article:18784362lifeskim:mentionsumls-concept:C1547011lld:lifeskim
pubmed-article:18784362pubmed:issue37lld:pubmed
pubmed-article:18784362pubmed:dateCreated2008-9-17lld:pubmed
pubmed-article:18784362pubmed:abstractTextPim-1 kinase exerts potent cardioprotective effects in the myocardium downstream of AKT, but the participation of Pim-1 in cardiac hypertrophy requires investigation. Cardiac-specific expression of Pim-1 (Pim-WT) or the dominant-negative mutant of Pim-1 (Pim-DN) in transgenic mice together with adenoviral-mediated overexpression of these Pim-1 constructs was used to delineate the role of Pim-1 in hypertrophy. Transgenic overexpression of Pim-1 protects mice from pressure-overload-induced hypertrophy relative to wild-type controls as evidenced by improved hemodynamic function, decreased apoptosis, increases in antihypertrophic proteins, smaller myocyte size, and inhibition of hypertrophic signaling after challenge. Similarly, Pim-1 overexpression in neonatal rat cardiomyocyte cultures inhibits hypertrophy induced by endothelin-1. On the cellular level, hearts of Pim-WT mice show enhanced incorporation of BrdU into myocytes and a hypercellular phenotype compared to wild-type controls after hypertrophic challenge. In comparison, transgenic overexpression of Pim-DN leads to dilated cardiomyopathy characterized by increased apoptosis, fibrosis, and severely depressed cardiac function. Furthermore, overexpression of Pim-DN leads to reduced contractility as evidenced by reduced Ca(2+) transient amplitude and decreased percentage of cell shortening in isolated myocytes. These data support a pivotal role for Pim-1 in modulation of hypertrophy by impacting responses on molecular, cellular, and organ levels.lld:pubmed
pubmed-article:18784362pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:commentsCorrectionshttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:languageenglld:pubmed
pubmed-article:18784362pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:citationSubsetIMlld:pubmed
pubmed-article:18784362pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18784362pubmed:statusMEDLINElld:pubmed
pubmed-article:18784362pubmed:monthSeplld:pubmed
pubmed-article:18784362pubmed:issn1091-6490lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:SchaeferErikElld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:KajsturaJanJlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:AnversaPieroPlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:SussmanMark...lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:WangZepingZlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:RotaMarcelloMlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:FischerKimber...lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:GudeNatalieNlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:MuraskiJohn...lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:WuWeitaoWlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:MagnusonNancy...lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:CottageChrist...lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:QuijadaPearlPlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:MasonMattMlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:DinShabanaSlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:AlvarezRobert...lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:ChenXiongenXlld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:MacDonnelScot...lld:pubmed
pubmed-article:18784362pubmed:authorpubmed-author:HouserStephen...lld:pubmed
pubmed-article:18784362pubmed:issnTypeElectroniclld:pubmed
pubmed-article:18784362pubmed:day16lld:pubmed
pubmed-article:18784362pubmed:volume105lld:pubmed
pubmed-article:18784362pubmed:ownerNLMlld:pubmed
pubmed-article:18784362pubmed:authorsCompleteYlld:pubmed
pubmed-article:18784362pubmed:pagination13889-94lld:pubmed
pubmed-article:18784362pubmed:dateRevised2011-9-26lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:meshHeadingpubmed-meshheading:18784362...lld:pubmed
pubmed-article:18784362pubmed:year2008lld:pubmed
pubmed-article:18784362pubmed:articleTitlePim-1 kinase antagonizes aspects of myocardial hypertrophy and compensation to pathological pressure overload.lld:pubmed
pubmed-article:18784362pubmed:affiliationSan Diego State Heart Institute, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182, USA.lld:pubmed
pubmed-article:18784362pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18784362pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:18784362pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
entrez-gene:24649entrezgene:pubmedpubmed-article:18784362lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:18784362lld:entrezgene
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18784362lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18784362lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18784362lld:pubmed
More...