Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:15563472rdf:typepubmed:Citationlld:pubmed
pubmed-article:15563472lifeskim:mentionsumls-concept:C0086418lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C0021756lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C0812201lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C0022688lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C0017262lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C1334509lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C1366765lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C0851285lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C2911684lld:lifeskim
pubmed-article:15563472lifeskim:mentionsumls-concept:C0185117lld:lifeskim
pubmed-article:15563472pubmed:issue6lld:pubmed
pubmed-article:15563472pubmed:dateCreated2005-2-7lld:pubmed
pubmed-article:15563472pubmed:abstractTextInterleukins (IL)-2 and IL-15 regulate natural killer (NK) cell proliferation, survival, and cytolytic activity. Ets1 is a transcription factor expressed early in NK cell differentiation. Because IL-2Rbeta, IL-2Rgamma, IL-15, and Ets1 knock-out mice similarly lack NK cells, we explored a molecular connection between IL-2R signaling and Ets1. Here we report the post-transcriptional regulation of Ets1 by IL-2R signaling in human NK cells. IL-2 and IL-15 stimulation leads to increased Ets1 protein levels with no significant change in mRNA levels. Pulse and pulse-chase experiments show that IL-2 stimulation results in both a marked increase in the nascent translation of Ets1 and an increased protein half-life. Pharmacological inhibition of MEK specifically blocks IL-2- and IL-15-induced translation, whereas p38, phosphatidylinositol 3-kinase, and mTOR inhibitors had no effect on Ets1 levels. Fli1, an Ets family member, exhibited a different mechanism of regulation, illustrating the specificity of IL-2R beta and gamma subunit signaling on the regulation of Ets1 expression. Expression of a dominant negative form of MNK1, a regulator of the translation initiation factor eIF4E, blocks the expression of Ets1 as do the dominant negative forms of the common IL-2R beta and gamma chains. Expression of Ets1 is regulated similarly in normal peripheral human NK cells. Taken together, our findings provide a direct link between IL-2R subunit signaling and Ets1 expression and helps to explain the interdependence of the IL-2R subunits and Ets1 for NK cell development and function.lld:pubmed
pubmed-article:15563472pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:languageenglld:pubmed
pubmed-article:15563472pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:citationSubsetIMlld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15563472pubmed:statusMEDLINElld:pubmed
pubmed-article:15563472pubmed:monthFeblld:pubmed
pubmed-article:15563472pubmed:issn0021-9258lld:pubmed
pubmed-article:15563472pubmed:authorpubmed-author:WatsonDennis...lld:pubmed
pubmed-article:15563472pubmed:authorpubmed-author:SpyropoulosDe...lld:pubmed
pubmed-article:15563472pubmed:authorpubmed-author:Muise-Helmeri...lld:pubmed
pubmed-article:15563472pubmed:authorpubmed-author:GrundEric MEMlld:pubmed
pubmed-article:15563472pubmed:issnTypePrintlld:pubmed
pubmed-article:15563472pubmed:day11lld:pubmed
pubmed-article:15563472pubmed:volume280lld:pubmed
pubmed-article:15563472pubmed:ownerNLMlld:pubmed
pubmed-article:15563472pubmed:authorsCompleteYlld:pubmed
pubmed-article:15563472pubmed:pagination4772-8lld:pubmed
pubmed-article:15563472pubmed:dateRevised2010-11-18lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:meshHeadingpubmed-meshheading:15563472...lld:pubmed
pubmed-article:15563472pubmed:year2005lld:pubmed
pubmed-article:15563472pubmed:articleTitleInterleukins 2 and 15 regulate Ets1 expression via ERK1/2 and MNK1 in human natural killer cells.lld:pubmed
pubmed-article:15563472pubmed:affiliationDepartment of Cell Biology and Anatomy, Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina 29425, USA.lld:pubmed
pubmed-article:15563472pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15563472pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
entrez-gene:3558entrezgene:pubmedpubmed-article:15563472lld:entrezgene
entrez-gene:3600entrezgene:pubmedpubmed-article:15563472lld:entrezgene
entrez-gene:5594entrezgene:pubmedpubmed-article:15563472lld:entrezgene
entrez-gene:5595entrezgene:pubmedpubmed-article:15563472lld:entrezgene
entrez-gene:8569entrezgene:pubmedpubmed-article:15563472lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:15563472lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:15563472lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:15563472lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:15563472lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:15563472lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:15563472lld:entrezgene
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:15563472lld:pubmed
More...