Linked Life Data

19880579

Source:http://linkedlifedata.com/resource/pubmed/id/19880579

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pubmed-article:19880579pubmed:abstractTextSustained extracellular signal-regulated kinase (ERK)-signaling plays a critical role in T-cell-mediated IL-2 production. Although many downstream targets are known for ERK, details remain unknown about which molecules play functional roles in IL-2 production. Here, we addressed this question using proteomic analysis of nuclear proteins from TCR-activated T cells and identified hnRNP-K as one of the ERK targets essential for IL-2 production. hnRNP-K was previously shown by others to be a direct substrate of ERK and form complexes with multiple signaling proteins as well as DNA and RNA. Our data showed a clear ERK-dependent increase in one form of hnRNP-K after TCR stimulation. Small interfering RNA-mediated gene knockdown of hnRNP-K expression abrogated IL-2 production by T cells. Moreover, reduction of hnRNP-K expression caused a notable increase in proteolysis of Vav1, a binding target of hnRNP-K. Since Vav1 is an essential molecule for T-cell activation, the data suggest that ERK signaling is required for T-cell activation partly by inhibiting activation-induced proteolysis of Vav1.lld:pubmed
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pubmed-article:19880579pubmed:dateRevised2011-3-3lld:pubmed
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pubmed-article:19880579pubmed:articleTitlehnRNP-K is a nuclear target of TCR-activated ERK and required for T-cell late activation.lld:pubmed
pubmed-article:19880579pubmed:affiliationDepartment of Medicine, Immunotherapy Center, Medical College of Georgia, Augusta, GA 30912-2600, USA.lld:pubmed
pubmed-article:19880579pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19880579pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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