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hnRNP-K is a nuclear target of TCR-activated ERK and required for T-cell late activation
International Immunology, 11/06/09
Chang JW et al. – The 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.
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