Nuclear to cytoplasmic translocation of hnRNP U enhances TLR-induced proinflammatory cytokines production by stabilizing mRNAs in macrophages
会议名称：《“细胞活动 生命活力”——中国细胞生物学学会全体会员代表大会暨第十二次学术大会》
会议日期：2011年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100104[医学-病理学与病理生理学] 10[医学]
关 键 词：TLR hnRNP U RNA stability proinflammatory cytokine
摘 要：TLR signaling is associated with the transcription of various proinflammatory cytokines including TNF-α, IL-6 and IL-1β.After transcription,the mRNA of these proinflammatory cytokines needs to be tightly controlled at the post-transcriptional level to achieve an optimal ***,the precise mechanism of post-transcriptional regulation is not fully *** the present study,we found the expression of hnRNP U,also termed scaffold attachment factor A(SAF-A),was greatly induced by TLR stimulation in ***-down of hnRNP U expression greatly attenuated TLR-induced expression of TNF-α, IL-6 and IL-1β,but not IL-12,while hnRNP U overexpression greatly increased TLR-induced expression of TNF-α,IL-6 and IL-1β.Furthermore,hnRNP U knock-down accelerated the turnover and decreased the half-life of TNF-在,IL-6,and IL-1β*** immunoprecipitation(RIP) demonstrated that hnRNP U bound to the mRNA of these proinflammatory cytokines through the RGG ***,we showed that TLR stimulation provided a stimulus for hnRNP U nuclear to cytoplasmic ***,we propose that hnRNP U induced by TLR signaling binds to the mRNA of a subset of proinflammatory cytokines and positively regulates the expression of these cytokines by stabilizing mRNA.