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目的:探讨β-arrestin2对肿瘤坏死因子α(TNFα)信号转导的调控作用.方法:在HT-29细胞过表达β-arrestin2和干扰β-arrestin2表达后,用TNFα刺激相应时间点,用免疫共沉淀和Western印迹法观察TNFα诱导的下游信号转导分子IKKα/β(I-kappa-B kinaseα/β),IκBα,TAK1(TGF-betaacti-vated kinase1),JNK(c-junN-terminal kinase),p38的活化及可能机制.结果:β-arrestin2通过结合RIP1并抑制TNFα诱导的RIP1的多聚泛素化,抑制TNFα诱导的IKKα/β及下游信号通路活化,TAK1及其下游信号通路则活化增强.干扰β-arrestin2表达从反向说明β-arrestin2对TNFα的信号转导调控.结论:β-arrestin2通过结合并抑制RIP1多聚泛素化抑制TNFα诱导的IKKα/β活化,而促进TAK1活化.
Objective: To investigate the regulatory effect of β-arrestin2 on tumor necrosis factor α (TNFα) signal transduction.Methods: After the expression of β-arrestin2 and β-arrestin2 were over-expressed in HT-29 cells, TNFα was used to stimulate the corresponding time points, The expression of IKKα / β, IκBα, TAK1 and JNK (c-junN-terminal kinase) were detected by coprecipitation and Western blotting. , p38 activation and its possible mechanism.β-arrestin2 inhibits TNFα-induced polyclonalization of RIP1 by inhibiting RIPα-induced RIPA-induced activation of IKKα / β and downstream signaling pathways, activating TAK1 and its downstream signaling pathway Β-arrestin2 could reverse the signal transduction of β-arrestin2 on TNFα.Conclusion: β-arrestin2 can promote TAK1 activation by binding and inhibiting RIP1 poly-ubiquitination to inhibit TNFα-induced IKKα / β activation .