Receptor-interacting protein shuttles between cell death and survival signaling pathways.
Receptor-interacting protein shuttles between cell death and survival signaling pathways.
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DOI：
10.1091/mbc.e09-06-0530
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发表时间：
2010-02-01
影响因子：
3.3
通讯作者：
Kapila YL
中科院分区：
文献类型：
--
作者：
Kamarajan P;Bunek J;Lin Y;Nunez G;Kapila YL
RIP在CD95/Fas死亡和FAK存活信号之间穿梭，以调节失巢凋亡。细胞凋亡和存活信号通路之间的串扰对于调节组织过程和减轻疾病至关重要。我们报道，失巢凋亡--由细胞外基质接触缺失引发--激活CD95/Fas介导的信号通路，受受体相互作用蛋白(RIP)调节，RIP是一种在CD95/Fas介导的细胞死亡和整合素/粘着斑激酶(FAK)介导的生存通路之间穿梭的激酶。RIP的死亡结构域对于RIP和Fas的联合调节失巢至关重要。Fas或RIP的减弱减少了这种联系并抑制了失巢凋亡，而它们的过度表达则起到了相反的作用。过量表达FAK可恢复RIP和FAK的联系，并抑制失巢凋亡。因此，RIP在CD95/Fas死亡和FAK存活信号之间穿梭，以调节失巢。
RIP shuttles between CD95/Fas death and FAK survival signaling to mediate anoikis. Cross-talk between apoptosis and survival signaling pathways is crucial for regulating tissue processes and mitigating disease. We report that anoikis—apoptosis triggered by loss of extracellular matrix contacts—activates a CD95/Fas-mediated signaling pathway regulated by receptor-interacting protein (RIP), a kinase that shuttles between CD95/Fas-mediated cell death and integrin/focal adhesion kinase (FAK)-mediated survival pathways. RIP's death domain was critical for RIP and Fas association to mediate anoikis. Fas or RIP attenuation reduced this association and suppressed anoikis, whereas their overexpression had the reverse effect. Overexpressing FAK restored RIP and FAK association and inhibited anoikis. Thus, RIP shuttles between CD95/Fas death and FAK survival signaling to mediate anoikis.
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