X-linked inhibitor of apoptosis protein functions as a cofactor in transforming growth factor-β signaling
X-linked inhibitor of apoptosis protein functions as a cofactor in transforming growth factor-β signaling
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DOI：
10.1074/jbc.m100331200
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发表时间：
2001-07-13
影响因子：
4.8
通讯作者：
Duckett, CS
中科院分区：
文献类型：
--
作者：
Reffey, SB;Wurthner, JU;Duckett, CS
X-linked inhibitor of apoptosis protein （XIAP）是一种有效的凋亡细胞死亡抑制剂，它通过直接抑制caspases（凋亡的主要效应因子）起作用。在这里，我们报道XIAP也可以作为一个辅助因子，通过转化生长因子- β (tgf - β)， XIAP，而不是相关蛋白c-IAP1或c-IAP2来调节基因表达，这些蛋白与tgf - β受体超家族的几个I型成员相关，并增强tgf - β诱导的信号传导。尽管发现XIAP介导的c-Jun n -末端激酶和核因子kappaB的激活需要tgf - β信号传导的中间体Smad4。发现XIAP抑制细胞凋亡的能力与smad4无关，这些数据表明XIAP在tgf - β介导的信号传导中起着不同于其抗凋亡功能的作用。
X-linked inhibitor of apoptosis protein (XIAP) is a potent suppressor of apoptotic cell death, which functions by directly inhibiting caspases, the principal effecters of apoptosis. Here we report that XIAP can also function as a cofactor in the regulation of gene expression by transforming growth factor-beta (TGF-beta), XIAP, but not the related proteins c-IAP1 or c-IAP2, associated with several members of the type I class of the TGF-beta receptor superfamily and potentiated TGF-beta -induced signaling, Although XIAP-mediated activation of c-Jun N-terminal kinase and nuclear factor kappaB was found to require the TGF-beta signaling intermediate Smad4, the ability of XIAP to suppress apoptosis was found to be Smad4-independent, These data implicate a role for XIAP in TGF-beta -mediated signaling that is distinct from its anti-apoptotic functions.