The internal ribosome entry site-mediated translation of antiapoptotic protein XIAP is modulated by the heterogeneous nuclear ribonucleoproteins C1 and C2
The internal ribosome entry site-mediated translation of antiapoptotic protein XIAP is modulated by the heterogeneous nuclear ribonucleoproteins C1 and C2
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DOI：
10.1128/mcb.23.1.280-288.2003
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发表时间：
2003-01-01
影响因子：
5.3
通讯作者：
Korneluk, RG
中科院分区：
文献类型：
--
作者：
Holcík, M;Gordon, BW;Korneluk, RG
X染色体连锁的凋亡抑制因子XIAP是最强大和普遍存在的内源性凋亡抑制因子。我们以前已经表明，XIAP的翻译是由一个有效的内部核糖体进入位点（IRES）元件控制。IRES介导的XIAP翻译在细胞应激反应中增加，表明IRES翻译在细胞应激过程中起关键作用。在这里，我们表明，异质核核糖核蛋白C1和C2（hnRNPC 1和-C2）的RNP复合物的一部分，形成XIAP IRES。此外，hnRNPC 1和-C2的细胞水平平行XIAP IRES的活性和hnRNPC 1和-C2的过表达特异性增强XIAP IRES的翻译，表明hnRNPC 1和-C2可以调节XIAP表达。鉴于XIAP在细胞凋亡调控中的核心作用，这些结果对于我们理解细胞凋亡的控制是重要的。
The X-chromosome-linked inhibitor of apoptosis, XIAP, is the most powerful and ubiquitous intrinsic inhibitor of apoptosis. We have shown previously that the translation of XIAP is controlled by a potent internal ribosome entry site (IRES) element. IRES-mediated translation of XIAP is increased in response to cellular stress, suggesting the critical role for IRES translation during cellular stress. Here, we demonstrate that heterogeneous nuclear ribonucleoproteins C1 and C2 (hnRNPC1 and -C2) are part of the RNP complex that forms on XIAP IRES. Furthermore, the cellular levels of hnRNPC1 and -C2 parallel the activity of XIAP IRES and the overexpression of hnRNPC1 and -C2 specifically enhanced translation of XIAP IRES, suggesting that hnRNPC1 and -C2 may modulate XIAP expression. Given the central role of XIAP in the regulation of apoptosis these results are important for our understanding of the control of apoptosis.