Receptor for activated C kinase 1 stimulates nascent polypeptide-dependent translation arrest
Receptor for activated C kinase 1 stimulates nascent polypeptide-dependent translation arrest
复制标题
DOI：
10.1038/embor.2010.169
复制
发表时间：
2010-12-01
期刊：
影响因子：
7.7
通讯作者：
Inada, Toshifumi
中科院分区：
文献类型：
--
作者：
Kuroha, Kazushige;Akamatsu, Mayuko;Inada, Toshifumi
初生肽依赖性翻译阻滞对真核生物基因表达的质量控制至关重要。我们发现活化C激酶1的受体（RACK1）参与新生肽依赖的翻译阻滞，并且它与40S亚基的结合对此至关重要。新生肽的翻译阻滞导致mRNA的不依赖于Dom34/ hbs1的内切裂解，这是由RACK1刺激的。我们提出RACK1刺激由碱性氨基酸序列诱导的翻译阻滞，导致mRNA的核内裂解，以及共翻译蛋白的降解。
Nascent peptide-dependent translation arrest is crucial for the quality control of eukaryotic gene expression. Here we show that the receptor for activated C kinase 1 (RACK1) participates in nascent peptide-dependent translation arrest, and that its binding to the 40S subunit is crucial for this. Translation arrest by a nascent peptide results in Dom34/Hbs1-independent endonucleolytic cleavage of mRNA, and this is stimulated by RACK1. We propose that RACK1 stimulates the translation arrest that is induced by basic amino-acid sequences that leads to endonucleolytic cleavage of the mRNA, as well as to co-translational protein degradation.