Translational regulation in the cellular response to biosynthetic load on the endoplasmic reticulum
Translational regulation in the cellular response to biosynthetic load on the endoplasmic reticulum
复制标题
DOI：
10.1101/sqb.2001.66.499
复制
发表时间：
2001-01-01
期刊：
影响因子：
--
通讯作者：
Ron, D
中科院分区：
文献类型：
--
作者：
Harding, HP;Novoa, I;Ron, D
500 HARDING等响应特定信号。几种eIF 2 α激酶已经进化为将特异性应激信号与eIF 2 α在Ser-51上的磷酸化偶联。例如，干扰素诱导的PKR被病毒感染细胞中的双链RNA激活，并参与宿主适应，使入侵病毒无法使用细胞的蛋白质合成机制（考夫曼2000），HRI是一种血红素抑制的eIF 2 α激酶，可确保红系前体中的珠蛋白生物合成与血红素辅基的产生相匹配（Chen 2000）。
500 HARDING ET AL. sponse to specific signals. Several eIF2α kinases have evolved to couple specific stress signals to phosphorylation of eIF2α on Ser-51. For example, the interferon-induced PKR is activated by double-stranded RNA in virally infected cells and participates in a host adaptation that deprives the invading virus of use of the cell’s protein synthesizing machinery (Kaufman 2000), and HRI, a heme-repressed eIF2α kinase, ensures the matching of globin biosynthesis in erythroid precursors to the production of the heme prosthetic group (Chen 2000).