Mechanism of inhibition of polypeptide chain initiation in heat-shocked Ehrlich ascites tumour cells.
Mechanism of inhibition of polypeptide chain initiation in heat-shocked Ehrlich ascites tumour cells.
复制标题
热休克艾氏腹水肿瘤细胞中多肽链起始的抑制机制。
DOI：
10.1111/j.1432-1033.1984.tb08088.x
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Henshaw,EC
中科院分区：
文献类型：
--
作者：
Panniers,R;Henshaw,EC
在43℃孵育的Ehrlich细胞中，多肽合成速率比37℃孵育的Ehrlich细胞抑制了80%。翻译的调节位点位于多肽链起始。在更高的温度下，多肽合成不会恢复；然而，通过将细胞返回到37℃，这种抑制被逆转。在37℃下恢复，既不需要新的RNA合成，也不需要蛋白质合成，消除了mRNA的降解和多肽链起始所必需的蛋白质的不可逆变性。与对照组相比，热休克细胞中40-S引发络合物的浓度显著降低。这在由热休克细胞和对照细胞制备的无细胞蛋白质合成系统中得到了证实。因此，影响eIF2功能的成分活性的可逆变化可能是热休克Ehrlich细胞的一种调节机制。在热休克细胞提取物中，Met-tRNA合成酶活性与对照提取物相比没有变化。
The rate of polypeptide synthesis is inhibited by 80% in Ehrlich cells incubated at 43°C compared to those at 37°C. The regulatory site of translation resides at polypeptide chain initiation. Polypeptide synthesis does not recover at the higher temperature; however, the inhibition is reversed by returning the cells to 37°C. Neither new RNA synthesis or protein synthesis is required for recovery at 37°C, eliminating degradation of mRNA and irreversible denaturation of a protein essential for polypeptide chain initiation. The concentration of 40‐S initiation complexes was found to be reduced markedly in heat‐shocked cells compared to controls. This was confirmed in the cell‐free protein‐synthesizing systems prepared from heat‐shocked and control cells. Reversible alteration in the activity of components affecting eIF2 function is, therefore, a likely mechanism of regulation in heat‐shocked Ehrlich cells. In extracts from heat‐shocked cells, Met‐tRNA synthetase activity was unaltered compared to control extracts.