REGULATION OF TYROSINE AMINOTRANSFERASE MESSENGER RIBONUCLEIC-ACID IN RAT-LIVER - EFFECT OF CYCLOHEXIMIDE ON MESSENGER RIBONUCLEIC-ACID TURNOVER
REGULATION OF TYROSINE AMINOTRANSFERASE MESSENGER RIBONUCLEIC-ACID IN RAT-LIVER - EFFECT OF CYCLOHEXIMIDE ON MESSENGER RIBONUCLEIC-ACID TURNOVER
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DOI：
10.1021/bi00269a022
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发表时间：
1982-01-01
期刊：
影响因子：
2.9
通讯作者：
ERNEST, MJ
中科院分区：
文献类型：
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作者：
ERNEST, MJ
在体内给予醋酸氢化可的松、二丁酰cAMP或蛋白质合成抑制剂放线菌酮后，大鼠肝脏中酪氨酸氨基转移酶[达特] mRNA活性迅速增加3- 6倍。类固醇激素或环核苷酸与放线菌酮的组合治疗导致达特mRNA水平比对照值高10至20倍。这些mRNA活性的变化不伴随白蛋白mRNA或总肝脏模板活性的变化。放线菌酮处理防止达特mRNA活性的快速下降虫草素抑制从头RNA合成。当用环己酰亚胺代替帕他霉素时，没有观察到这种保护作用，这表明蛋白质合成本身的抑制并不负责达特mRNA的稳定。根据放线菌酮和太平洋霉素对大鼠肝多核糖体结构的影响，可以得出结论，放线菌酮介导的达特mRNA活性的增加是mRNA分子的稳定化的结果，这使得该信息不易于在细胞质中失活和降解。放线菌酮的作用对达特、磷酸烯醇式丙酮酸羧激酶以及可能编码响应激素或代谢刺激而迅速翻转的次要肝蛋白的其他几种mRNA非常特异。
Tyrosine aminotransferase [TAT] mRNA activity in rat liver was rapidly increased 3- to 6-fold following in vivo administration of hydrocortisone acetate, dibutyryl cAMP or the protein synthesis inhibitor cycloheximide. Treatment with the steroid hormone or cyclic nucleotide in combination with cycloheximide resulted in levels of TAT mRNA 10- to 20-fold greater than control values. These changes in mRNA activity were not accompanied by changes in albumin mRNA or total liver template activity. The rapid decline in TAT mRNA activity following cordycepin inhibition of de novo RNA synthesis was prevented by cycloheximide treatment. This protection was not observed when pactamycin was substituted for cycloheximide, demonstrating that the inhibition of protein synthesis per se was not responsible for the stabilization of TAT mRNA. Based upon the effects of cycloheximide and pactamycin on rat liver polysome structure, it is concluded that the cycloheximide-mediated increase in TAT mRNA activity is the result of stabilization of the mRNA molecule which renders the message less susceptible to inactivation and degradation in the cytoplasm. The action of cycloheximide is very specific for TAT, phosphoenolpyruvate carboxykinase, and probably several other mRNA that code for minor liver proteins that turn over rapidly in response to hormonal or metabolic stimuli.