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海拉细胞的有丝分裂原刺激会增加缺氧应激蛋白LDH 6/k的活性:被queuine抑制。

Mitogenic stimulation of HeLa cells increases the activity of the anoxic stress protein, LDH 6/k: suppression by queuine.

作者信息

Reisser T, Eicher A, Langgut W

机构信息

Institut für Biochemie der Medizinischen Fakultät, Universität Erlangen-Nürnberg, Germany.

出版信息

Biochem Biophys Res Commun. 1993 Dec 30;197(3):1319-25. doi: 10.1006/bbrc.1993.2621.

DOI:10.1006/bbrc.1993.2621
PMID:8280149
Abstract

Mitogenic stimulation of quiescent mammalian cells triggers an array of early events crucial for cell cycle progression. Here we show that the activity of the anoxic stress protein, lactate dehydrogenase 6/k, transiently increased after mitogenic stimulation of serum-starved HeLa cells. Regulation of lactate dehydrogenase 6/k activity in early G1 depended on the activity of a receptor tyrosine kinase and on protein and mRNA synthesis, but did not involve protein kinase C. The guanine analog, queuine, an ubiquitously occurring tRNA base of bacterial origin, suppressed the mitogen-induced protein synthesis and also the transient increase in lactate dehydrogenase 6/k activity. The results suggest that queuine relieves hypoxic stress resulting from mitogenic stimulation by suppressing protein synthesis during G0/G1 transition.

摘要

对静止的哺乳动物细胞进行有丝分裂原刺激会引发一系列对细胞周期进程至关重要的早期事件。在此我们表明,在血清饥饿的HeLa细胞经有丝分裂原刺激后,缺氧应激蛋白乳酸脱氢酶6/k的活性会短暂增加。早期G1期乳酸脱氢酶6/k活性的调节取决于受体酪氨酸激酶的活性以及蛋白质和mRNA的合成,但不涉及蛋白激酶C。鸟嘌呤类似物queuine是一种普遍存在的源自细菌的tRNA碱基,它抑制有丝分裂原诱导的蛋白质合成以及乳酸脱氢酶6/k活性的短暂增加。结果表明,queuine通过在G0/G1期转换过程中抑制蛋白质合成来减轻有丝分裂原刺激引起的缺氧应激。

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J Bacteriol. 1995 Sep;177(18):5284-8. doi: 10.1128/jb.177.18.5284-5288.1995.
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Activation of transfer RNA-guanine ribosyltransferase by protein kinase C.蛋白激酶C对转运RNA-鸟嘌呤核糖基转移酶的激活作用。
Nucleic Acids Res. 1995 Jul 11;23(13):2492-8. doi: 10.1093/nar/23.13.2492.
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