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细胞周期调控蛋白p34cdc2的小鼠同源物在T淋巴细胞中的表达。

Expression of the murine homologue of the cell cycle control protein p34cdc2 in T lymphocytes.

作者信息

Kim Y H, Proust J J, Buchholz M J, Chrest F J, Nordin A A

机构信息

Clinical Immunology Section, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224.

出版信息

J Immunol. 1992 Jul 1;149(1):17-23.

PMID:1637418
Abstract

The mammalian homologue of the cdc2 gene of the fission yeast Schizosaccharomyces pombe encodes a p34cdc2 cyclin-dependent kinase that regulates the cell cycle of a wide variety of cell types. Resting murine T lymphocytes contained no detectable p34cdc2 protein, histone kinase activity, or specific mRNA for the cdc2 gene. Activation of the T cells by immobilized anti-CD3 resulted in the expression of specific mRNA late in the G1 phase of the cell cycle, and p34cdc2 protein was detectable at or near G1/S. At this point in the cell cycle, the protein was phosphorylated at tyrosine and displayed no H1 histone kinase activity. As the cells progressed through the cycle, the amount of specific mRNA and p34cdc2 increased, and H1 histone kinase activity was detectable when the cells were blocked at G2/M by nocodazole. The activation of T cells by phorbol dibutyrate induced the expression of IL-2R but failed to induce the synthesis of IL-2 or the expression of cdc2-specific mRNA. Under these conditions, the activated cells failed to enter the S phase of the cell cycle. Because the presence of IL-2 added exogenously during activation by phorbol dibutyrate resulted in the expression of cdc2-specific mRNA and progression through the cell cycle, either IL-2 or the interaction with IL-2R may be involved in the expression of cdc2 and regulation of the G1/S transition.

摘要

粟酒裂殖酵母的细胞分裂周期蛋白2(cdc2)基因的哺乳动物同源物编码一种p34cdc2细胞周期蛋白依赖性激酶,该激酶调节多种细胞类型的细胞周期。静息的鼠T淋巴细胞中未检测到p34cdc2蛋白、组蛋白激酶活性或cdc2基因的特异性mRNA。固定化抗CD3激活T细胞导致在细胞周期G1期晚期表达特异性mRNA,在G1/S期或其附近可检测到p34cdc2蛋白。在细胞周期的这一阶段,该蛋白在酪氨酸位点被磷酸化,且不显示H1组蛋白激酶活性。随着细胞在周期中进展,特异性mRNA和p34cdc2的量增加,当细胞被诺考达唑阻断在G2/M期时可检测到H1组蛋白激酶活性。佛波酯二丁酸酯激活T细胞诱导白细胞介素2受体(IL-2R)的表达,但未能诱导IL-2的合成或cdc2特异性mRNA的表达。在这些条件下,活化的细胞未能进入细胞周期的S期。因为在佛波酯二丁酸酯激活过程中外源添加IL-2会导致cdc2特异性mRNA的表达和细胞周期进展,所以IL-2或与IL-2R的相互作用可能参与cdc2的表达和G1/S期转换的调节。

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