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胸腺细胞凋亡不需要Cdc2激活。

Cdc2 activation is not required for thymocyte apoptosis.

作者信息

Norbury C, MacFarlane M, Fearnhead H, Cohen G M

机构信息

ICRF Molecular Oncology Laboratory, University of Oxford Institute of Molecular Medicine, John Radcliffe Hospital, UK.

出版信息

Biochem Biophys Res Commun. 1994 Aug 15;202(3):1400-6. doi: 10.1006/bbrc.1994.2086.

Abstract

Apoptosis is a mode of cell death characterized by chromatin condensation and disassembly of the nuclear lamina, processes that are also characteristic of mitosis. The apparent similarity between the two events, together with observations that apoptosis can occur following G2 arrest, has led to the suggestion that apoptosis could be a defective form of mitosis. Further support for this idea comes from the recent description of activation of the p34cdc2 protein kinase (Cdc2), the universal M-phase promoter, during death induced by a lymphocyte granule protease. We have monitored the protein kinase activity of Cdc2 during apoptosis of primary rat thymocytes, which die from a quiescent (G0) state. We demonstrate unequivocally that activation of Cdc2 is not involved in the induction of apoptosis in thymocytes, indicating that chromatin condensation and lamina disassembly occur in this system by processes different from those that operate in mitosis.

摘要

细胞凋亡是一种细胞死亡方式,其特征为染色质浓缩和核纤层解体,这些过程也是有丝分裂的特征。这两种事件之间明显的相似性,以及细胞凋亡可在G2期阻滞之后发生的观察结果,导致有人提出细胞凋亡可能是一种有缺陷的有丝分裂形式。对这一观点的进一步支持来自最近对p34cdc2蛋白激酶(Cdc2)(通用的M期启动子)在淋巴细胞颗粒蛋白酶诱导的死亡过程中被激活的描述。我们监测了原代大鼠胸腺细胞凋亡过程中Cdc2的蛋白激酶活性,这些细胞从静止(G0)状态开始死亡。我们明确证明,Cdc2的激活不参与胸腺细胞凋亡的诱导,这表明在该系统中染色质浓缩和核纤层解体是通过与有丝分裂中起作用的过程不同的过程发生的。

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