原癌基因bcl-2在细胞凋亡过程中的作用。评论文章。

Sbornik lekarsky Pub Date : 2002-01-01
Z Humlová
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引用次数: 0

摘要

细胞凋亡是一种受基因调控的细胞死亡形式,与多细胞生物组织稳态的维持密切相关。线粒体在这一过程中发挥关键作用,参与ATP的合成、氧自由基的产生、Ca2+离子的控制、细胞色素c、凋亡诱导因子、Smac/DIABLO蛋白和几种原葡聚糖酶等凋亡分子的挤出。细胞凋亡的早期阶段是离子和水通过线粒体内膜的通量变化的特征,在此期间,基质体积的增加可能导致线粒体膜电位(δ psi m)的崩溃。这些变化受到Bax促进的Bcl-2/Bcl-XL的抑制,并至少由所谓的通透性过渡孔复合物介导,这是线粒体膜通透性(MMP)的可能机制之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protooncogene bcl-2 in process of apoptosis. Review article.

The process of apoptosis is genetically regulated form of cell death, which is tightly connected, with maintaining of tissue homeostasis in multicellular organisms. Mitochondria play a key role in this process being involved in ATP synthesis, production of oxygen free radicals, control of Ca2+ ions, extrusion of apoptogenic molecules such as cytochrome c, apoptosis inducing factor, Smac/DIABLO protein and several procaspases. Changes in the flux of ions and water across the inner mitochondrial membrane characterize the early phase of apoptosis, during which an increase in matrix volume may precede a collapse of mitochondrial membrane potential (delta psi m). These changes are suppressed by Bcl-2/Bcl-XL facilitated by Bax, and mediated at least by so-called permeability transition pore complex which is one of possible mechanisms involved in mitochondrial membrane permeabilization (MMP).

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