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Mitochondrial Transmembrane Potential and Cell Apoptosis

Xun Cai, Guoqiang Chen, Chen Zhu, Wang Zhenyi

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Abstract

Apoptosis, an intrinsic cell death model which is regulated by organisms, is essential for the maintenance of tissue homeostasis in multicellular organisms. Recently, researchers on cell apoptosis have paid more attention on mitochondrion than on nucleus. Different death stimulus induces opening of PT pore, degradation of mitochondrial transmembrane potential, activation of caspase and inducing cell apoptosis. Bcl 2 and Bcl X L inhibit cell apoptosis via mitochondrion while Bax, Bak and Bad induce apoptosis by means of regulation of mitochondrion.

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What this paper is about

Apoptosis, an intrinsic cell death model which is regulated by organisms, is essential for the maintenance of tissue homeostasis in multicellular organisms. Recently, researchers on cell apoptosis have paid more attention on mitochondrion than on nucleus. Different death stimulus induces opening of PT pore, degradation of mitochondrial transmembrane potential, activation of caspase and inducing cell apoptosis. Bcl 2 and Bcl X L inhibit cell apoptosis via mitochondrion while Bax, Bak and Bad induce apoptosis by means of regulation of mitochondrion.

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Available abstract

Apoptosis, an intrinsic cell death model which is regulated by organisms, is essential for the maintenance of tissue homeostasis in multicellular organisms. Recently, researchers on cell apoptosis have paid more attention on mitochondrion than on nucleus. Different death stimulus induces opening of PT pore, degradation of mitochondrial transmembrane potential, activation of caspase and inducing cell apoptosis. Bcl 2 and Bcl X L inhibit cell apoptosis via mitochondrion while Bax, Bak and Bad induce apoptosis by means of regulation of mitochondrion.

Key concepts: Cell biology, Apoptosis, Mitochondrion, Programmed cell death, Multicellular organism, Cell, Intrinsic apoptosis, Biology

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