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Mitochondrial membrane voltage-dependent anion channel
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Mitochondrial membrane voltage-dependent anion channel
Voltage-dependent anion channel (voltage-dependent anion channels, VDAC) in the outer mitochondrial membrane, its closure can inhibit mitochondrial function, leading to mitochondrial membrane permeability change, release of proteins such as cytochrome C, Smac / Diablo, apoptosis factors, etc. eventually lead to apoptosis [1,2]. VDAC affected by many factors, such as hypoxia, cell hypoxia, ethanol, reactive oxygen species and reactive nitrogen, cytokines, kinase, NADH can inhibit the increase in VDAC, the promotion of respiratory chain substrates such as short-chain fatty acids and oxidation of acetaldehyde. A lot of evidence that the VDAC on the mitochondria and the regulation of cell function is very important.
1 VDAC basic characteristics of
1.1 VDAC characteristics of the molecular structure of the VDAC in the mitochondrial outer membrane is very important [3]. Now extracted from a variety of creatures mitochondrial VDAC, including plants, animals, fungi, protozoa and so on. VDAC has three kinds of isomers, the most primitive of the model is the β -sheet, the membrane structure is composed of 10 amino acids, the structure of highly conserved, but not all are of the β -sheet across the mitochondrial membrane, the channel structure from a drum a β helix and 13 β -sheet form [5], mammalian VDAC right La3 sensitive, but N.crassaVDAC insensitive. On the contrary, N.crassaVDAC by the G-actin regulation, while mammals are not the regulator.
The distribution of VDAC in a variety of organisms are not the same. N.crassa There is a VDAC, while S.cerebiciae (yeast), there are two VDAC, rat, there are three kinds of wheat VDAC isomers, its molecular weight is about 30kD [4]. VDAC knock out three kinds of isomers of a can lead to serious consequences, such as the knockout will be induced in rats VDAC3 infertility, while the knockout VDAC1 or VDAC2 can cause respiratory function decli
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