Bax increases the pore size of rat brain mitochondrial voltage-dependent anion channel in the presence of tBid.
Voltage-dependent anion channel (VDAC), Bax, and tBid play a central role in apoptosis regulation but their functioning is still very controversial. VDAC forms voltage gated pore in planar lipid bilayers, and acts as the pathway for the movement of substances in and out of the mitochondria by passive diffusion. Here we report that there is increase in the pore size of VDAC in the presence of Bax and tBid through bilayer electrophysiological experiments. We hereby hypothesize that this increase in pore size might cause swelling in the mitochondria, leading to the rupture of mitochondrial outer membrane and release of cytochrome c causing brain cell death.
Banerjee
Jyotirmoy
J
Department of Biophysics, University of Delhi South Campus, New Delhi 110021, India.
Ghosh
Subhendu
S
D000818:Animals; D000838:Anions / Q000737:chemistry*; D051023:BH3 Interacting Domain Death Agonist Protein; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002352:Carrier Proteins / Q000737:chemistry*; D016923:Cell Death; D045304:Cytochromes c / Q000378:metabolism; D004058:Diffusion; D004594:Electrophysiology; D008051:Lipid Bilayers; D008055:Lipids / Q000737:chemistry; D008928:Mitochondria / Q000378:metabolism*; D018272:Porins / Q000737:chemistry / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051381:Rats; D050994:Voltage-Dependent Anion Channels; D051028:bcl-2-Associated X Protein
D000838:Anions; D051023:BH3 Interacting Domain Death Agonist Protein; C494828:Bax protein, rat; C494816:Bid protein, rat; D002352:Carrier Proteins; D008051:Lipid Bilayers; D008055:Lipids; D018272:Porins; D019253:Proto-Oncogene Proteins c-bcl-2; D050994:Voltage-Dependent Anion Channels; D051028:bcl-2-Associated X Protein; D045304:Cytochromes c