Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death

By Christopher P. Baines, R. A. Kaiser, T. Sheiko, W. Craigen, J. Molkentin. Nature Cell Biology, 2007

956 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c9038b86fd1d435a5d04f51f1448eff6700777c0

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Citations in the corpus

Dimers of mitochondrial ATP synthase form the permeability transition pore (2013, background): “The long-standing idea that the PTP forms at contact sites of the inner and outer membranes through voltage-dependent anion channel (VDAC) and the adenine nucleotide translocator (ANT) (15) proved incorrect, because VDAC-and ANT-null mitochondria still display a CsA-sensitive PT (16 – 18).”
Molecular mechanisms of necroptosis: an ordered cellular explosion (2010, background): “As it stands, CYPD seems to be the leading player of the PTPC, as genetic ablation of peptidylprolyl isomerase F ( Ppif ; the CYPD-encoding gene), but not of the genes coding for all known VDAC and ANT isoform”
Mitochondria in cancer cells: what is so special about them? (2008, neutral): “However, a recent genetic study indicated that mitochondrial VDAC is dispensablefor MPTinductionandapoptoticcelldeath[ 54 ].It appears that the role of VDAC in permeabilization of OMM during apoptosis requires further study.”
Mitochondria and cell death: outer membrane permeabilization and beyond (2010, background): “However, loss of all three VDAC isoforms imparts no resistance of cells or isolated mitochondria to either MOMP or apoptosi”
Biogenesis of β-barrel membrane proteins in bacteria and eukaryotes: evolutionary conservation and divergence (2009, background): “However, the physiological importance of VDAC proteins to apoptosis was challenged by the finding that fibroblasts lacking all three VDAC isoforms exhibited MPT and cell death indistinguishable from wild-type cells [74].”
Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “However, it appears that neither VDAC nor ANT are required components of MPT (17, 137).”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “and Slc25a5, which encode ANT1 and ANT2, respectively [390], or that of Vdac1, Vdac2, and Vdac3 [391, 392] fails to prevent the induction of MPT by oxidative stress or Ca”