Title : Knockout of VDAC1 in H9c2 Cells Promotes Oxidative Stress-Induced Cell Apoptosis through Decreased Mitochondrial Hexokinase II Binding and Enhanced Glycolytic Stress.

Pub. Date : 2020 Sep 9

PMID : 32901466






4 Functional Relationships(s)
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1 However, compared to the wildtype (WT) cells, exposure to either tBHP or ROT enhanced the production of ROS, ECAR, and the proton (H+) production rate (PPR) from glycolysis, as well as promoted apoptotic cell death in VDAC1-/- H9c2 cells. tert-Butylhydroperoxide voltage-dependent anion channel 1 Rattus norvegicus
2 Restoration of VDAC1 in VDAC1-/- H9c2 cells reinstated mitochondria-bound HKII and concomitantly decreased tBHP and ROT-induced ROS production and cell death. tert-Butylhydroperoxide voltage-dependent anion channel 1 Rattus norvegicus
3 Restoration of VDAC1 in VDAC1-/- H9c2 cells reinstated mitochondria-bound HKII and concomitantly decreased tBHP and ROT-induced ROS production and cell death. tert-Butylhydroperoxide voltage-dependent anion channel 1 Rattus norvegicus
4 Interestingly, mitochondrial respiration remained the same after tBHP treatment in VDAC1-/- and WT H9c2 cells. tert-Butylhydroperoxide voltage-dependent anion channel 1 Rattus norvegicus