Meiying Yang, Jie Sun, David F Stowe, Emad Tajkhorshid, Wai-Meng Kwok, and
Amadou KS Camara.
Knockout of VDAC1 in H9c2 cells promotes oxidative stress-induced
cell apoptosis through decreased mitochondrial hexokinase II binding and
enhanced glycolytic stress.
Cellular Physiology & Biochemistry, 54:853-874, 2020.
Published.
YANG2020-ET
The role of VDAC1, the most abundant mitochondrial outer membrane protein,
in cell death depends on cell types and stimuli. Both silencing and upregulation
of VDAC1 in
various type of cancer cell lines can stimulate apoptosis. In contrast, in mouse
embryonic stem (MES) cells and mouse embryonic fibroblasts (MEFs), the roles
of VDAC1
knockout (VDAC1^-/-) in apoptotic cell death are contradictory. The
contribution and underlying mechanism of VDAC1^-/- in oxidative stress-
induced cell death in
cardiac cells has not been established. We hypothesized that VDAC1 is an
essential regulator of oxidative stress-induced cell death in H9c2 cells.
