J
John G. Pastorino
Researcher at Thomas Jefferson University
Publications - 31
Citations - 5066
John G. Pastorino is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Mitochondrial permeability transition pore & Mitochondrion. The author has an hindex of 25, co-authored 31 publications receiving 4888 citations. Previous affiliations of John G. Pastorino include University of Medicine and Dentistry of New Jersey & Rowan University.
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Mitochondrial Binding of Hexokinase II Inhibits Bax-induced Cytochrome c Release and Apoptosis
TL;DR: It is demonstrated that HXK II interferes with the ability of Bax to bind to mitochondria and release cytochrome c, and results were found in intact cells, in which the detachment of mitochondrial bound HxK II or its overexpression potentiated and inhibited, respectively, Bax-induced mitochondrial dysfunction and cell death.
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The Overexpression of Bax Produces Cell Death upon Induction of the Mitochondrial Permeability Transition
TL;DR: It is concluded that Bax induces the mitochondrial permeability transition (MPT), a critical event in the loss of cell viability, and mediates other typical manifestations of apoptosis in this model, namely release of cytochrome c, caspase activation with PARP cleavage, and DNA fragmentation.
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Ethanol, oxidative stress, and cytokine-induced liver cell injury
Jan B. Hoek,John G. Pastorino +1 more
TL;DR: How the shift in the balance of cytokine-induced defensive and damage responses in hepatocytes contributes to the liver injury that occurs in alcoholic hepatitis remains poorly characterized and should be a rewarding area for future studies.
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Alcohol and mitochondria: a dysfunctional relationship.
TL;DR: How mitochondrial actions of ethanol influence oxidative stress management of liver cells is considered, which may promote both apoptotic and necrotic cell death in response to otherwise benign or beneficial challenges and contribute to the onset or progression of alcohol-induced liver diseases.
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Activation of Glycogen Synthase Kinase 3β Disrupts the Binding of Hexokinase II to Mitochondria by Phosphorylating Voltage-Dependent Anion Channel and Potentiates Chemotherapy-Induced Cytotoxicity
TL;DR: Interference with the binding of HXK II to mitochondria may be a practicable modality by which to potentiate the efficacy of conventional chemotherapeutic agents.