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- W2026063842 abstract "Eukaryotic cell viability is largely regulated at the level of mitochondria, with cell death executed by endogenous proteins that act to increase the permeability of the inner and/or outer membranes of these organelles. The gastric pathogen, Helicobacter pylori, can mimic this mechanism by producing the pro-apoptotic toxin, VacA, which was recently demonstrated to (i) localize to mitochondria within epithelial cells, (ii) rapidly transport into mitochondria in vitro, and (iii) induce changes consistent with permeabilization of mitochondrial membranes by a mechanism dependent on cellular entry and toxin membrane channel activity. The targeting of mitochondrial membranes is emerging as a strategy used by pathogenic microbes to control cell viability while circumventing upstream pathways and checkpoints of cell death. Eukaryotic cell viability is largely regulated at the level of mitochondria, with cell death executed by endogenous proteins that act to increase the permeability of the inner and/or outer membranes of these organelles. The gastric pathogen, Helicobacter pylori, can mimic this mechanism by producing the pro-apoptotic toxin, VacA, which was recently demonstrated to (i) localize to mitochondria within epithelial cells, (ii) rapidly transport into mitochondria in vitro, and (iii) induce changes consistent with permeabilization of mitochondrial membranes by a mechanism dependent on cellular entry and toxin membrane channel activity. The targeting of mitochondrial membranes is emerging as a strategy used by pathogenic microbes to control cell viability while circumventing upstream pathways and checkpoints of cell death. adenine nucleotide translocase, a component of the permeability transition pore. programmed cell death within eukaryotic cells: occurs by several conserved mechanisms as an essential process during development. Apoptosis is one form of cell death in eukaryotes, and under ideal circumstances, results in the clearance of apoptotic cells by professional phagocytes in such a manner as to minimize an inflammatory response within the host. the assembly of this complex is central to the activation of apoptosis. It comprises the vertebrate homologue of the nematode, Ced-4 protein, Apaf-1, holo-cytochrome c (released from mitochondria), deoxy-adenosinetriphosphate and pro-Caspase-9. Bcl-2 antagonist/killer. Bak is pro-apoptosis. Bcl-2 associated x protein. Bax is a member of the Bcl-2 family and is pro-apoptosis. endogenous proteins involved in modulating mitochondrial membrane permeability within mammalian cells. There are both pro-apoptotic and anti-apoptotic Bcl-2 proteins. B-cell lymphoma 2. Belongs to the Bcl-2 family of proteins. Bcl-2 inhibits cell death. long form of Bcl-x. A Bcl-2-related gene that functions as a dominant regulator of apoptotic cell death. Bcl-xL inhibits cell death. cysteinyl aspartic acid proteases involved in executing cell damage during apoptosis. inner mitochondrial membrane permeabilization, manifested by the dissipation of trans-membrane potential (ΔΨm). organelles that make use of molecular oxygen. They generate ATP, the major molecule by which cellular energy is transferred or spent. In addition, mitohcondria serve as the central sensors and executioners of eukaryotic cell death. mitochondrial membrane permeabilization. Changes in the permeability of mitochondrial inner and outer membranes are nearly a universal hallmark of apoptosis. a form of cell death resulting from anoxia, trauma, or any other form of irreversible damage to the cell; involves the release of toxic cellular material into the intercellular space, poisoning surrounding cells. outer mitochondrial membrane permeabilization, manifested by the release of effectors from the intermembrane space of the mitochondrion. calcium dependent, non-specific mitochondrial membrane permeabilization. a complex of the voltage-dependent anion channel (VDAC), the adenine nucleotide translocase and cyclophilin-D (CyP-D) at contact sites between the mitochondrial outer and inner membranes. voltage-dependent anion channel, a component of the permeability transition pore." @default.
- W2026063842 created "2016-06-24" @default.
- W2026063842 creator A5030797083 @default.
- W2026063842 date "2005-02-01" @default.
- W2026063842 modified "2023-10-16" @default.
- W2026063842 title "Micro-managing the executioner: pathogen targeting of mitochondria" @default.
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- W2026063842 doi "https://doi.org/10.1016/j.tim.2004.12.007" @default.
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