Effect of Bcl-x(L) overexpression on reactive oxygen species, intracellular calcium, and mitochondrial membrane potential following injury in astrocytes. (Q44088277)

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scientific article published in August 2002

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English	Effect of Bcl-x(L) overexpression on reactive oxygen species, intracellular calcium, and mitochondrial membrane potential following injury in astrocytes.	scientific article published in August 2002

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scholarly article

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11 November 2019

Effect of Bcl-x(L) overexpression on reactive oxygen species, intracellular calcium, and mitochondrial membrane potential following injury in astrocytes (English)

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11 November 2019

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reactive oxygen species

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3

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11 November 2019

author name string

Yi-Bing Ouyang

1

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11 November 2019

Sean G Carriedo

2

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11 November 2019

publication date

1 August 2002

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11 November 2019

Free Radical Biology and Medicine

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11 November 2019

33

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4

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11 November 2019

544-551

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11 November 2019

The mitochondrial death/life regulator in apoptosis and necrosis

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Mitochondria and apoptosis

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Bcl-xL regulates the membrane potential and volume homeostasis of mitochondria

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Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked

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The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis

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VDAC regulation by the Bcl-2 family of proteins

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The role of the Bcl-2 family in the regulation of outer mitochondrial membrane permeability

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BCL-2 family members and the mitochondria in apoptosis

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BCL-2 proteins: regulators of the mitochondrial apoptotic program

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7 January 2021

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Bcl-2 proteins: regulators of apoptosis or of mitochondrial homeostasis?

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Bcl-x(L) prevents the initial decrease in mitochondrial membrane potential and subsequent reactive oxygen species production during tumor necrosis factor alpha-induced apoptosis

1 reference

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Overexpression of bcl-xL protects astrocytes from glucose deprivation and is associated with higher glutathione, ferritin, and iron levels.

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Expression of bcl-2 inhibits necrotic neural cell death.

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Dissipation of potassium and proton gradients inhibits mitochondrial hyperpolarization and cytochrome c release during neural apoptosis

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bcl-x is expressed in embryonic and postnatal neural tissues and functions to prevent neuronal cell death

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Lack of oxidative phosphorylation and low mitochondrial membrane potential decrease susceptibility to apoptosis and do not modulate the protective effect of Bcl-x(L) in osteosarcoma cells.

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Potentiation of murine astrocyte antioxidant defence by bcl-2: protection in part reflects elevated glutathione levels.

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Increasing vulnerability of astrocytes to oxidative injury with age despite constant antioxidant defenses.

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The mitochondrial permeability transition pore and nitric oxide synthase mediate early mitochondrial depolarization in astrocytes during oxygen-glucose deprivation.

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Superoxide production in rat hippocampal neurons: selective imaging with hydroethidine

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1 reference

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Pivotal role of mitochondrial calcium uptake in neural cell apoptosis and necrosis

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Differential sensitivity of murine astrocytes and neurons from different brain regions to injury

1 reference

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Effect of overexpression of BCL-2 on cellular oxidative damage, nitric oxide production, antioxidant defenses, and the proteasome

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Programmed cell death and Bcl-2 protection in very low oxygen.

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7 January 2021

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Evidence against the hypothesis that BCL-2 inhibits apoptosis through an anti-oxidant effect

1 reference

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Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair

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Enhanced oxidative stress and altered antioxidants in brains of Bcl-2-deficient mice

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Inhibitors of permeability transition interfere with the disruption of the mitochondrial transmembrane potential during apoptosis.

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Mitochondrial control of nuclear apoptosis.

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Mitochondrial permeability transition is a central coordinating event of apoptosis

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Bcl-xL prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange

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Functional F1-ATPase essential in maintaining growth and membrane potential of human mitochondrial DNA-depleted rho degrees cells

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Bcl-2 prevents apoptotic mitochondrial dysfunction by regulating proton flux

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Identifiers

10.1016/S0891-5849(02)00912-7

1 reference

Europe PubMed Central

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:12160936%20AND%20SRC:MED&resulttype=core&format=json

11 November 2019

1 reference

Europe PubMed Central

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:12160936%20AND%20SRC:MED&resulttype=core&format=json

11 November 2019

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