The permeability transition pore triggers Bax translocation to mitochondria during neuronal apoptosis (Q24337594)

positive regulation of neuron apoptotic process

GOA release 2020-03-11

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GOA release 2020-03-11

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T A Precht

1

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R A Phelps

2

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D A Linseman

3

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B D Butts

4

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S S Le

5

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T A Laessig

6

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R J Bouchard

7

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K A Heidenreich

Cell Death & Differentiation

8

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language of work or name

English

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publication date

March 2005

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published in

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volume

12

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issue

3

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page(s)

255-65

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cites work

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ICE, neuronal apoptosis and neurodegeneration

21 January 2018

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Induction of apoptosis in cerebellar granule neurons by low potassium: inhibition of death by insulin-like growth factor I and cAMP.

21 January 2018

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Cascade of caspase activation in potassium-deprived cerebellar granule neurons: targets for treatment with peptide and protein inhibitors of apoptosis

21 January 2018

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Role of Bcl-2 family proteins in apoptosis: apoptosomes or mitochondria?

21 January 2018

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The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex

21 January 2018

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Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics

21 January 2018

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Identification of novel isoforms of the BH3 domain protein Bim which directly activate Bax to trigger apoptosis

21 January 2018

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Regulators of cell death

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Role of the mitochondrial permeability transition pore in apoptosis

21 January 2018

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The release of cytochrome c from mitochondria during apoptosis of NGF-deprived sympathetic neurons is a reversible event

21 January 2018

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The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore

21 January 2018

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The mitochondrion in apoptosis: how Pandora's box opens

21 January 2018

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Calphostin C-mediated translocation and integration of Bax into mitochondria induces cytochrome c release before mitochondrial dysfunction.

21 January 2018

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Transient and long-lasting openings of the mitochondrial permeability transition pore can be monitored directly in intact cells by changes in mitochondrial calcein fluorescence

21 January 2018

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Differential neuroprotection by cyclosporin A and FK506 following ischemia corresponds with differing abilities to inhibit calcineurin and the mitochondrial permeability transition

21 January 2018

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The 'harmless' release of cytochrome c.

21 January 2018

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An APAF-1.cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9

21 January 2018

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Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade

21 January 2018

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Induction of BIM, a proapoptotic BH3-only BCL-2 family member, is critical for neuronal apoptosis

21 January 2018

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Dominant-negative c-Jun promotes neuronal survival by reducing BIM expression and inhibiting mitochondrial cytochrome c release

21 January 2018

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Movement of Bax from the cytosol to mitochondria during apoptosis

21 January 2018

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Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria

21 January 2018

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Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c.

21 January 2018

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Conformation of the Bax C-terminus regulates subcellular location and cell death

21 January 2018

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Bax directly induces release of cytochrome c from isolated mitochondria

21 January 2018

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Disruption of the outer mitochondrial membrane as a result of large amplitude swelling: the impact of irreversible permeability transition.

21 January 2018

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Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis

21 January 2018

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Electrophysiological study of a novel large pore formed by Bax and the voltage-dependent anion channel that is permeable to cytochrome c.

21 January 2018

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Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria

21 January 2018

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14-3-3 Interacts directly with and negatively regulates pro-apoptotic Bax

21 January 2018

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Glycogen synthase kinase-3beta phosphorylates Bax and promotes its mitochondrial localization during neuronal apoptosis.

21 January 2018

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Insulin-like growth factor-I blocks Bcl-2 interacting mediator of cell death (Bim) induction and intrinsic death signaling in cerebellar granule neurons.

21 January 2018

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https://api.crossref.org/works/10.1038%2FSJ.CDD.4401552

7 January 2021

The permeability transition pore signals apoptosis by directing Bax translocation and multimerization.

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https://api.crossref.org/works/10.1038%2FSJ.CDD.4401552

7 January 2021

Insulin-like growth factor and potassium depolarization maintain neuronal survival by distinct pathways: possible involvement of PI 3-kinase in IGF-1 signaling.

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7 January 2021

Insulin-like growth factor-I overexpression attenuates cerebellar apoptosis by altering the expression of Bcl family proteins in a developmentally specific manner.

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7 January 2021

Transfection of adipocytes by gene gun-mediated transfer

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7 January 2021

Caspase-dependent apoptosis of COS-7 cells induced by Bax overexpression: differential effects of Bcl-2 and Bcl-xL on Bax-induced caspase activation and apoptosis

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7 January 2021

Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC

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https://api.crossref.org/works/10.1038%2FSJ.CDD.4401552

7 January 2021