The voltage-dependent anion channel: an essential player in apoptosis (Q28218549)

Breaking the mitochondrial barrier

Europe PubMed Central

title

The voltage-dependent anion channel: an essential player in apoptosis (English)

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Yoshihide Tsujimoto

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Shigeomi Shimizu

series ordinal

2

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language of work or name

English

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publication date

2002

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84

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issue

2-3

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page(s)

187-93

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cites work

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Mitochondrial endonuclease G is important for apoptosis in C. elegans.

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Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells

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Apoptotic pathways: paper wraps stone blunts scissors

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Molecular characterization of mitochondrial apoptosis-inducing factor

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Hsp60 accelerates the maturation of pro-caspase-3 by upstream activator proteases during apoptosis

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Presence of a pre-apoptotic complex of pro-caspase-3, Hsp60 and Hsp10 in the mitochondrial fraction of jurkat cells

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Endonuclease G is an apoptotic DNase when released from mitochondria

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The conserved N-terminal BH4 domain of Bcl-2 homologues is essential for inhibition of apoptosis and interaction with CED-4

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BH4 domain of antiapoptotic Bcl-2 family members closes voltage-dependent anion channel and inhibits apoptotic mitochondrial changes and cell death

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Bcl-2 family proteins as ion-channels

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

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Investigation of bax-induced release of cytochrome c from yeast mitochondria permeability of mitochondrial membranes, role of VDAC and ATP requirement

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Bax and Bcl-xL independently regulate apoptotic changes of yeast mitochondria that require VDAC but not adenine nucleotide translocator

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Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells

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Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity

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Colicin Pore-Forming Domains Bind toEscherichia ColiTrimeric Porins†

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Gelsolin inhibits apoptosis by blocking mitochondrial membrane potential loss and cytochrome c release

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Gelsolin in complex with phosphatidylinositol 4,5-bisphosphate inhibits caspase-3 and -9 to retard apoptotic progression

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Human gelsolin prevents apoptosis by inhibiting apoptotic mitochondrial changes via closing VDAC

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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

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Hepatitis B virus X protein colocalizes to mitochondria with a human voltage-dependent anion channel, HVDAC3, and alters its transmembrane potential

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Neisseria meningitidis porin PorB interacts with mitochondria and protects cells from apoptosis

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Targeting of the pro-apoptotic VDAC-like porin (PorB) of Neisseria gonorrhoeae to mitochondria of infected cells

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VDAC regulation by the Bcl-2 family of proteins

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The mitochondrial permeability transition.

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Mitochondrial control of cell death

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10.1016/S0300-9084(02)01370-6

Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

12022949

1 reference

Consolidated OpenCitations Corpus – April 2017