Lipidic pore formation by the concerted action of proapoptotic BAX and tBID. (Q47618625)

4 February 2018

title

Lipidic pore formation by the concerted action of proapoptotic BAX and tBID. (English)

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4 February 2018

author

Hong-Gang Wang

4

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4 February 2018

author name string

Oihana Terrones

1

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4 February 2018

Bruno Antonsson

2

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4 February 2018

Hirohito Yamaguchi

3

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4 February 2018

Jihua Liu

5

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4 February 2018

Ray M Lee

6

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4 February 2018

Andreas Herrmann

7

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4 February 2018

Gorka Basañez

8

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language of work or name

English

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publication date

11 May 2004

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4 February 2018

Journal of Biological Chemistry

published in

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volume

279

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issue

29

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4 February 2018

page(s)

30081-30091

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4 February 2018

Mitochondria: releasing power for life and unleashing the machineries of death

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Direct addition of BimL to mitochondria does not lead to cytochrome c release

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Bid acts on the permeability transition pore complex to induce apoptosis

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Activation of mitochondrial voltage-dependent anion channel by apro-apoptotic BH3-only protein Bim

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Bid, but not Bax, regulates VDAC channels.

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Ion channel activity of the BH3 only Bcl-2 family member, BID.

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Leakage and aggregation of phospholipid vesicles induced by the BH3-only Bcl-2 family member, BID.

21 January 2018

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Bid, a widely expressed proapoptotic protein of the Bcl-2 family, displays lipid transfer activity.

21 January 2018

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tBID Homooligomerizes in the mitochondrial membrane to induce apoptosis

21 January 2018

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The apoptotic protein tBid promotes leakage by altering membrane curvature

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Bcl-XL protects BimEL-induced Bax conformational change and cytochrome C release independent of interacting with Bax or BimEL.

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Interaction with a membrane surface triggers a reversible conformational change in Bax normally associated with induction of apoptosis

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Fatty acids enhance membrane permeabilization by pro-apoptotic Bax.

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Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors

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Proapoptotic Bid binds to monolysocardiolipin, a new molecular connection between mitochondrial membranes and cell death

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Membrane lipids and cell death: an overview.

21 January 2018

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Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations

21 January 2018

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Bax-type apoptotic proteins porate pure lipid bilayers through a mechanism sensitive to intrinsic monolayer curvature.

21 January 2018

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Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane

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Vesicles of variable sizes produced by a rapid extrusion procedure

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Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis

21 January 2018

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Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane

21 January 2018

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Bax oligomerization in mitochondrial membranes requires tBid (caspase-8-cleaved Bid) and a mitochondrial protein.

21 January 2018

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Cytochrome c release from mitochondria proceeds by a two-step process

21 January 2018

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Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilization

21 January 2018

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Bax, along with lipid conspirators, allows cytochrome c to escape mitochondria

21 January 2018

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Membrane fusion: the process and its energy suppliers

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21 January 2018

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21 January 2018

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21 January 2018

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21 January 2018

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21 January 2018

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21 January 2018

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Constitutive association of the proapoptotic protein Bim with Bcl-2-related proteins on mitochondria in T cells

21 January 2018

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Involvement of histone H1.2 in apoptosis induced by DNA double-strand breaks

21 January 2018

1 reference

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Mitochondrial p53 activates Bak and causes disruption of a Bak-Mcl1 complex.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M313420200

Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3

21 January 2018

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Transbilayer lipid diffusion promoted by Bax: implications for apoptosis.

21 January 2018

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21 January 2018

Identifiers

DOI

10.1074/JBC.M313420200

1 reference

4 February 2018

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4 February 2018