Cell permeable BH3-peptides overcome the cytoprotective effect of Bcl-2 and Bcl-X(L). (Q43829420)

27 November 2017

Cell permeable BH3-peptides overcome the cytoprotective effect of Bcl-2 and Bcl-X(L). (English)

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27 November 2017

10

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27 November 2017

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Bernard Roques

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27 November 2017

Patricia Boya

2

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author name string

Helena L A Vieira

1

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27 November 2017

Isabelle Cohen

3

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27 November 2017

Chahrazed El Hamel

4

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27 November 2017

Delphine Haouzi

5

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27 November 2017

Sabine Druillenec

6

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27 November 2017

Anne-Sophie Belzacq

7

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27 November 2017

Catherine Brenner

8

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27 November 2017

language of work or name

English

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publication date

1 March 2002

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27 November 2017

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27 November 2017

21

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27 November 2017

13

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27 November 2017

1963-1977

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1205270

27 November 2017

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BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis

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Oxidation of a critical thiol residue of the adenine nucleotide translocator enforces Bcl-2-independent permeability transition pore opening and apoptosis

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Cyclophilin-D binds strongly to complexes of the voltage-dependent anion channel and the adenine nucleotide translocase to form the permeability transition pore

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Identification of small-molecule inhibitors of interaction between the BH3 domain and Bcl-xL

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Apoptosis control in syncytia induced by the HIV type 1-envelope glycoprotein complex: role of mitochondria and caspases.

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PK11195, a ligand of the mitochondrial benzodiazepine receptor, facilitates the induction of apoptosis and reverses Bcl-2-mediated cytoprotection.

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Mutational inactivation of the proapoptotic gene BAX confers selective advantage during tumor clonal evolution

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Control of mitochondrial membrane permeabilization by adenine nucleotide translocator interacting with HIV-1 viral protein rR and Bcl-2

21 January 2018

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The HIV-1 viral protein R induces apoptosis via a direct effect on the mitochondrial permeability transition pore

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Bax directly induces release of cytochrome c from isolated mitochondria

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

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

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

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Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosis

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NMR structure of the (52-96) C-terminal domain of the HIV-1 regulatory protein Vpr: molecular insights into its biological functions

21 January 2018

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Haploid loss of bax leads to accelerated mammary tumor development in C3(1)/SV40-TAg transgenic mice: reduction in protective apoptotic response at the preneoplastic stage

21 January 2018

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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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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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Bcl-2 inhibits the mitochondrial release of an apoptogenic protease

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Antimycin A mimics a cell-death-inducing Bcl-2 homology domain 3.

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The adenine nucleotide translocator: a target of nitric oxide, peroxynitrite, and 4-hydroxynonenal

21 January 2018

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Permeabilization of the mitochondrial inner membrane during apoptosis: impact of the adenine nucleotide translocator

21 January 2018

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BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak

21 January 2018

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Human immunodeficiency virus induces a dual regulation of Bcl-2, resulting in persistent infection of CD4(+) T- or monocytic cell lines

21 January 2018

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7 January 2021

Efficient solid-phase synthesis of Vpr from HIV-1 using low quantities of uniformly 13C-, 15N-labeled amino acids for NMR structural studies

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7 January 2021

Regulation of apoptosis by BH3 domains in a cell-free system

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7 January 2021

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7 January 2021

Bak BH3 peptides antagonize Bcl-xL function and induce apoptosis through cytochrome c-independent activation of caspases

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7 January 2021

The BH3 domain of BAD fused to the Antennapedia peptide induces apoptosis via its alpha helical structure and independent of Bcl-2

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7 January 2021

Purification of mitochondria for apoptosis assays

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7 January 2021

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

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7 January 2021

Re-staging mitosis: a contemporary view of mitotic progression

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7 January 2021

Identifiers

DOI

10.1038/SJ.ONC.1205270

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Dimensions Publication ID

27 November 2017

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1 reference