BH3 peptides induce mitochondrial fission and cell death independent of BAX/BAK (Q27349157)

1

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Colleen M Snyder

2

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G R Scott Budinger

3

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Teng-Leong Chew

5

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Satya Khuon

6

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Harris Perlman

7

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Navdeep S Chandel

Creative Commons Attribution 4.0 International

8

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language of work or name

English

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publication date

2009

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published in

PLOS One

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volume

4

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issue

5

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page(s)

e5646

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copyright license

start time

21 May 2009

1 reference

April 2022 Public Data File from Crossref

copyright status

copyrighted

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cites work

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Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak

21 March 2017

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The mitochondrial fission protein hFis1 requires the endoplasmic reticulum gateway to induce apoptosis

21 March 2017

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Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function

21 March 2017

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21 March 2017

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tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c

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Bok is a pro-apoptotic Bcl-2 protein with restricted expression in reproductive tissues and heterodimerizes with selective anti-apoptotic Bcl-2 family members

21 March 2017

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

21 March 2017

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OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion

21 March 2017

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

21 March 2017

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Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons

21 March 2017

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BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly

7 April 2017

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Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes

7 April 2017

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

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Bax- or Bak-induced mitochondrial fission can be uncoupled from cytochrome C release

7 April 2017

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Opa1-mediated cristae opening is Bax/Bak and BH3 dependent, required for apoptosis, and independent of Bak oligomerization

29 September 2017

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Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization

29 September 2017

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Loss of Mcl-1 protein and inhibition of electron transport chain together induce anoxic cell death

29 September 2017

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Inhibiting the mitochondrial fission machinery does not prevent Bax/Bak-dependent apoptosis.

29 September 2017

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29 September 2017

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29 September 2017

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29 September 2017

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29 September 2017

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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

29 September 2017

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29 September 2017

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29 September 2017

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The coordinate release of cytochrome c during apoptosis is rapid, complete and kinetically invariant

2 June 2018

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GAPDH and autophagy preserve survival after apoptotic cytochrome c release in the absence of caspase activation.

2 June 2018

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Cytochrome c is released in a single step during apoptosis

27 November 2018

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DRP-1-mediated mitochondrial fragmentation during EGL-1-induced cell death in C. elegans

27 November 2018

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Mitochondrial dynamics and apoptosis: a painful separation

27 November 2018

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/19468307

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/19468307