(Q38269004)

1 September 2017

BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program (English)

1 reference

1 September 2017

1 reference

Decheng Ren

1

1 reference

1 September 2017

Ho-Chou Tu

2

1 reference

1 September 2017

Hyungjin Kim

3

1 reference

1 September 2017

Gary X Wang

4

1 reference

1 September 2017

Gregory R Bean

5

1 reference

1 September 2017

Osamu Takeuchi

6

1 reference

1 September 2017

John R Jeffers

7

1 reference

1 September 2017

Gerard P Zambetti

8

1 reference

1 September 2017

James J-D Hsieh

9

1 reference

1 September 2017

Emily H-Y Cheng

10

1 reference

1 September 2017

language of work or name

English

0 references

publication date

1 December 2010

1 reference

1 September 2017

1 reference

1 September 2017

330

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1 September 2017

6009

1 reference

1 September 2017

1390-1393

1 reference

Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis.

1 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Mechanism of apoptosis induction by inhibition of the anti-apoptotic BCL-2 proteins

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Membrane binding by tBid initiates an ordered series of events culminating in membrane permeabilization by Bax

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

BAX activation is initiated at a novel interaction site

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

The BCL-2 protein family: opposing activities that mediate cell death

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Proapoptotic multidomain Bcl-2/Bax-family proteins: mechanisms, physiological roles, and therapeutic opportunities

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

The limited role of NH2-terminal c-Jun phosphorylation in neuronal apoptosis: identification of the nuclear pore complex as a potential target of the JNK pathway.

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

An inhibitor of Bcl-2 family proteins induces regression of solid tumours

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Intrinsic and extrinsic pathway signaling during neuronal apoptosis: lessons from the analysis of mutant mice

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

The expanding role of mitochondria in apoptosis

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Disruption of the glucocorticoid receptor gene in the nervous system results in reduced anxiety

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

BCL-2 family members and the mitochondria in apoptosis

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

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

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Apaf1 is required for mitochondrial pathways of apoptosis and brain development

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Bax deletion further orders the cell death pathway in cerebellar granule cells and suggests a caspase-independent pathway to cell death.

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

Baxbeta: a constitutively active human Bax isoform that is under tight regulatory control by the proteasomal degradation mechanism

6 September 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=3163443

BH3-only Bcl-2 family members are coordinately regulated by the JNK pathway and require Bax to induce apoptosis in neurons

31 August 2018

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/21127253

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/21127253

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Upgrading the BCL-2 network

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/21127253

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Identifiers

DOI

10.1126/SCIENCE.1190217

1 reference

1 September 2017

1 reference

1 September 2017

PubMed publication ID

21127253

1 reference