BID-D59A is a potent inducer of apoptosis in primary embryonic fibroblasts (Q78767539)

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16 December 2019

title

BID-D59A is a potent inducer of apoptosis in primary embryonic fibroblasts (English)

1 reference

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16 December 2019

author name string

Rachel Sarig

1

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16 December 2019

Yehudit Zaltsman

2

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16 December 2019

Richard C Marcellus

3

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16 December 2019

Richard Flavell

4

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16 December 2019

Tak W Mak

5

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16 December 2019

Atan Gross

6

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16 December 2019

publication date

7 January 2003

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Journal of Biological Chemistry

16 December 2019

language of work or name

English

0 references

number of pages

9

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based on heuristic

inferred from page(s)

published in

1 reference

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16 December 2019

volume

278

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16 December 2019

issue

12

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16 December 2019

page(s)

10707-10715

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The Bcl2 family: regulators of the cellular life-or-death switch

16 December 2019

cites work

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

21 January 2018

Caspases: Enemies Within

1 reference

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Caspase knockouts: matters of life and death.

21 January 2018

1 reference

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Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis

21 January 2018

1 reference

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FLICE is activated by association with the CD95 death-inducing signaling complex (DISC).

21 January 2018

1 reference

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Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

tBID Homooligomerizes in the mitochondrial membrane to induce apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

The Destabilization of Lipid Membranes Induced by the C-terminal Fragment of Caspase 8-cleaved Bid Is Inhibited by the N-terminal Fragment

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Rapid Kinetics of tBid-induced Cytochrome c and Smac/DIABLO Release and Mitochondrial Depolarization

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Cytochrome c Release upon Fas Receptor Activation Depends on Translocation of Full-length Bid and the Induction of the Mitochondrial Permeability Transition

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Transcriptional activation by tetracyclines in mammalian cells

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

BID: a novel BH3 domain-only death agonist

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Cleavage of BID during cytotoxic drug and UV radiation-induced apoptosis occurs downstream of the point of Bcl-2 action and is catalysed by caspase-3: a potential feedback loop for amplification of apoptosis-associated mitochondrial cytochrome c rel

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

In situ immunodetection of activated caspase-3 in apoptotic neurons in the developing nervous system

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Cell-specific induction of apoptosis by microinjection of cytochrome c. Bcl-xL has activity independent of cytochrome c release

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Deficiency in caspase-9 or caspase-3 induces compensatory caspase activation

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Granzyme B-mediated cytochrome c release is regulated by the Bcl-2 family members bid and Bax.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Lysosomal protease pathways to apoptosis. Cleavage of bid, not pro-caspases, is the most likely route

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Bid is cleaved by calpain to an active fragment in vitro and during myocardial ischemia/reperfusion

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

Distinct stages of cytochrome c release from mitochondria: evidence for a feedback amplification loop linking caspase activation to mitochondrial dysfunction in genotoxic stress induced apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M210296200

21 January 2018

Identifiers

DOI

10.1074/JBC.M210296200

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:12519725%20AND%20SRC:MED&resulttype=core&format=json

16 December 2019

1 reference