(Q34060202)

30 July 2017

1 reference

title

Signal transduction mediated by Bid, a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathways (English)

1 reference

30 July 2017

1 reference

1 reference

Yin XM

1

1 reference

30 July 2017

publication date

1 September 2000

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30 July 2017

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30 July 2017

volume

10

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30 July 2017

issue

3

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30 July 2017

page(s)

161-167

1 reference

https://scigraph.springernature.com/pub.10.1038/sj.cr.7290045

30 July 2017

exact match

0 references

cites work

Apoptosis: A Basic Biological Phenomenon with Wideranging Implications in Tissue Kinetics

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

The genetics of programmed cell death in the nematode Caenorhabditis elegans.

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

21 January 2018

Caspases: enemies within

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

Death receptors: signaling and modulation

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

BCL-2 family members and the mitochondria in apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax.

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

BID: a novel BH3 domain-only death agonist

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

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/10.1038%2FSJ.CR.7290045

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/10.1038%2FSJ.CR.7290045

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/10.1038%2FSJ.CR.7290045

Lethal effect of the anti-Fas antibody in mice

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

Fas-mediated apoptosis in mouse hepatocytes involves the processing and activation of caspases

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

Involvement of the CD95 (APO-1/Fas) receptor and ligand in liver damage.

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

Bcl–2 protects from lethal hepatic apoptosis induced by an ant–Fas antibody in mice

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

inferred from DOI database lookup

7 January 2021

based on heuristic

Tumor necrosis factor is a terminal mediator in galactosamine/endotoxin-induced hepatitis in mice

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CR.7290045

inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1038/SJ.CR.7290045

1 reference

30 July 2017

1 reference