(Q40943000)

25 September 2017

title

NH2-terminal BH4 domain of Bcl-2 is functional for heterodimerization with Bax and inhibition of apoptosis (English)

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protein heterodimerization activity

25 September 2017

main subject

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Hirotani M

1

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25 September 2017

Zhang Y

2

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25 September 2017

Fujita N

3

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25 September 2017

Naito M

4

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25 September 2017

Tsuruo T

5

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25 September 2017

language of work or name

English

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publication date

1 July 1999

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Journal of Biological Chemistry

25 September 2017

number of pages

6

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based on heuristic

inferred from page(s)

published in

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25 September 2017

volume

274

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25 September 2017

issue

29

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25 September 2017

page(s)

20415-20420

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Apoptosis in the pathogenesis and treatment of disease

25 September 2017

cites work

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https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Caspases: killer proteases

21 January 2018

1 reference

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New members of the Bcl-2 family and their protein partners

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

The proto-oncogene Bcl-2 and its role in regulating apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death

21 January 2018

1 reference

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Interactions among members of the Bcl-2 protein family analyzed with a yeast two-hybrid system.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Multiple Bcl-2 family members demonstrate selective dimerizations with Bax

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

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/10.1074%2FJBC.274.29.20415

Proapoptotic protein Bax heterodimerizes with Bcl-2 and homodimerizes with Bax via a novel domain (BH3) distinct from BH1 and BH2

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Mutagenesis of the BH3 domain of BAX identifies residues critical for dimerization and killing

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Double identity for proteins of the Bcl-2 family

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Bcl-2 targets the protein kinase Raf-1 to mitochondria

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Suppression of signalling through transcription factor NF-AT by interactions between calcineurin and Bcl-2.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

The conserved N-terminal BH4 domain of Bcl-2 homologues is essential for inhibition of apoptosis and interaction with CED-4

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Functional dissection of the human Bc12 protein: sequence requirements for inhibition of apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Bax-independent inhibition of apoptosis by Bcl-XL.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

The protein bcl-2 alpha does not require membrane attachment, but two conserved domains to suppress apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Conversion of Bcl-2 to a Bax-like death effector by caspases

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Movement of Bax from the cytosol to mitochondria during apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Inhibition of Bax channel-forming activity by Bcl-2

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Comparison of the ion channel characteristics of proapoptotic BAX and antiapoptotic BCL-2.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

A common binding site mediates heterodimerization and homodimerization of Bcl-2 family members

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

A peptide sequence from Bax that converts Bcl-2 into an activator of apoptosis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

The C. elegans protein EGL-1 is required for programmed cell death and interacts with the Bcl-2-like protein CED-9

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Bcl-2 and Bax function independently to regulate cell death

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Alphaviruses induce apoptosis in Bcl-2-overexpressing cells: evidence for a caspase-mediated, proteolytic inactivation of Bcl-2.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

Evidence for alpha-helical conformation of an essential N-terminal region in the human Bcl2 protein.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.274.29.20415

21 January 2018

Identifiers

DOI

10.1074/JBC.274.29.20415

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25 September 2017

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