BCL-2, BCL-XL Sequester BH3 Domain-Only Molecules Preventing BAX- and BAK-Mediated Mitochondrial Apoptosis
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- 1 September 2001
- journal article
- Published by Elsevier in Molecular Cell
- Vol. 8 (3) , 705-711
- https://doi.org/10.1016/s1097-2765(01)00320-3
Abstract
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This publication has 34 references indexed in Scilit:
- Noxa, a BH3-Only Member of the Bcl-2 Family and Candidate Mediator of p53-Induced ApoptosisScience, 2000
- Bax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of ApoptosisScience, 1998
- The Bcl-2 Protein Family: Arbiters of Cell SurvivalScience, 1998
- Mitochondria and ApoptosisScience, 1998
- Movement of Bax from the Cytosol to Mitochondria during ApoptosisThe Journal of cell biology, 1997
- Structure of Bcl-x L -Bak Peptide Complex: Recognition Between Regulators of ApoptosisScience, 1997
- Bax-independent inhibition of apoptosis by Bcl-XLNature, 1996
- Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell deathCell, 1995
- Activation of C. elegans cell death protein CED-9 by an ammo-acid substitution in a domain conserved in Bcl-2Nature, 1994
- Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell deathCell, 1993