Mutation to Bax beyond the BH3 Domain Disrupts Interactions with Pro-survival Proteins and Promotes Apoptosis
Open Access
- 1 March 2011
- journal article
- research article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 286 (9) , 7123-7131
- https://doi.org/10.1074/jbc.m110.161281
Abstract
No abstract availableKeywords
This publication has 58 references indexed in Scilit:
- Evidence that inhibition of BAX activation by BCL-2 involves its tight and preferential interaction with the BH3 domain of BAXCell Research, 2010
- Novel Bcl-2 Homology-3 Domain-like Sequences Identified from Screening Randomized Peptide Libraries for Inhibitors of the Pro-survival Bcl-2 ProteinsJournal of Biological Chemistry, 2009
- High‐Resolution Structural Characterization of a Helical α/β‐Peptide Foldamer Bound to the Anti‐Apoptotic Protein Bcl‐xLAngewandte Chemie International Edition in English, 2009
- Apoptosis is triggered when prosurvival Bcl-2 proteins cannot restrain BaxProceedings of the National Academy of Sciences, 2008
- BAX activation is initiated at a novel interaction siteNature, 2008
- Loss of Hus1 sensitizes cells to etoposide-induced apoptosis by regulating BH3-only proteinsOncogene, 2008
- The BCL-2 protein family: opposing activities that mediate cell deathNature Reviews Molecular Cell Biology, 2008
- Structural insights into the degradation of Mcl-1 induced by BH3 domainsProceedings of the National Academy of Sciences, 2007
- The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralizedCancer Cell, 2006
- [20] Processing of X-ray diffraction data collected in oscillation modePublished by Elsevier ,1997