BIM and tBID Are Not Mechanistically Equivalent When Assisting BAX to Permeabilize Bilayer Membranes
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference63 articles.
1. The Pathophysiology of Mitochondrial Cell Death
2. The BCL-2 protein family: opposing activities that mediate cell death
3. Embedded together: The life and death consequences of interaction of the Bcl-2 family with membranes
4. A Bax/Bak-independent Mechanism of Cytochrome c Release
5. Upgrading the BCL-2 Network
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1. Bim escapes displacement by BH3-mimetic anti-cancer drugs by double-bolt locking both Bcl-XL and Bcl-2;eLife;2019-03-12
2. Mcl-1 and Bcl-xL sequestration of Bak confers differential resistance to BH3-only proteins;Cell Death & Differentiation;2018-02-19
3. Membrane insertion of the BAX core, but not latch domain, drives apoptotic pore formation;Scientific Reports;2017-11-24
4. JNK3 phosphorylates Bax protein and induces ability to form pore on bilayer lipid membrane;Biochimie Open;2017-06
5. Mitochondrial apoptosis and BH3 mimetics;F1000Research;2016-12-01
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