BCL2 and related prosurvival proteins require BAK1 and BAX to affect autophagy
Author(s)
Lindqvist, LM; Vaux, DL;
Details
Publication Year 2014-06-27, Volume 10, Issue #8, Page 1474-1475
Journal Title
Autophagy
Publication Type
Journal Article
Abstract
It is widely thought that prosurvival BCL2 family members not only inhibit apoptosis, but also block autophagy by directly binding to BECN1/Beclin 1. To distinguish whether BCL2, BCL2L1/BCL-XL, or MCL1 influence autophagy directly, or indirectly, through their effects on apoptosis, we compared normal cells to those lacking BAX and BAK1. In cells able to undergo mitochondria-mediated apoptosis, inhibiting the endogenous prosurvival BCL2 family members induces both autophagy and cell death, but when BAX and BAK1 are deleted, neither inhibiting nor overexpressing BCL2, BCL2L1, or MCL1 causes any detectable effect on LC3B lipidation, LC3B turnover, or autolysosome formation. These results show that prosurvival BCL2 family members influence autophagy only indirectly, by inhibiting activation of BAX and BAK1.
Publisher
Landes
WEHI Research Division(s)
Cell Signalling And Cell Death
NHMRC Grants
NHMRC/1016701 NHMRC/1020136
Rights Notice
© 2014 Landes Bioscience


Creation Date: 2014-07-09 07:54:57
Last Modified: 2015-05-25 03:31:30
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