Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Aug 4;24(11):1963–1974. doi: 10.1038/cdd.2017.123

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

PMC Copyright notice

Differential regulation of cell death by high or low ABT-737. High ABT-737 exposure does not by itself cause cell death, but it induces the loss of full-length Bcl-xL through a non-specific proteolysis-dependent mechanism and indirectly causes mitochondrial depolarization and energy loss (1). Loss of Bcl-xL also releases BID to be ready to activate Bax upon a death stimulus (primed for death status; (1)). Under conditions of glutamate toxicity, caspase activation leads to specific cleavage of full-length Bcl-xL to form ΔN-Bcl-xL (2). Both calcium influx and ΔN-Bcl-xL act together to depolarize mitochondrial inner membrane (3), leading to Bax activation (4), cytochrome c release and further activation of caspases, initiating a positive feedback loop (5) of enhanced propensity toward neuronal death. Low ABT binds to ΔN-Bcl-xL (6), preventing the depolarization of the mitochondrial inner membrane, mPT and Bax activation, thereby preventing downstream neuronal death (7)