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

. 2014 Jul 31;5(7):e1358. doi: 10.1038/cddis.2014.316

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

Copyright © 2014 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported 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/3.0/

PMC Copyright notice

(a) Levels of full-length Bid and pT59 Bid assessed by western blot assays in cancer cells in response to ALDH1L1. (b) Proposed mechanism of JNK-mediated Bid accumulation. In response to certain stimuli (ALDH1L1 folate stress enzyme in this case) the activation of JNK1/2 results in Bid phosphorylation at T59 within the caspase-8 cleavage site. This prevents cleavage of Bid to tBid and leads to the accumulation of full-length Bid. Full-length Bid translocates to mitochondria and induces apoptosis. It is proposed that the phosphorylation at T59 also allows the cleavage to jBid by yet unidentified proteases