VDAC2 and the BCL-2 family of proteins
- Author(s)
- Yuan, Z; Dewson, G; Czabotar, PE; Birkinshaw, RW;
- Details
- Publication Year 2021-12-16,Volume 49,Issue #6,Page 2787-2795
- Journal Title
- Biochemical Society Transactions
- Abstract
- The BCL-2 protein family govern whether a cell dies or survives by controlling mitochondrial apoptosis. As dysregulation of mitochondrial apoptosis is a common feature of cancer cells, targeting protein-protein interactions within the BCL-2 protein family is a key strategy to seize control of apoptosis and provide favourable outcomes for cancer patients. Non-BCL-2 family proteins are emerging as novel regulators of apoptosis and are potential drug targets. Voltage dependent anion channel 2 (VDAC2) can regulate apoptosis. However, it is unclear how this occurs at the molecular level, with conflicting evidence in the literature for its role in regulating the BCL-2 effector proteins, BAK and BAX. Notably, VDAC2 is required for efficient BAX-mediated apoptosis, but conversely inhibits BAK-mediated apoptosis. This review focuses on the role of VDAC2 in apoptosis, discussing the current knowledge of the interaction between VDAC2 and BCL-2 family proteins and the recent development of an apoptosis inhibitor that targets the VDAC2-BAK interaction.
- Publisher
- Portland Press
- Keywords
- Bak; Bax; BCL-2 family proteins; Vdac2; apoptosis; voltage-gated channels
- Research Division(s)
- Structural Biology; Ubiquitin Signalling
- PubMed ID
- 34913469
- Publisher's Version
- https://doi.org/10.1042/bst20210753
- Open Access at Publisher's Site
https://doi.org/10.1042/BST20210753- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2022-03-04 01:43:23
Last Modified: 2022-03-04 02:05:25