Physiological and Pharmacological Control of BAK, BAX, and Beyond
Open accessAbstract
Cellular commitment to the mitochondrial pathway of apoptosis is accomplished when proapoptotic B cell chronic lymphocytic leukemia/lymphoma (BCL)-2 proteins compromise mitochondrial integrity through the process of mitochondrial outer membrane permeabilization (MOMP). For nearly three decades, intensive efforts focused on the identification and interactions of two key proapoptotic BCL-2 proteins: BCL-2 antagonist killer (BAK) and BCL-2-associated X (BAX). Indeed, we now have critical insights into which BCL-2 proteins interact with BAK/BAX to either preserve survival or initiate MOMP. In contrast, while mitochondria are targeted by BAK/BAX, a molecular understanding of how these organelles govern BAK/BAX function remains less clear. Here, we integrate recent mechanistic insights of proapoptotic BCL-2 protein function in the context of mitochondrial environment, and discuss current and potential pharmacological opportunities to control MOMP in disease.
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In response to apoptotic stimuli, MOMP is mediated by BAX and/or BAK.
“In response to apoptotic stimuli, MOMP is mediated by BCL2 associated X, apoptosis regulator (BAX), and/or BCL2 antagonist/killer 1 (BAK1; best known as BAK), both of which contain four BH domains and a conserved transmembrane domain [44–46].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [45]
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References 85 · Cited by 142
- Authors
- Luna-Vargas, M. P. A., & Chipuk, J. E.
- Affiliations
- Tisch Cancer Institute (US)
- Corresponding author
- Chipuk, Jerry Edward
- ORCID
- Chipuk, Jerry Edward
- Venue
- Trends in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2016-12
- Volume
- 26
- Issue
- 12
- Pages
- 906-917
- ISSN
- 0962-8924 (ISSN-L)
- PMC
- PMC5118054
- OpenAlex
- W2495523499
- Cited by
- 142
- References
- 85
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 14 · 2023: 20 · 2022: 13 · 2021: 14 · 2020: 15 · 2019: 10 · 2018: 22 · 2017: 21 · 2016: 6
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA157740, R01CA206005)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK020541)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- Bak, Bax, mitochondrial outer membrane permeabilization, mitochondrial apoptosis, Bcl-2 family proteins, apoptosis regulation, BCL-2 inhibitor, chronic lymphocytic leukemia
- MeSH terms
- Amino Acid Sequence, Animals, Humans, Mitochondria, Models, Biological, Apoptosis, bcl-2 Homologous Antagonist-Killer Protein, bcl-2-Associated X Protein, Membrane Potential, Mitochondrial
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