ArticlePLoS biology2024
Key residues in the VDAC2-BAK complex can be targeted to modulate apoptosis.
Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Computational Insights into PB1-F2 Mediated Modulation of VDAC1: An Allosteric Mechanism in Mitochondrial Dysfunction.ACS omega · 2026Article
- Research progress on VDAC2 in mitochondrial dysfunction-related diseases.Molecular biology reports · 2026Review
- Mitochondrial Voltage-Dependent Anion Channel: From a Passive Pore to a Cellular Hub Through Protein Complexation.International journal of molecular sciences · 2026Review
- Perspectives from machine learning and multi-omics to decoding the effects of VDAC2 malignant subsets on tumor evolution.NPJ precision oncology · 2026Article
- VDAC2: an emerging pivotal and multifaceted regulator in tumor biology.Apoptosis : an international journal on programmed cell death · 2026Review
- Chlamydial membrane vesicles deliver the beta barrel outer membrane protein OmpA to mitochondria to inhibit apoptosis.PLoS pathogens · 2026Article
- Article
- Mendelian randomization analysis and molecular mechanism study of childhood asthma and obstructive sleep apnea.Human genetics · 2025Article
- Differential regulation of BAX and BAK apoptotic activity revealed by small molecules.Science advances · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
BAK and BAX execute intrinsic apoptosis by permeabilising the mitochondrial outer membrane. Their activity is regulated through interactions with pro-survival BCL-2 family proteins and with non-BCL-2 proteins including the mitochondrial channel protein VDAC2. VDAC2 is important for bringing both BAK and BAX to mitochondria where they execute their apoptotic function. Despite this important function in apoptosis, while interactions with pro-survival family members are well characterised and have culminated in the development of drugs that target these interfaces to induce cancer cell apoptosis, the interaction between BAK and VDAC2 remains largely undefined. Deep scanning mutagenesis coupled with cysteine linkage identified key residues in the interaction between BAK and VDAC2. Obstructive labelling of specific residues in the BH3 domain or hydrophobic groove of BAK disrupted this interaction. Conversely, mutating specific residues in a cytosol-exposed region of VDAC2 stabilised the interaction with BAK and inhibited BAK apoptotic activity. Thus, this VDAC2-BAK interaction site can potentially be targeted to either inhibit BAK-mediated apoptosis in scenarios where excessive apoptosis contributes to disease or to promote BAK-mediated apoptosis for cancer therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.