ArticleProceedings of the National Academy of Sciences of the United States of America2015
Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 88 citations in OpenAlex.
- A membrane-disruptive action of VBIT-4 challenges its role as a widely used VDAC1 oligomerization inhibitor.eLife · 2026Article
- Direct binding of the C-terminal sequences of Bim and Bak contributes to efficient Bak activation.Cell death and differentiation · 2026Article
- 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
- Deciphering Bax Dynamics: Regulation, Retrotranslocation, and Mitochondrial Interplay in the Commitment to Apoptosis: A Narrative Review.Health science reports · 2026Article
- VDAC2: an emerging pivotal and multifaceted regulator in tumor biology.Apoptosis : an international journal on programmed cell death · 2026Review
- Mitochondrial membrane hyperpolarization modulates nuclear DNA methylation and gene expression through phospholipid remodeling.Nature communications · 2025Article
- Conformational plasticity of mitochondrial VDAC2 controls the kinetics of its interaction with cytosolic proteins.Science advances · 2025Article
- Postbiotic Parabacteroides Distasonis Supplementation Enhances Intestinal and Skeletal Muscle Function in Aged Mice.Aging and disease · 2025Article
- Article
- Investigation of new autoantibodies in urothelial bladder cancer for biomarker discovery using immunoproteomics.Discover oncology · 2025Article
- VDAC2 and Bak scarcity in liver mitochondria enables targeting hepatocarcinoma while sparing hepatocytes.Nature communications · 2025Article
- Differential regulation of BAX and BAK apoptotic activity revealed by small molecules.Science advances · 2025Article
- The C-terminal sequences of Bcl-2 family proteins mediate interactions that regulate cell death.The Biochemical journal · 2024Review
- Lipid unsaturation promotes BAX and BAK pore activity during apoptosis.Nature communications · 2024Article
- A novel inhibitory BAK antibody enables assessment of non-activated BAK in cancer cells.Cell death and differentiation · 2024Article
- Key residues in the VDAC2-BAK complex can be targeted to modulate apoptosis.PLoS biology · 2024Article
- Mechanistic engineering of celastrol liposomes induces ferroptosis and apoptosis by directly targeting VDAC2 in hepatocellular carcinoma.Asian journal of pharmaceutical sciences · 2023Article
- Repurposing of Tibolone in Alzheimer's Disease.Biomolecules · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Voltage-dependent anion channel (VDAC) proteins are major components of the outer mitochondrial membrane. VDAC has three isoforms with >70% sequence similarity and redundant roles in metabolite and ion transport. However, only Vdac2(-/-) (V2(-/-)) mice are embryonic lethal, indicating a unique and fundamental function of VDAC2 (V2). Recently, a specific V2 requirement was demonstrated for mitochondrial Bak import and truncated Bid (tBid)-induced apoptosis. To determine the relevant domain(s) of V2 involved, VDAC1 (V1) and V2 chimeric constructs were created and used to rescue V2(-/-) fibroblasts. Surprisingly, the commonly cited V2-specific N-terminal extension and cysteines were found to be dispensable for Bak import and high tBid sensitivity. In gain-of-function studies, V2 (123-179) was the minimal sequence sufficient to render V1 competent to support Bak insertion. Furthermore, in loss-of-function experiments, T168 and D170 were identified as critical residues. These motifs are conserved in zebrafish V2 (zfV2) that also rescued V2-deficient fibroblasts. Because high-resolution structures of zfV2 and mammalian V1 have become available, we could superimpose these structures and recognized that the critical V2-specific residues help to create a distinctive open "pocket" on the cytoplasmic surface that could facilitate Bak recruitment.
Indexed as
Identifiers
What OpenQuestion holds
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.