ArticleEMBO reports2009
VDAC2 is required for truncated BID-induced mitochondrial apoptosis by recruiting BAK to the mitochondria.
Article in EMBO reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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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.
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Who cites it
82 citing papers in PubMed, 129 citations in OpenAlex.
- Direct binding of the C-terminal sequences of Bim and Bak contributes to efficient Bak activation.Cell death and differentiation · 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
- What does BCL-2 do? From new molecular insights to the clinical implications.Cell death and differentiation · 2026Review
- Membrane lipid composition modulates the organization of VDAC1, a mitochondrial gatekeeper.Communications biology · 2025Article
- VDAC2 Mediates the Apoptosis of Cashmere Goat Hair Follicle Stem Cells Through the P53 Signaling Pathway.Animals : an open access journal from MDPI · 2025Article
- VDAC2 and Bak scarcity in liver mitochondria enables targeting hepatocarcinoma while sparing hepatocytes.Nature communications · 2025Article
- Multiple entanglements of different cell death pathways, in which caspase-8 and BID interact with cardiolipin*, have been identified.Frontiers in cell and developmental biology · 2025Review
- Modulation of mitochondrial voltage dependent anion channel: studies on bilayer electrophysiology.Frontiers in physiology · 2025Review
- Mitochondria and cell death.Nature cell biology · 2024Review
- Canonical and Noncanonical Functions of the BH3 Domain Protein Bid in Apoptosis, Oncogenesis, Cancer Therapeutics, and Aging.Cancers · 2024Review
- VDAC in Retinal Health and Disease.Biomolecules · 2024Review
- Lipid unsaturation promotes BAX and BAK pore activity during apoptosis.Nature communications · 2024Article
- Key residues in the VDAC2-BAK complex can be targeted to modulate apoptosis.PLoS biology · 2024Article
- Hepatocyte Deubiquitinating Enzyme OTUD5 Deficiency is a Key Aggravator for Metabolic Dysfunction-Associated Steatohepatitis by Disturbing Mitochondrial Homeostasis.Cellular and molecular gastroenterology and hepatology · 2024Article
- Fusion-negative rhabdomyosarcoma 3D organoids to predict effective drug combinations: A proof-of-concept on cell death inducers.Cell reports. Medicine · 2023Article
- Duck Tembusu virus NS3 protein induces apoptosis by activating the PERK/PKR pathway and mitochondrial pathway.Journal of virology · 2023Article
- Pore-forming proteins as drivers of membrane permeabilization in cell death pathways.Nature reviews. Molecular cell biology · 2023Review
- Mitochondrial E3 ubiquitin ligase MARCHF5 controls BAK apoptotic activity independently of BH3-only proteins.Cell death and differentiation · 2023Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Truncated BID (tBID), a proapoptotic BCL2 family protein, induces BAK/BAX-dependent release of cytochrome c and other mitochondrial intermembrane proteins to the cytosol to induce apoptosis. The voltage-dependent anion channels (VDACs) are the primary gates for solutes across the outer mitochondrial membrane (OMM); however, their role in apoptotic OMM permeabilization remains controversial. Here, we report that VDAC2(-/-) (V2(-/-)) mouse embryonic fibroblasts (MEFs) are virtually insensitive to tBID-induced OMM permeabilization and apoptosis, whereas VDAC1(-/-), VDAC3(-/-) and VDAC1(-/-)/VDAC3(-/-) MEFs respond normally to tBID. V2(-/-) MEFs regain tBID sensitivity after VDAC2 expression. Furthermore, V2(-/-) MEFs are deficient in mitochondrial BAK despite normal tBID-mitochondrial binding and BAX/BAK expression. tBID sensitivity of BAK(-/-) MEFs is also reduced, although not to the same extent as V2(-/-) MEFs, which might result from their strong overexpression of BAX. Indeed, addition of recombinant BAX also sensitized V2(-/-) MEFs to tBID. Thus, VDAC2 acts as a crucial component in mitochondrial apoptosis by allowing the mitochondrial recruitment of BAK, thereby controlling tBID-induced OMM permeabilization and cell death.
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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.