Affinage

VDAC1

Non-selective voltage-gated ion channel VDAC1 · UniProt P21796

Round 2 corrected
Length
283 aa
Mass
30.8 kDa
Annotated
2026-04-28
130 papers in source corpus 39 papers cited in narrative 39 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

VDAC1 is a 19-stranded β-barrel channel in the outer mitochondrial membrane that serves as the principal conduit for metabolite and ion exchange between mitochondria and the cytosol, and as a signaling platform that integrates apoptosis, mitophagy, and innate immune responses (PMID:18832158, PMID:18755977). Pro-apoptotic Bcl-2 family members Bax and Bak open VDAC1 to permit cytochrome c release, whereas anti-apoptotic Bcl-xL closes it; hexokinase I/II binding to the N-terminal domain and multiple β-strands further suppresses apoptosis by partially occluding the pore (PMID:10365962, PMID:22589539, PMID:19094960). Calcium-promoted VDAC1 oligomerization forms a mega-pore that releases cytochrome c and mitochondrial DNA, activating caspase-dependent apoptosis and cGAS–STING innate immune signaling; site-specific Parkin-mediated ubiquitination at K53 disrupts oligomerization to restrain these pathways, while polyubiquitination at K27 and monoubiquitination at K274 differentially regulate mitophagy and mitochondrial calcium uptake through MCU (PMID:23542128, PMID:36658227, PMID:32047033, PMID:20098416). Phosphorylation at S193 by Nek1 maintains appropriate mitochondrial membrane permeability and cell survival, and pharmacological agents that bind VDAC1 (itraconazole, VBIT-3/4) modulate AMPK–mTOR signaling and oligomerization-dependent cell death (PMID:19158487, PMID:26655341, PMID:27738100).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1992 High

    Identification of VDAC as the 32-kDa subunit of the mitochondrial benzodiazepine receptor complex established it as a component of a multiprotein signaling hub at mitochondrial contact sites, beyond its role as a simple metabolite channel.

    Evidence Biochemical solubilization, radioligand binding, selective antibody identification, and photoaffinity labeling of the mBzR complex

    PMID:1373486

    Open questions at the time
    • Stoichiometry and structural arrangement of VDAC within the mBzR complex undefined
    • Functional significance of VDAC–ANT–TSPO assembly not established
  2. 1999 High

    Demonstration that Bcl-2 family proteins directly regulate VDAC gating to control cytochrome c release established VDAC1 as a central effector of mitochondrial apoptosis, resolving how outer membrane permeabilization is achieved at the molecular level.

    Evidence Liposome reconstitution with purified VDAC, cytochrome c passage assays, and VDAC1-null yeast mitochondria; co-immunoprecipitation of Bax/Bak with VDAC from isolated mitochondria

    PMID:10365962 PMID:9843949

    Open questions at the time
    • Structural basis of Bax/Bak-induced VDAC opening unknown
    • Whether VDAC1 monomers or oligomers mediate cytochrome c passage not resolved
  3. 2008 High

    Determination of the 19-stranded β-barrel structure by NMR and X-ray crystallography provided the atomic framework needed to map ligand-binding sites (Bcl-xL at strands 17–18, NADH, cholesterol) and rationalize VDAC1's unique odd-strand topology among membrane proteins.

    Evidence NMR spectroscopy and X-ray crystallography of recombinant human VDAC1; chemical shift perturbation mapping

    PMID:18755977 PMID:18832158

    Open questions at the time
    • No high-resolution structure of VDAC1 in complex with Bcl-2 family members
    • Conformational dynamics of channel gating not captured in static structures
  4. 2008 High

    Functional dissection of VDAC1's interactions with hexokinase I and its epistatic relationship with Bax/Bak in cisplatin-induced apoptosis revealed VDAC1 as a hierarchical regulator: it acts downstream of Bak but upstream of Bax conformational activation, and HK-I binding to the N-terminal domain confers anti-apoptotic protection.

    Evidence Site-directed mutagenesis and peptide competition disrupting HK-I binding; siRNA knockdown and DIDS inhibition with Bax/Bak conformational activation assays

    PMID:18250166 PMID:18362892 PMID:19094960

    Open questions at the time
    • Structural details of the VDAC1–hexokinase interface at atomic resolution not available
    • How VDAC1 triggers Bax conformational change mechanistically undefined
  5. 2009 High

    Identification of Nek1-mediated phosphorylation of VDAC1 at S193 as a survival signal answered how post-translational modification tunes VDAC1 permeability: loss of this phosphorylation causes excessive membrane permeabilization and cell death.

    Evidence Yeast two-hybrid, GST pull-down, co-IP, kinase-dead Nek1 mutant, VDAC1-S193A/S193E mutagenesis with membrane permeability and survival assays

    PMID:19158487

    Open questions at the time
    • Upstream signals activating Nek1 toward VDAC1 not fully mapped
    • Whether S193 phosphorylation affects VDAC1 oligomerization not tested
  6. 2010 High

    Discovery that PINK1/Parkin-mediated K27-linked polyubiquitination of VDAC1 recruits p62 for mitochondrial clearance placed VDAC1 at the intersection of mitophagy signaling, though subsequent VDAC1/3-knockout studies showed VDAC1 is sufficient but not strictly required for Parkin-induced mitophagy.

    Evidence Ubiquitin linkage analysis, siRNA, immunoprecipitation, and imaging in multiple cell types; VDAC1/3-null MEFs with K63-ubiquitin and p62 recruitment assays

    PMID:20098416 PMID:20890124

    Open questions at the time
    • Relative contribution of VDAC1 versus other OMM substrates (e.g., Mfn1/2) to mitophagy signaling unclear
    • Whether K27-linked chains are necessary or whether other linkage types suffice not resolved
  7. 2011 High

    Mapping of VDAC1 oligomerization interfaces to β-strands 1, 2, 16, and 19, and the demonstration that oligomers form a mega-pore for cytochrome c release, established oligomerization as the structural basis of VDAC1-mediated apoptosis distinct from simple gating.

    Evidence Structure-based mutagenesis, cysteine cross-linking with BMOE, native gel electrophoresis

    PMID:22117062

    Open questions at the time
    • High-resolution structure of the oligomeric mega-pore not determined
    • Stoichiometry of the functional oligomer (dimer, tetramer, hexamer) debated
  8. 2013 Medium

    Calcium was identified as a key promoter of VDAC1 oligomerization: chelation blocks and ionophore-induced elevation triggers oligomerization and apoptosis, linking mitochondrial Ca²⁺ dynamics to the oligomerization switch.

    Evidence BAPTA-AM chelation, Ca²⁺ ionophore, mitochondrial Ca²⁺ transport inhibitor AzRu, cross-linking oligomerization and apoptosis assays

    PMID:23542128

    Open questions at the time
    • Direct Ca²⁺ binding site on VDAC1 not identified
    • Whether Ca²⁺ acts on VDAC1 directly or through an intermediary not distinguished
  9. 2016 High

    Development of small-molecule VDAC1 oligomerization inhibitors (VBIT-3/4, DIDS, DPC) that directly bind VDAC1, reduce channel conductance, and block apoptosis validated oligomerization as a druggable target and provided tool compounds for subsequent studies.

    Evidence Microscale thermophoresis, bilayer electrophysiology, BRET2 in living cells, cross-linking, apoptosis and mitochondrial membrane potential assays

    PMID:26253170 PMID:27064145 PMID:27738100

    Open questions at the time
    • In vivo efficacy and specificity of VBIT compounds in disease models incompletely characterized at this stage
    • Binding site on VDAC1 for VBIT-3/4 not structurally resolved
  10. 2020 High

    Site-specific mutagenesis of Parkin ubiquitination sites (K274R mono, Poly-KR) revealed that monoubiquitination and polyubiquitination of VDAC1 differentially control apoptosis versus mitophagy, with K274 monoubiquitination restraining MCU-dependent mitochondrial Ca²⁺ uptake — validated in Drosophila where the corresponding Porin K273R causes Parkinson-like phenotypes rescued by MCU suppression.

    Evidence VDAC1 ubiquitination-site mutants, mitophagy and apoptosis assays, mitochondrial Ca²⁺ measurements, Drosophila transgenic behavioral and neuronal phenotyping

    PMID:32047033

    Open questions at the time
    • Structural mechanism by which monoubiquitination at K274 gates MCU activity unknown
    • Whether the same ubiquitin code operates in mammalian neurons not directly shown
  11. 2023 High

    Parkin-mediated ubiquitination at K53 was shown to disrupt VDAC1 oligomerization and prevent mtDNA release into the cytoplasm, linking VDAC1 oligomerization control to cGAS–STING innate immune signaling and establishing a new function for VDAC1 beyond apoptosis and mitophagy.

    Evidence VDAC1-K53R mutagenesis, Parkin-KO mice with CCl₄ liver fibrosis, mtDNA release and STING signaling assays, oligomerization analysis

    PMID:36658227

    Open questions at the time
    • Whether K53 ubiquitination status is dynamically regulated during infection or sterile inflammation unknown
    • Interplay between K53 and K274 ubiquitination events not dissected
  12. 2023 Medium

    Multiple new VDAC1 oligomerization regulators were identified — TMBIM6 prevents oligomerization to sustain mitochondrial Ca²⁺ homeostasis, GPCPD1 relocalizes under hypoxia to promote PRKN-accessible monomers, and MCU–VDAC1 interaction enhances dimerization — expanding the regulatory network around the oligomerization switch.

    Evidence Co-IP, KO/transgenic mouse models (TMBIM6 cardiac KO, MCU heterozygous KO), palmitoylation assays, mitophagy and oligomerization assays

    PMID:36603706 PMID:36642847 PMID:36803235

    Open questions at the time
    • How these regulators are coordinated under physiological stress remains unclear
    • Direct binding interfaces for TMBIM6 and GPCPD1 on VDAC1 not structurally defined
  13. 2024 Medium

    VDAC1 oligomerization was linked to ferroptosis execution: oligomerization inhibitors and mitochondria-targeted antioxidants suppress cysteine-deprivation- and RSL3-induced ferroptosis, with complex III identified as the primary mitochondrial ROS source driving this process.

    Evidence Pharmacological VDAC1 oligomerization inhibitors, MitoQ/MitoT antioxidants, complex III inhibition, ROS and ferroptosis quantification

    PMID:39521767

    Open questions at the time
    • Whether VDAC1 oligomerization is required or merely amplifies ferroptotic signaling not genetically resolved
    • VDAC1 oligomerization state during lipid peroxidation not directly visualized

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution structure of the VDAC1 oligomeric mega-pore — and the precise conformational transitions linking monomer gating, dimer formation, and higher-order oligomerization to distinct cell-fate outcomes (apoptosis, mitophagy, ferroptosis, innate immunity) — remains unresolved.
  • No cryo-EM or crystal structure of VDAC1 oligomers
  • Integrated model connecting all ubiquitination sites (K27, K53, K274) and phosphorylation (S193) to oligomerization dynamics lacking
  • In vivo cell-type-specific functions of VDAC1 oligomerization in disease models incompletely characterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0005215 transporter activity 4
Localization
GO:0005739 mitochondrion 10 GO:0005886 plasma membrane 1
Pathway
R-HSA-5357801 Programmed Cell Death 9 R-HSA-9612973 Autophagy 7 R-HSA-382551 Transport of small molecules 4 R-HSA-168256 Immune System 1
Partners
BAK1BAXBCL2L1HK1HK2MCUNEK1PRKNTMBIM6TSPO
Complex memberships
TSPO/VDAC1/ANT (mitochondrial benzodiazepine receptor)VDAC1/hexokinase complex

Evidence

Reading pass · 39 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Bcl-2 family proteins regulate cytochrome c release through direct interaction with VDAC: pro-apoptotic Bax and Bak accelerate VDAC opening and allow cytochrome c to pass through VDAC-containing liposomes, while anti-apoptotic Bcl-xL closes VDAC by binding to it directly. VDAC1-deficient yeast mitochondria failed to exhibit Bax/Bak-induced membrane potential loss and cytochrome c release. Liposome reconstitution with purified VDAC, cytochrome c release assay, VDAC1-deficient yeast mutant mitochondria Nature High 10365962
1998 Pro-apoptotic Bax and Bak interact physically with VDAC (voltage-dependent anion channel), a component of the mitochondrial permeability transition (PT) pore, to induce PT and cytochrome c release from isolated mitochondria in a Ca2+-dependent, cyclosporin A-sensitive manner. Co-immunoprecipitation of Bax/Bak with VDAC from isolated mitochondria; isolated mitochondria swelling and cytochrome c release assays Proceedings of the National Academy of Sciences of the United States of America High 9843949
2008 Human VDAC1 adopts a 19-stranded beta-barrel architecture with an alpha-helix located horizontally midway within the pore, solved conjointly by NMR spectroscopy and X-ray crystallography. This structure is common to all VDAC proteins and is also adopted by the general import pore TOM40. NMR spectroscopy and X-ray crystallography of recombinant human VDAC1 Proceedings of the National Academy of Sciences of the United States of America High 18832158
2008 NMR solution structure of human VDAC-1 in detergent micelles reveals a 19-stranded beta-barrel with parallel first and last strands (an odd number, unprecedented in integral membrane proteins). NMR measurements identified binding sites for Bcl-xL (at strands 17 and 18 of the barrel), for NADH, and for cholesterol. Solution NMR structure determination; NMR chemical shift perturbation mapping of ligand binding sites; functional reconstitution in phospholipid bilayers Science High 18755977
2010 PINK1/Parkin-mediated mitophagy requires VDAC1 as a substrate: Parkin mediates Lys27 poly-ubiquitylation of VDAC1 on depolarized mitochondria, and this ubiquitylation is essential for p62/SQSTM1-dependent mitochondrial clearance. PINK1 kinase activity and its mitochondrial localization are prerequisites for Parkin translocation. siRNA knockdown, immunoprecipitation, ubiquitin chain linkage analysis, fluorescence microscopy of mitochondrial clustering and clearance in non-neuronal and neuronal cells Nature cell biology High 20098416
2010 VDAC1 is dispensable for Parkin-induced mitophagy: although VDAC1 is ubiquitinated following mitochondrial depolarization, VDAC1/3-null mouse embryonic fibroblasts still show K63-linked ubiquitin immunoreactivity and undergo p62 recruitment, mitochondrial clustering, and mitophagy normally. VDAC1/3 knockout MEFs, immunofluorescence, immunoprecipitation, K63-ubiquitin linkage analysis Autophagy High 20890124
2008 VDAC1 acts downstream of Bak and upstream of Bax in cisplatin-induced apoptosis: VDAC1 knockdown or chemical inhibition prevents cisplatin-induced Bax conformational activation but not Bak activation. VDAC1 thus functions as a hierarchical regulator of mitochondrial membrane permeabilization. siRNA knockdown, chemical inhibition (DIDS), Bax/Bak conformational activation assays, mitochondrial membrane potential measurement, plasma membrane permeabilization assay Oncogene High 18362892
2008 Phosphorylated StAR interacts with VDAC1 on the outer mitochondrial membrane, which facilitates processing of the 37-kDa phospho-StAR to the 32-kDa intermediate required for steroidogenesis. In the absence of VDAC1, phospho-StAR is degraded by cysteine proteases. Phosphate carrier protein contacts StAR before VDAC1. Co-immunoprecipitation, VDAC1 knockdown/knockout cellular assays, steroidogenesis activity assays, mass spectrometry identification The Journal of biological chemistry High 18250166
2008 VDAC1 interacts with hexokinase I (HK-I) through charged residues in multiple beta-strands and the N-terminal domain. Mutation of these residues or expression of N-terminal VDAC1 peptides disrupts HK-I binding, detaches HK-I-GFP from mitochondria, and diminishes HK anti-apoptotic activity. VDAC1 mutagenesis, VDAC1-based peptide expression, HK-I-GFP mitochondrial localization assay, apoptosis assays Biochimica et biophysica acta High 19094960
2009 Nek1 kinase directly phosphorylates VDAC1 at serine 193. Nek1 associates with VDAC1 by yeast two-hybrid, GST pull-down, and co-immunoprecipitation. Loss of Nek1 or expression of a VDAC1-S193A phosphorylation-deficient mutant results in exaggerated mitochondrial membrane permeability and cell death; a phosphomimetic VDAC1-S193E mutant rescues these defects. Yeast two-hybrid, GST pull-down, co-immunoprecipitation, kinase-dead Nek1 mutant, VDAC1 S193A/S193E site-directed mutagenesis, mitochondrial membrane permeability assay Cell cycle High 19158487
2011 VDAC1 oligomerization occurs through interfaces involving beta-strands 1, 2, 16, and 19. Replacing hydrophobic amino acids with charged residues in these strands interferes with oligomerization. Cysteine cross-linking confirmed proximity of these strands within dimers. VDAC1 exists as a dimer under physiological conditions and undergoes conformational changes to form higher oligomers upon apoptosis induction. Structure-based computation, site-directed mutagenesis, cysteine replacement, chemical cross-linking with BMOE, native gel electrophoresis The Journal of biological chemistry High 22117062
2012 Bcl-xL interacts directly with VDAC1 and this interaction mediates its anti-apoptotic function. Bcl-xL(Δ21) binds purified VDAC1 as measured by microscale thermophoresis and reduces VDAC1 channel conductance in bilayer reconstitution. Specific VDAC1 mutations prevent Bcl-xL interaction. VDAC1 N-terminal domain and two internal sequences bind Bcl-xL, as shown by surface plasmon resonance. Microscale thermophoresis, bilayer electrophysiology reconstitution, VDAC1 mutagenesis, surface plasmon resonance, cell-based apoptosis assays with VDAC1 mutants The Journal of biological chemistry High 22589539
2013 Calcium promotes VDAC1 oligomerization and apoptosis. Chelation of intracellular Ca2+ with BAPTA-AM inhibits VDAC1 oligomerization and apoptosis; increasing Ca2+ with ionophore induces VDAC1 oligomerization and apoptosis without additional apoptotic stimuli. Inhibition of mitochondrial Ca2+ transport (AzRu) decreases VDAC1 oligomerization, implicating mitochondrial Ca2+ as required for oligomerization. Chemical manipulation of Ca2+ levels, VDAC1 cross-linking oligomerization assay, apoptosis assays, mitochondrial Ca2+ transport inhibition Biochimica et biophysica acta Medium 23542128
2013 Parkin ubiquitylates numerous outer mitochondrial membrane proteins upon depolarization, with VDAC1 identified as a ubiquitylation substrate at specific lysine residues. Quantitative diGly proteomics defined the ubiquitylation site specificity and topology of Parkin-dependent target modification. Quantitative diGly capture proteomics, affinity purification mass spectrometry, PARKIN active-site mutant (C431) Nature High 23503661
2014 TSPO binds VDAC1 on the outer mitochondrial membrane and inhibits mitophagy downstream of the PINK1-Parkin pathway by preventing ubiquitination of mitochondrial proteins. This effect is independent of cholesterol regulation and instead depends on VDAC1 interaction, which promotes ROS overproduction that counteracts Parkin-mediated ubiquitination. Co-immunoprecipitation, mitochondrial membrane coupling measurements, ROS measurements, LC3 and p62 recruitment assays, siRNA knockdown Autophagy Medium 25470454
2015 Itraconazole targets VDAC1 in endothelial cells: VDAC1 knockdown mimics itraconazole's inhibition of mTOR and cell proliferation. Itraconazole binding to VDAC1 disrupts mitochondrial metabolism, increasing AMP:ATP ratio and activating AMPK, an upstream inhibitor of mTOR. VDAC1-knockout cells are resistant to itraconazole-induced AMPK activation and mTOR inhibition. VDAC1 siRNA knockdown, VDAC1-knockout cells, AMPK/mTOR signaling assays, mitochondrial metabolism measurements, drug binding studies Proceedings of the National Academy of Sciences of the United States of America High 26655341
2015 A new fungal diterpene (cyathin-R) induces apoptosis independently of Bax/Bak via promoting VDAC1 oligomerization and subsequent cytochrome c release. VDAC1 silencing prevents cyathin-R-induced apoptosis, and VDAC1 oligomerization inhibitor (DPC) blocks the effect, demonstrating that VDAC1 can mediate apoptosis in a Bax/Bak-independent manner. Bax/Bak-deficient MEFs, VDAC1 siRNA, VDAC1 oligomerization cross-linking assay, cytochrome c release assay, xenograft tumor model The Journal of biological chemistry High 26253170
2016 VDAC1-interacting anion transport inhibitors (DIDS, SITS, H2DIDS, DNDS, DPC) directly bind VDAC1 as shown by microscale thermophoresis and reduce bilayer-reconstituted VDAC conductance. These compounds inhibit apoptosis-stimuli-induced VDAC1 oligomerization (monitored by cross-linking and BRET2 in living cells), pro-apoptotic protein release, and apoptosis. Microscale thermophoresis, bilayer electrophysiology, chemical cross-linking, BRET2 in living cells, apoptosis assays Biochimica et biophysica acta High 27064145
2016 Novel small molecules (VBIT-3, VBIT-4) directly interact with VDAC1 and prevent VDAC1 oligomerization, inhibiting apoptosis. These compounds also restore dissipated mitochondrial membrane potential, decrease ROS production, prevent hexokinase detachment from mitochondria, and normalize intracellular Ca2+ levels. High-throughput compound screening, direct binding assays, VDAC1 cross-linking oligomerization assay, mitochondrial membrane potential measurements, ROS assay, HK binding assay, Ca2+ measurements The Journal of biological chemistry High 27738100
2010 VDAC1 cysteine residues (Cys127 and Cys232) have distinct topologies: one faces the pore (blocked by bulky charged 5-FM but not NEM) and one faces the lipid bilayer. Cysteine-less VDAC1 mutants retain normal channel activity and mitochondrial localization and undergo apoptosis normally, indicating the cysteines are not required for channel function or apoptosis. Thiol-modifying agent treatment of bilayer-reconstituted VDAC1, cysteine-specific cross-linker BMOE, cysteine-to-alanine mutagenesis, cell apoptosis assays The Biochemical journal High 20192921
2019 Yeast Por1 (VDAC ortholog) associates with newly imported Tom22, sequestering it to modulate Tom22 integration into the TOM complex. Por1 binding to Tom22 dissociated from the trimeric TOM complex enhances the dimeric TOM complex, which is preferable for import of TIM40/MIA-dependent proteins. Por1 also chaperones monomeric Tom22 during cell-cycle-controlled TOM complex remodeling. Co-immunoprecipitation, mitochondrial import assays, genetic analysis in yeast, native gel electrophoresis of TOM complexes Molecular cell Medium 30738703
2019 Mutant SOD1 (SOD1G93A and SOD1G85R, but not wild-type SOD1) binds specifically to the N-terminal domain of VDAC1 and reduces VDAC1 channel conductance. A VDAC1-derived N-terminal peptide inhibited mutant SOD1-induced toxicity and enhanced survival of motor neuron-like cells. Direct binding assay of purified proteins, truncated VDAC1 (N-terminal deletion) controls, electrophysiology of bilayer-reconstituted VDAC1, peptide treatment of NSC-34 cells and mouse embryonic stem cell-derived motor neurons Frontiers in cellular neuroscience High 31474832
2020 VDAC1 can be either mono- or polyubiquitinated by Parkin in a PINK1-dependent manner, and these two forms differentially regulate mitophagy vs. apoptosis. Polyubiquitination-deficient VDAC1 (Poly-KR) hampers mitophagy; monoubiquitination-deficient VDAC1 (K274R) promotes apoptosis by augmenting mitochondrial calcium uptake through the MCU channel. Drosophila expressing corresponding Porin K273R show Parkinson disease phenotypes rescued by MCU suppression. VDAC1 ubiquitination-deficient mutants, mitophagy assays, apoptosis assays, mitochondrial calcium measurements, Drosophila transgenic model with behavioral and neuronal phenotyping Proceedings of the National Academy of Sciences of the United States of America High 32047033
2020 TLK1 activates Nek1 by phosphorylating Nek1-T141, which in turn phosphorylates VDAC1 to maintain mitochondrial integrity. Cells overexpressing kinase-inactive Nek1-T141A show reduced oxygen consumption, increased glycolysis, and cytochrome c leakage upon DNA damage, consistent with loss of VDAC1 phosphorylation-dependent channel regulation. Nek1-T141A mutant overexpression, oxygen consumption measurement, cell cycle analysis, cytochrome c fractionation, doxorubicin treatment Cell cycle Medium 31914854
2021 Structural modeling and molecular dynamics simulations combined with electrophysiology revealed that HKII inserts its H-anchor into the outer mitochondrial membrane before forming a complex with VDAC1 on the cytosolic leaflet. The HKII/VDAC1 complex partially blocks VDAC1's permeation pathway, confirmed by electrophysiological measurements. VDAC1 phosphorylation disrupts HKII binding. Molecular dynamics simulations, Brownian dynamics simulations, electrophysiology of VDAC1 with and without HKII, phosphorylation mimetic mutant analysis Communications biology Medium 34083717
2018 Post-translational modifications of VDAC1 cysteines in rat liver mitochondria include over-oxidation and succination, detected by UHPLC/High Resolution ESI-MS/MS after tryptic and chymotryptic proteolysis. Cysteine over-oxidation appears to be exclusive to VDACs and not present in other transmembrane mitochondrial proteins. Tryptic/chymotryptic proteolysis, UHPLC/High Resolution ESI-MS/MS mass spectrometry Biochimica et biophysica acta. Bioenergetics Medium 29890122
1992 The mitochondrial benzodiazepine receptor (mBzR) comprises three protein subunits of 18, 30, and 32 kDa. Selective antibodies and reagents identify the 32-kDa protein as VDAC (voltage-dependent anion channel) and the 30-kDa protein as the adenine nucleotide carrier. VDAC and the adenine nucleotide carrier together with the 18-kDa subunit comprise mBzR at mitochondrial membrane contact sites. Solubilization of mBzR, radioligand binding, selective antibody identification, photoaffinity labeling Proceedings of the National Academy of Sciences of the United States of America High 1373486
2023 Site-specific ubiquitination of VDAC1 at lysine 53 by Parkin interrupts VDAC1 oligomerization and prevents mitochondrial DNA release into the cytoplasm. The ubiquitination-defective VDAC1 K53R mutant predominantly forms oligomers that release mtDNA and activate STING signaling even in the presence of Parkin. Parkin knockout mice (CCl4 liver fibrosis model), site-directed mutagenesis (VDAC1 K53R), mtDNA release assay, STING signaling assay, VDAC1 oligomerization analysis Experimental & molecular medicine High 36658227
2023 TMBIM6 (an ER Ca2+ leak protein) interacts with and prevents oligomerization of VDAC1, thereby sustaining mitochondrial Ca2+ homeostasis and mitochondrial quality control. Co-IP, mutant TMBIM6 transfection, and molecular docking confirmed the TMBIM6-VDAC1 interaction. TMBIM6 cardiac-specific knockout exacerbates LPS-induced mitochondrial dysfunction and septic cardiomyopathy. Co-immunoprecipitation, mutant TMBIM6 plasmid transfection, molecular docking, cardiomyocyte-specific KO and transgenic mice, mitochondrial respiration and ATP assays Metabolism: clinical and experimental High 36603706
2023 GPCPD1 depalmitoylated by LYPLA1 under hypoxia relocates to the outer mitochondrial membrane, binds VDAC1, and interferes with VDAC1 oligomerization, thereby increasing VDAC1 monomers that serve as anchor sites for PRKN-mediated polyubiquitination, triggering mitophagy. Co-immunoprecipitation, palmitoylation assay (HAM), confocal imaging of GPCPD1 relocalization, VDAC1 oligomerization assay, mitophagy assay, PRKN ubiquitination assay Autophagy Medium 36803235
2023 MCU upregulation by Cd intensifies interaction with VDAC1, enhances VDAC1 dimerization and ubiquitination, resulting in excessive mitophagy and hepatotoxicity. MCU inhibition (siRNA or Ru360) or heterozygous MCU knockout reduces Cd-induced VDAC1 dimerization and mitophagy. Co-immunoprecipitation, siRNA knockdown of MCU, Ru360 pharmacological inhibition, MCU heterozygous knockout mice, VDAC1 oligomerization analysis, mitophagy assays Advanced science Medium 36642847
2024 VDAC1 oligomerization is required for ferroptosis induced by cysteine deprivation or RSL3. Mitochondria-targeted antioxidants and pharmacological inhibitors of VDAC1 oligomerization suppress ferroptosis and reduce mitochondrial ROS; complex III of the electron transport chain is the primary source of ROS driving this process. MitoQ/MitoT mitochondria-targeted antioxidants, VDAC1 oligomerization inhibitors (pharmacological), complex III inhibition, ROS measurement, ferroptosis quantification Cell death & disease Medium 39521767
2018 miR-675 (encoded by lncRNA H19) directly targets the 3'UTR of VDAC1, repressing its expression. Loss of H19/miR-675 leads to VDAC1 upregulation and increased cardiomyocyte apoptosis under high glucose conditions; enforced H19 expression reduces VDAC1 levels and inhibits apoptosis. Luciferase reporter assay with VDAC1 3'UTR, miR-675 mimic/antagomir transfection, H19 siRNA, western blot, apoptosis assay Scientific reports Medium 27796346
2022 VDAC1 is required for phagophore recruitment during mitophagy of functional mitochondria in human terminal erythropoiesis. VDAC1 shRNA knockdown accelerates early erythroblast maturation but blocks enucleation at the orthochromatic stage with mitochondrial retention, demonstrating VDAC1 controls selective mitophagy in erythroid differentiation. shRNA lentiviral knockdown in human erythroblasts, flow cytometry of differentiation stages, mitochondria clearance assays, electron microscopy Haematologica Medium 33406813
2025 VSTM2L forms a complex with VDAC1 and HK2, enhancing their binding affinity and preventing VDAC1 oligomerization, thereby inhibiting ferroptosis and maintaining mitochondrial homeostasis in prostate cancer cells. VSTM2L knockdown sensitizes cells to RSL3-induced ferroptosis. Co-immunoprecipitation, VSTM2L knockdown, ferroptosis assays (RSL3), VDAC1 oligomerization assay, in vivo xenograft Nature communications Medium 39880844
2000 VDAC (porin) is present in the plasma membrane of hematopoietic cells, localized mostly in caveolae or caveolae-like domains. Purification from intact cell plasma membranes using membrane-impermeable NHS-SS-biotin labeling and streptavidin affinity chromatography confirmed extramitochondrial VDAC with channel properties similar to mitochondrial VDAC. Cell surface biotinylation with membrane-impermeable NHS-SS-biotin, streptavidin affinity purification, patch-clamp of intact cells Journal of bioenergetics and biomembranes Medium 11768765
2023 Alisol B (ALB) directly binds VDAC1 at amino acid residues S196 and H184 in the ATP-binding region, disrupting mitochondrial ATP export, increasing AMP/ATP ratio, and activating AMPK to inhibit SREBP-mediated lipid synthesis. Thermal shift assay confirmed binding was lost when VDAC1 was mutated at S196 and H184. Cellular thermal shift assay (CETSA), molecular dynamics, ultrafiltration-LC/MS, site-directed mutagenesis of VDAC1 S196A/H184A, AMPK/mTOR/SREBP signaling assays Phytomedicine Medium 38520833
2018 BRD4 regulates VDAC1 transcription: chromatin immunoprecipitation (ChIP) demonstrated BRD4 binding to the VDAC1 promoter, and the BRD4 inhibitor JQ1 decreases VDAC1 expression. VDAC1 expression contributes to JQ1 resistance in breast cancer cells. ChIP-qPCR, bromodomain inhibitor (JQ1) treatment, cell proliferation assays, western blot Oncology letters Low 31452730
2018 VDAC1 promotes cardiomyocyte autophagy after anoxia/reoxygenation via the PINK1/Parkin pathway. VDAC1 upregulation correlates with increased Beclin 1, LC3-II/I, and Parkin recruitment to mitochondria; VDAC1 RNAi knockdown inhibits PINK1/Parkin pathway activation and reduces autophagic flux and ROS. VDAC1 RNAi, immunofluorescence of Parkin mitochondrial recruitment, LC3-II/I and Beclin 1 western blot, ROS measurement, mitochondrial membrane potential assay Cell biology international Medium 33675282

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. Cell 2861 17081983
2010 PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1. Nature cell biology 2347 20098416
1999 Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC. Nature 1811 10365962
2012 Insights into RNA biology from an atlas of mammalian mRNA-binding proteins. Cell 1718 22658674
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2004 Large-scale characterization of HeLa cell nuclear phosphoproteins. Proceedings of the National Academy of Sciences of the United States of America 1159 15302935
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2005 Nucleolar proteome dynamics. Nature 934 15635413
2004 Immunoaffinity profiling of tyrosine phosphorylation in cancer cells. Nature biotechnology 916 15592455
2013 Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization. Nature 870 23503661
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
1998 Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. Proceedings of the National Academy of Sciences of the United States of America 823 9843949
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2007 Large-scale mapping of human protein-protein interactions by mass spectrometry. Molecular systems biology 733 17353931
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2010 p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both. Autophagy 640 20890124
1992 Isolation of the mitochondrial benzodiazepine receptor: association with the voltage-dependent anion channel and the adenine nucleotide carrier. Proceedings of the National Academy of Sciences of the United States of America 638 1373486
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