Affinage

VDAC1

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

Length
283 aa
Mass
30.8 kDa
Annotated
2026-06-11
100 papers in source corpus 36 papers cited in narrative 36 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/10 claims corpus-supported (90%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

VDAC1 is a large voltage-gated channel of the outer mitochondrial membrane that forms a ~1.2–2 nm pore permeable to hydrophilic solutes up to ~6 kDa, gated by electric fields and metabolic state, positioning it as the principal gateway for metabolite and ion flux across the outer membrane (PMID:2415299). Beyond conductance, VDAC1 is a central effector of mitochondria-mediated cell death: it dimerizes under physiological conditions through contacts involving beta-strands 1, 2, 16, and 19 and converts to higher-order oligomers upon apoptotic stimulation, a transition promoted by elevated intracellular Ca2+ and required for cytochrome c release (PMID:22117062, PMID:23542128). VDAC1 oligomerization can drive apoptosis even in Bax/Bak-deficient cells, and in cisplatin-induced death VDAC1 acts downstream of Bak and upstream of Bax activation (PMID:18362892, PMID:26253170). This oligomeric, death-promoting state is constrained by direct binding partners: hexokinase I/II dock onto charged beta-strand and N-terminal residues to partially occlude the pore and confer anti-apoptotic, pro-survival activity, while Bcl-xL binds the N-terminal domain to reduce channel conductance and mediate its protective effect (PMID:22589539, PMID:19094960, PMID:34083717). Multiple chemical probes that bind VDAC1 directly—DIDS-class anion-transport inhibitors and the VBIT-3/VBIT-4 compounds—block oligomerization and suppress apoptosis, ROS, and Ca2+ elevation, validating oligomerization as the pharmacological lever (PMID:27064145, PMID:27738100). VDAC1 is a major node in PINK1/Parkin mitophagy, undergoing site-specific ubiquitination by Parkin with opposing outcomes: K27 poly-ubiquitination recruits p62/SQSTM1 for mitochondrial clearance, K274 mono-ubiquitination suppresses apoptosis by limiting MCU-mediated Ca2+ uptake, and K53 poly-ubiquitination restricts oligomerization and blocks mtDNA release and downstream STING activation (PMID:20098416, PMID:32047033, PMID:36658227). These modifications are countered by ataxin-3-mediated deubiquitination, whose loss in SCA3 impairs canonical mitophagy (PMID:35682609). Phosphorylation of VDAC1 at Ser193 by Nek1—itself activated by TLK1—maintains membrane integrity and disrupts hexokinase binding (PMID:19158487, PMID:31914854). VDAC1 also serves non-apoptotic roles, acting as the molecular target through which itraconazole and alisol B (binding H184/S196) lower mitochondrial ATP, raise the AMP:ATP ratio, and activate AMPK to inhibit mTOR (PMID:26655341, PMID:38520833), and functioning as a plasma-membrane NADH-ferricyanide reductase (PMID:14573604). Studies of yeast and Drosophila orthologs extend its functions to mitochondrial morphology via the fission/fusion machinery, TOM complex assembly through chaperoning of Tom22, and cardiolipin/phospholipid metabolism via Mdm31/Mdm35 (PMID:20949033, PMID:30738703, PMID:30237174).

Mechanistic history

Synthesis pass · year-by-year structured walk · 29 steps
  1. 1985 Medium

    Established the foundational biophysical identity of VDAC1 as a large, voltage- and metabolite-gated outer-membrane pore, defining the channel whose gating later studies would link to death and signaling.

    Evidence planar lipid bilayer electrophysiology and molecular sieving of purified mitochondrial porin

    PMID:2415299

    Open questions at the time
    • Did not define the molecular determinants of gating
    • No connection to apoptosis or signaling at this stage
  2. 1991 Low

    Framed VDAC as a scaffold for metabolic microcompartmentation by binding hexokinase and glycerol kinase at the outer membrane, an early concept of channel–enzyme coupling.

    Evidence review of biochemical outer-membrane binding assays for hexokinase and glycerol kinase

    PMID:1710914

    Open questions at the time
    • Review-level summary of single-method pulldown data
    • Binding residues and functional consequence not defined here
  3. 2003 Medium

    Showed VDAC1 has an enzymatic activity beyond pore conduction—NADH-ferricyanide reductase at the plasma membrane—indicating a moonlighting function distinct from its mitochondrial role.

    Evidence subcellular fractionation, immunoprecipitation of enzymatic activity, and plasma-membrane targeting constructs

    PMID:14573604

    Open questions at the time
    • Physiological substrate/electron acceptor in vivo unclear
    • Relationship of this activity to mitochondrial VDAC1 function unresolved
  4. 2005 High

    Identified VDAC1 as a host target of influenza PB1-F2 that triggers permeability transition and cytochrome c release, linking VDAC1 to pathogen-induced apoptosis.

    Evidence GST pulldown with MS, purified-mitochondria permeabilization assay, and PTPC inhibitor rescue

    PMID:16201016

    Open questions at the time
    • Binding interface on VDAC1 not mapped
    • Relative contribution of VDAC1 versus ANT3 not resolved
  5. 2008 Medium

    Placed VDAC1 in a hierarchical apoptotic pathway (downstream of Bak, upstream of Bax) and defined hexokinase docking residues, establishing VDAC1 as a regulated apoptotic checkpoint and HK as a survival ligand.

    Evidence siRNA, chemical inhibition (DIDS), Bax/Bak epistasis; VDAC1 mutagenesis and HK-detaching peptides with apoptosis readouts

    PMID:18362892 PMID:19094960

    Open questions at the time
    • Mechanism coupling VDAC1 to Bax conformational change not defined
    • Whether HK binding acts solely by pore occlusion unresolved
  6. 2009 High

    Showed Nek1 phosphorylates VDAC1 at Ser193 to restrain excessive membrane permeability, revealing kinase control of VDAC1 death function.

    Evidence yeast two-hybrid, reciprocal Co-IP, kinase-dead and S193A/S193E phospho-mutant rescue of mitochondrial permeability

    PMID:19158487

    Open questions at the time
    • Structural effect of S193 phosphorylation on the channel not defined
    • Upstream activation of Nek1 not addressed here
  7. 2010 High

    Defined VDAC1 as a Parkin substrate ubiquitinated at K27 to recruit p62 during PINK1/Parkin mitophagy, integrating VDAC1 into mitochondrial quality control.

    Evidence siRNA, reciprocal Co-IP, ubiquitin chain-linkage analysis, mitophagy assays in multiple cell types

    PMID:20098416

    Open questions at the time
    • Whether VDAC1 ubiquitination is required versus accessory for mitophagy not fully resolved
    • Other Parkin sites not yet distinguished
  8. 2010 Medium

    Linked VDAC to mitochondrial morphology by demonstrating ortholog loss/overexpression shifts the fission/fusion balance via Drp1 and mitofusins.

    Evidence Drosophila porin mutants, morphology imaging, genetic epistasis with Drp1/mitofusins, locomotor assays

    PMID:20949033

    Open questions at the time
    • Ortholog study; direct relevance to human VDAC1 not tested
    • Molecular mechanism connecting VDAC to fission/fusion machinery unknown
  9. 2010 High

    Mapped cysteine topology and showed cysteines are dispensable for channel and apoptotic function, ruling out a required redox-cysteine gating mechanism.

    Evidence bilayer conductance with thiol-modifying reagents and cysteine-to-alanine mutagenesis with apoptosis readout

    PMID:20192921

    Open questions at the time
    • Does not exclude regulatory roles of cysteine oxidation under stress
    • Native redox state of cysteines in vivo not addressed
  10. 2011 High

    Identified the structural oligomerization interface (beta-strands 1, 2, 16, 19) and showed VDAC1 is a physiological dimer that climbs to higher oligomers upon apoptosis, providing the structural basis for pore-formation models.

    Evidence structure-based mutagenesis and cysteine cross-linking (BMOE) of dimer contacts

    PMID:22117062

    Open questions at the time
    • Architecture of the apoptotic high-order oligomer not resolved at atomic level
    • How cargo such as cytochrome c traverses the oligomer unclear
  11. 2012 High

    Established direct Bcl-xL–VDAC1 binding via the N-terminal domain as a conductance-reducing, anti-apoptotic interaction, mechanistically distinct from HK binding.

    Evidence MST, SPR, bilayer conductance, site-directed mutagenesis, viability assays

    PMID:22589539

    Open questions at the time
    • Whether Bcl-xL acts on monomer or blocks oligomerization not distinguished
    • In vivo relevance to tissue apoptosis not addressed
  12. 2013 Medium

    Showed Ca2+ is a direct trigger of VDAC1 oligomerization and apoptosis, connecting calcium signaling to pore formation.

    Evidence cross-linking oligomerization assays with Ca2+ chelator, ionophore, and mitochondrial Ca2+-transport inhibition

    PMID:23542128

    Open questions at the time
    • Whether Ca2+ acts directly on VDAC1 or via partners not resolved
    • Ca2+ sensing site on VDAC1 not identified
  13. 2014 Medium

    Identified TSPO–VDAC1 binding as a negative regulator of mitophagy by promoting ROS and counteracting Parkin ubiquitination.

    Evidence Co-IP, VDAC1 knockdown/overexpression, mitophagy flux and ROS assays

    PMID:25470454

    Open questions at the time
    • Single-lab Co-IP; binding interface unmapped
    • Mechanism by which TSPO–VDAC1 raises ROS not defined
  14. 2015 High

    Defined VDAC1 as the molecular target through which itraconazole lowers ATP and activates AMPK to inhibit mTOR, establishing VDAC1 as an upstream metabolic regulator.

    Evidence VDAC1 KO/KD rescue, AMPK/mTOR western blots, AMP:ATP measurements

    PMID:26655341

    Open questions at the time
    • Drug binding site not mapped in this study
    • Whether AMPK activation requires channel inhibition versus oligomerization unclear
  15. 2015 Medium

    Demonstrated a small molecule (cyathin-R) can force VDAC1 oligomerization to drive apoptosis independently of Bax/Bak, reinforcing VDAC1 as an autonomous death effector.

    Evidence Bax/Bak-null MEFs, VDAC1 siRNA, cross-linking oligomerization, cytochrome c release, xenograft

    PMID:26253170

    Open questions at the time
    • Direct binding of cyathin-R to VDAC1 not shown
    • Mechanism of oligomer induction not defined
  16. 2016 High

    Validated VDAC1 oligomerization as a druggable target through two compound classes (DIDS-type inhibitors and VBIT-3/4) that directly bind VDAC1 and block oligomerization and apoptosis.

    Evidence MST/direct binding, bilayer conductance, BRET2 oligomerization in living cells, apoptosis/ROS/Ca2+/HK assays

    PMID:27064145 PMID:27738100

    Open questions at the time
    • Compound binding sites on VDAC1 not resolved structurally
    • Selectivity over VDAC2/3 not fully established
  17. 2018 Medium

    Showed kinase-pathway control of HK2–VDAC1 binding (zinc/p53 via Akt/GSK3β phosphorylating VDAC1) and reported VDAC-specific cysteine over-oxidation, expanding the PTM landscape regulating VDAC1.

    Evidence Co-IP, VDAC1 phosphorylation blots, kinase inhibition, xenograft; high-resolution MS of native VDAC cysteines

    PMID:29890122 PMID:30528266

    Open questions at the time
    • Specific phospho-sites in the zinc/p53 axis not mapped
    • Functional consequence of cysteine over-oxidation/succination unknown
  18. 2018 Medium

    Established a conserved role for VDAC/porin in mitochondrial phospholipid metabolism through Mdm31/Mdm35 interactions controlling cardiolipin levels.

    Evidence yeast two-hybrid, Co-IP, lipidomics, interaction-defective Por1 mutants, validated in HeLa knockdown

    PMID:30237174

    Open questions at the time
    • Mammalian VDAC1 partners equivalent to Mdm31/Mdm35 not identified
    • Mechanism linking VDAC to lipid-transfer machinery unclear
  19. 2019 Medium

    Defined a TOM-assembly function for porin as a Tom22 sink balancing trimeric/dimeric TOM complexes, extending VDAC's role into protein import.

    Evidence Co-IP, in vitro import assays, native-gel TOM analysis in yeast

    PMID:30738703

    Open questions at the time
    • Conservation of the Tom22-chaperoning role in human VDAC1 not tested
    • Structural basis of the porin–Tom22 interaction unknown
  20. 2019 Medium

    Showed mutant SOD1 (ALS-associated) binds the VDAC1 N-terminus and reduces conductance, with an N-terminal peptide mitigating toxicity, implicating VDAC1 in motor neuron disease.

    Evidence direct binding to purified VDAC1, bilayer conductance, N-terminal truncation, motor-neuron viability with peptide

    PMID:31474832

    Open questions at the time
    • In vivo relevance in ALS models not established here
    • Whether reduced conductance is the toxic mechanism unclear
  21. 2020 High

    Discriminated opposing outcomes of Parkin mono- versus poly-ubiquitination of VDAC1: poly-Ub drives mitophagy while K274 mono-Ub suppresses apoptosis by limiting MCU Ca2+ uptake, refining the ubiquitin code on VDAC1.

    Evidence ubiquitin mutants, transgenic Drosophila, mitochondrial Ca2+ measurements, MCU epistasis

    PMID:32047033

    Open questions at the time
    • How K274 mono-Ub mechanistically limits MCU coupling not resolved
    • Mammalian in vivo confirmation of K274 phenotype pending
  22. 2020 Medium

    Placed the Nek1–VDAC1 axis under TLK1 control, showing TLK1 phosphorylation of Nek1-T141 supports VDAC1 phosphorylation, stability, and mitochondrial integrity.

    Evidence Nek1-T141A mutant, VDAC1 phosphorylation blots, mitochondrial permeability and respiration assays

    PMID:31914854

    Open questions at the time
    • Direct TLK1→Nek1→VDAC1 chain not fully reconstituted
    • Quantitative contribution to VDAC1 stability unclear
  23. 2021 Medium

    Provided a structural model of the HKII–VDAC1 binary complex showing partial pore occlusion and phosphorylation-dependent disruption of binding, mechanistically uniting earlier HK and phospho-regulation findings.

    Evidence molecular/Brownian dynamics docking with electrophysiological validation and phospho-mimetics

    PMID:34083717

    Open questions at the time
    • Computational model lacks experimental atomic structure
    • Which phospho-site drives disruption not pinned down
  24. 2022 Medium

    Linked ataxin-3-mediated VDAC1 deubiquitination to mitophagy, showing expanded ataxin-3 in SCA3 impairs Parkin recruitment and canonical mitophagy.

    Evidence SCA3 patient fibroblasts, VDAC1 ubiquitination and Parkin translocation assays, mitophagy flux, OXPHOS/ATP

    PMID:35682609

    Open questions at the time
    • VDAC1 ubiquitin sites targeted by ataxin-3 not defined
    • Causality of VDAC1 deubiquitination in SCA3 pathology not established
  25. 2022 Medium

    Demonstrated a developmental requirement for VDAC1 in terminal erythropoiesis, recruiting phagophore membranes for selective mitophagy needed for enucleation.

    Evidence shRNA knockdown in human erythroblasts, differentiation staging, mitophagy flux, confocal

    PMID:33406813

    Open questions at the time
    • Molecular basis of phagophore recruitment by VDAC1 unknown
    • Dependence on Parkin/PINK1 in this context not resolved
  26. 2023 High

    Defined K53 Parkin ubiquitination as a brake on VDAC1 oligomerization that prevents mtDNA release and STING-driven inflammation, connecting VDAC1 oligomerization to innate immune signaling.

    Evidence K53R mutagenesis, oligomerization and mtDNA-release assays, STING readout, Parkin-KO mice

    PMID:36658227

    Open questions at the time
    • How K53 ubiquitination sterically blocks oligomerization unclear
    • Generality across cell types beyond hepatic stellate cells untested
  27. 2023 Medium

    Identified multiple oligomerization-regulating partners and contexts—GPCPD1 increasing monomers to enable mitophagy, MCU enhancing dimerization/ubiquitination, and BAP31 controlling oligomerization to gate ferroptosis—showing oligomeric state as a convergent regulatory hub.

    Evidence Co-IP, cross-linking oligomerization, ubiquitination and ferroptosis/mitophagy assays, MCU-KO mice, HNF4A ChIP

    PMID:36642847 PMID:36803235 PMID:37296105

    Open questions at the time
    • Direct binding interfaces for these partners not mapped
    • Whether these regulators act independently or in shared complexes unknown
  28. 2023 Medium

    Mapped a defined small-molecule binding site (S196/H184 in the ATP-binding region) for alisol B that mediates AMPK activation via reduced ATP, refining the VDAC1–AMPK/mTOR mechanism.

    Evidence CETSA, ultrafiltration-LC/MS, site-directed mutagenesis ablating binding, AMP:ATP measurement

    PMID:38520833

    Open questions at the time
    • Whether endogenous ligands occupy this site unknown
    • Relationship of this site to oligomerization not addressed
  29. 2025 Medium

    Showed VSTM2L stabilizes the HK2–VDAC1 complex to suppress VDAC1 oligomerization and inhibit ferroptosis, extending the survival-promoting role of HK binding to redox cell death.

    Evidence Co-IP of ternary complex, oligomerization assay, siRNA, in vitro/in vivo ferroptosis assays

    PMID:39880844

    Open questions at the time
    • VSTM2L binding interface on the complex not mapped
    • Generality beyond prostate cancer cells untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • The atomic architecture of the apoptotic high-order VDAC1 oligomer and the route by which it conducts cytochrome c and mtDNA remain undefined, as does the unifying logic by which the many partners, PTMs, and small molecules converge on a single oligomerization switch.
  • No high-resolution structure of the death-associated oligomer
  • No reconstituted system showing macromolecular cargo passage
  • Integration of competing ubiquitination/phosphorylation signals on oligomeric state unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 2 GO:0098772 molecular function regulator activity 2 GO:0016491 oxidoreductase activity 1
Localization
GO:0005739 mitochondrion 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-9612973 Autophagy 4 R-HSA-5357801 Programmed Cell Death 3 R-HSA-1430728 Metabolism 2 R-HSA-162582 Signal Transduction 2 R-HSA-392499 Metabolism of proteins 1
Partners
ATXN3BCL2L1HK1HK2MCUNEK1PRKNTSPO
Complex memberships
TOM complex (yeast Por1)VDAC1 oligomerVDAC1-hexokinase complex

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 VDAC1 is a target for Parkin-mediated Lys27 poly-ubiquitylation during PINK1/Parkin-directed mitophagy; PINK1 kinase activity and mitochondrial localization are prerequisites for Parkin translocation to depolarized mitochondria, after which Parkin ubiquitylates VDAC1 to recruit the autophagic adaptor p62/SQSTM1 for mitochondrial clearance. siRNA knockdown, co-immunoprecipitation, ubiquitin chain-linkage analysis, cell-based mitophagy assays in non-neuronal and neuronal cells Nature cell biology High 20098416
2020 VDAC1 can be either mono- or poly-ubiquitinated by Parkin in a PINK1-dependent manner; poly-ubiquitination is required for mitophagy induction, whereas mono-ubiquitination at K274 suppresses apoptosis by limiting mitochondrial calcium uptake through the MCU channel. VDAC1 K274R mutation (blocking monoubiquitination) promotes apoptosis and Parkinson disease-related phenotypes in Drosophila. Ubiquitin mutant expression, transgenic Drosophila genetics, mitochondrial calcium measurements, MCU suppression epistasis Proceedings of the National Academy of Sciences of the United States of America High 32047033
2005 Influenza virus PB1-F2 protein physically interacts with VDAC1 on the outer mitochondrial membrane (and with ANT3 on the inner membrane), triggering mitochondrial permeability transition, cytochrome c release, and enhancement of tBid-induced membrane permeabilization; permeability transition pore blockers inhibit PB1-F2-induced permeabilization. GST pulldown with mass spectrometry, purified mitochondria permeabilization assay, pharmacological PTPC inhibition PLoS pathogens High 16201016
2009 Nek1 kinase physically associates with VDAC1 and phosphorylates it on serine 193; this phosphorylation is required to maintain normal mitochondrial membrane permeability and prevent excessive cell death. A phospho-mimetic S193E mutant rescues exaggerated MMP after DNA damage, while a non-phosphorylatable S193A mutant induces cell death. Yeast two-hybrid, GST pulldown, reciprocal immunoprecipitation, kinase-dead mutant expression, siRNA knockdown, mitochondrial membrane permeability assays, VDAC1 phospho-mutant rescue experiments Cell cycle (Georgetown, Tex.) High 19158487
2014 TSPO binds VDAC1 on the outer mitochondrial membrane; this interaction reduces mitochondrial coupling, promotes ROS overproduction, and thereby counteracts PARK2-mediated ubiquitination of proteins, inhibiting PINK1-PARK2-dependent mitophagy and abolishing SQSTM1/p62 and LC3 recruitment to mitochondria. Co-immunoprecipitation, VDAC1 knockdown/overexpression, mitophagy flux assays, ROS measurements, PARK2-ubiquitination assays Autophagy Medium 25470454
2008 In cisplatin-induced apoptosis, VDAC1 acts downstream of Bak and upstream of Bax in a hierarchical pathway governing mitochondrial membrane permeabilization; VDAC1 knockdown or chemical inhibition prevents Bax conformational activation without affecting Bak activation. siRNA screen, VDAC1 chemical inhibition (DIDS), Bax/Bak knockdown epistasis, mitochondrial membrane potential assay, plasma membrane permeabilization assay Oncogene Medium 18362892
2012 Bcl-xL directly interacts with VDAC1; the interaction requires specific VDAC1 residues including the N-terminal domain, reduces VDAC1 channel conductance in bilayer reconstitution, and mediates Bcl-xL antiapoptotic activity, since Bcl-xL fails to protect against apoptosis in cells expressing VDAC1 mutants that cannot bind Bcl-xL. Microscale thermophoresis, bilayer-reconstituted conductance assay, surface plasmon resonance, site-directed mutagenesis, cell viability assays with staurosporine The Journal of biological chemistry High 22589539
2003 VDAC1 expressed in the plasma membrane functions as a NADH-ferricyanide reductase; purified VDAC1 from both plasma membrane and mitochondria fractions exhibits this enzymatic activity, and targeting VDAC1 to the plasma membrane via an N-terminal signal peptide significantly increases cellular NADH-ferricyanide reductase activity. Subcellular fractionation, immunoprecipitation of enzymatic activity, VDAC1-GFP plasma-membrane targeting construct, confocal microscopy, FACS, enzymatic activity assay The Journal of biological chemistry Medium 14573604
2008 Hexokinase I and II bind VDAC1 through charged residues in several beta-strands and the N-terminal domain; disrupting the HK-VDAC1 interaction by mutagenesis or VDAC1-based peptides detaches HK from mitochondria, diminishes HK antiapoptotic activity, and reduces tumor cell survival. Site-directed mutagenesis of VDAC1, VDAC1-based peptide expression, HK-I-GFP mitochondrial localization assay, apoptosis assays Biochimica et biophysica acta Medium 19094960
2008 Phosphorylated StAR interacts with VDAC1 on the outer mitochondrial membrane; this interaction facilitates processing of 37-kDa phospho-StAR to the 32-kDa intermediate required for steroidogenesis. In the absence of VDAC1, phospho-StAR is degraded by cysteine proteases before mitochondrial import. Co-immunoprecipitation, VDAC1 knockdown, protease inhibitor experiments, biochemical processing assays The Journal of biological chemistry Medium 18250166
2011 VDAC1 oligomerization contact sites involve beta-strands 1, 2, 16, and 19; replacing hydrophobic residues in these strands with charged residues interferes with oligomerization. Cysteine-scanning cross-linking confirms proximity of these strands in dimers. VDAC1 exists as a dimer under physiological conditions and undergoes conformational changes to higher oligomers upon apoptosis induction. Structure-based mutagenesis, cysteine-replacement cross-linking with BMOE, chemical cross-linking, computation-guided dimerization interface prediction The Journal of biological chemistry High 22117062
2010 VDAC1 cysteine residues Cys127 and Cys232 have distinct topologies: one faces the pore (accessible to bulky 5-FM but blocked by prior NEM labeling) and one faces the lipid bilayer. However, cysteine-less VDAC1 (both Cys→Ala) retains normal channel activity and supports apoptosis when overexpressed, demonstrating that the cysteines are not required for channel gating or apoptotic function. Bilayer reconstitution conductance assay, thiol-modifying agents (NEM, 5-FM, BMOE), cysteine-to-alanine mutagenesis, cell apoptosis assay, mitochondrial localization by fluorescence The Biochemical journal High 20192921
2015 Itraconazole targets VDAC1 as its primary molecular target in endothelial cells; VDAC1 inhibition disrupts mitochondrial metabolism, raises the AMP:ATP ratio, activates AMPK, and thereby inhibits mTOR signaling. VDAC1-knockout cells are resistant to AMPK activation and mTOR inhibition by itraconazole, demonstrating VDAC1 as the mediator. VDAC1 knockdown and knockout cell lines, cellular thermal shift assay (implied by target identification), AMPK/mTOR pathway western blots, AMP:ATP ratio measurements, VDAC1-KO rescue experiments Proceedings of the National Academy of Sciences of the United States of America High 26655341
2013 Elevated intracellular Ca2+ promotes VDAC1 oligomerization and apoptosis; Ca2+ chelation with BAPTA-AM inhibits VDAC1 oligomerization and apoptosis, while Ca2+ ionophore treatment induces VDAC1 oligomerization in the absence of other apoptotic stimuli. Inhibition of mitochondrial Ca2+ transport decreases VDAC1 oligomerization, and increased [Ca2+]i upregulates VDAC1 expression. Chemical cross-linking to monitor oligomerization, Ca2+ chelator (BAPTA-AM), Ca2+ ionophore treatment, AzRu-mediated inhibition of mitochondrial Ca2+ transport, cell apoptosis assays Biochimica et biophysica acta Medium 23542128
2016 DIDS and related anion transport inhibitors (SITS, H2DIDS, DNDS, DPC) directly interact with VDAC1 (shown by microscale thermophoresis and reduced bilayer conductance), inhibit VDAC1 oligomerization, and consequently suppress pro-apoptotic protein release, apoptosis, Ca2+ elevation, ROS production, and mitochondrial membrane potential dissipation. Microscale thermophoresis, bilayer-reconstituted VDAC1 conductance, chemical cross-linking, BRET2 in living cells, apoptosis assays Biochimica et biophysica acta High 27064145
2016 Novel compounds (VBIT-3 and VBIT-4) directly interact with VDAC1, prevent VDAC1 oligomerization, inhibit apoptosis, restore mitochondrial membrane potential, decrease ROS production, prevent hexokinase detachment from mitochondria, and normalize intracellular Ca2+ levels. High-throughput compound screening, direct VDAC1 binding assays, chemical cross-linking for oligomerization, mitochondrial membrane potential assay, ROS assay, hexokinase binding assay, cell viability assays The Journal of biological chemistry Medium 27738100
2015 Cyathin-R, a fungal diterpene, promotes VDAC1 oligomerization to mediate cytochrome c release and apoptosis in Bax/Bak-deficient cells; VDAC1 silencing prevents cyathin-R-induced apoptosis, demonstrating that VDAC1 can mediate apoptosis independently of Bax/Bak. Bax/Bak-deficient MEF cells, VDAC1 siRNA knockdown, chemical cross-linking for oligomerization, cytochrome c release assay, xenograft mouse model The Journal of biological chemistry Medium 26253170
2019 Mutant SOD1 (G93A and G85R, but not wild-type SOD1) directly interacts with the N-terminal domain of VDAC1, reducing its channel conductance; a VDAC1 N-terminal domain-derived peptide inhibits mutant SOD1 toxicity in motor neuron-like cells and mouse embryonic stem cell-derived motor neurons. Direct binding assay with purified VDAC1, bilayer conductance measurement, N-terminally truncated VDAC1 construct, cell viability assay with peptide treatment Frontiers in cellular neuroscience Medium 31474832
2023 Under hypoxia, GPCPD1 is depalmitoylated by LYPLA1 and relocates to the outer mitochondrial membrane where it binds VDAC1, interferes with VDAC1 oligomerization, increasing VDAC1 monomers, which provide more anchor sites for PRKN-mediated polyubiquitination and consequent mitophagy induction. Co-immunoprecipitation, VDAC1 oligomerization assay (chemical cross-linking), PRKN ubiquitination assay, GPCPD1 depalmitoylation/localization tracking, siRNA knockdown Autophagy Medium 36803235
2023 Parkin ubiquitinates VDAC1 at lysine 53; this site-specific ubiquitination interrupts VDAC1 oligomerization and prevents mitochondrial DNA release into the cytoplasm. VDAC1 K53R mutant (ubiquitination-deficient) forms oligomers resistant to Parkin suppression and triggers STING pathway activation in hepatic stellate cells. Site-directed mutagenesis (K53R), E3 ligase activity assay, VDAC1 oligomerization assay, mtDNA release assay, STING signaling readout, Parkin knockout mice Experimental & molecular medicine High 36658227
2021 HKII and VDAC1 form a binary complex in which HKII partially (not completely) occludes VDAC1's permeation pathway after membrane insertion of HKII's H-anchor. Phosphorylation of VDAC1 disrupts HKII binding, as confirmed by electrophysiology. Molecular dynamics simulations, Brownian dynamics docking, electrophysiology (channel conductance in presence/absence of HKII), VDAC1 phosphorylation mimetics Communications biology Medium 34083717
2020 TLK1 phosphorylates Nek1 at T141, and this activating phosphorylation contributes to Nek1-mediated phosphorylation and stability of VDAC1, thereby maintaining mitochondrial membrane integrity. Cells overexpressing kinase-dead Nek1-T141A show reduced VDAC1 phosphorylation, exaggerated mitochondrial permeability, reduced mitochondrial respiration, and increased apoptosis. Nek1-T141A mutant overexpression, VDAC1 phosphorylation western blot, mitochondrial permeability/cytochrome c release assay, oxygen consumption measurements, drug sensitivity assays Cell cycle (Georgetown, Tex.) Medium 31914854
2018 VDAC1 and VDAC2 cysteine residues from rat liver mitochondria undergo over-oxidation and succination as post-translational modifications, with cysteine over-oxidation appearing to be an exclusive feature of VDACs not found in other transmembrane mitochondrial proteins. Tryptic and chymotryptic proteolysis, UHPLC/High-Resolution ESI-MS/MS Biochimica et biophysica acta. Bioenergetics Medium 29890122
2010 Loss of Drosophila Porin (VDAC) causes elongated mitochondria in indirect flight muscle, while Porin overexpression produces fragmented mitochondria. Genetic epistasis with Drp1 (fission) and mitofusins (fusion) demonstrates that Porin regulates mitochondrial morphology through the fission/fusion machinery, and increased mitochondrial fission rescues locomotor defects in porin mutants. Drosophila porin mutant generation, mitochondrial morphology imaging, genetic epistasis with Drp1 and mitofusin mutants, locomotor behavior assays PloS one Medium 20949033
2019 In yeast (Por1/VDAC ortholog), porin associates with Tom22 to act as a sink for newly imported Tom22, modulating Tom22 integration into the TOM complex and thereby regulating the dynamic equilibrium between trimeric (3-channel, Tom22-containing) and dimeric (2-channel) TOM complexes. Porin also facilitates import of TIM40/MIA-dependent proteins by promoting the dimeric TOM complex. Co-immunoprecipitation, in vitro import assays, TOM complex native gel analysis, cell-cycle-dependent Tom22 phosphorylation analysis Molecular cell Medium 30738703
2018 Yeast porins (Por1/Por2) interact with Mdm31 and Mdm35, and their depletion destabilizes Ups1 and Ups2, decreases cardiolipin levels by ~90%, and abolishes Ups2-dependent phosphatidylethanolamine synthesis. Por1 mutations that disrupt Mdm31/Mdm35 interactions (without affecting respiratory growth) also decrease cardiolipin levels, demonstrating a specific role in mitochondrial phospholipid metabolism conserved to mammalian VDAC. Yeast two-hybrid, co-immunoprecipitation, lipidomic analysis, Por1 interaction-defective mutants, HeLa cell VDAC knockdown The Journal of biological chemistry Medium 30237174
2022 VDAC1 downregulation by shRNA in human erythroblasts accelerates early maturation but blocks differentiation at the orthochromatic stage, reducing enucleation and increasing cell death. VDAC1 is required for phagophore membrane recruitment to regulate selective mitophagy of functional mitochondria during terminal erythropoiesis. shRNA knockdown, erythroid differentiation staging, mitochondrial retention assay, mitophagy flux assay, confocal microscopy Haematologica Medium 33406813
2022 Wild-type ataxin-3 deubiquitinates VDAC1; in SCA3 patients with expanded ataxin-3, VDAC1 deubiquitination and Parkin recruitment to depolarized mitochondria are inhibited, leading to impaired canonical mitophagy and compensatory increase in p62-linked mitophagy and autophagy. Patient-derived fibroblast cell lines, VDAC1 ubiquitination assay, Parkin translocation assay, mitophagy flux, OXPHOS complex measurement, ATP production assay International journal of molecular sciences Medium 35682609
1991 Porin (VDAC) interacts with hexokinase and glycerol kinase on the outer mitochondrial membrane surface, providing these enzymes with preferred access to mitochondrially-generated ATP through metabolic microcompartmentation. Biochemical interaction studies, mitochondrial outer membrane protein binding assays (review of primary experimental evidence) Biochemical medicine and metabolic biology Low 1710914
2023 MCU upregulation by cadmium intensifies MCU-VDAC1 interaction, enhances VDAC1 dimerization and ubiquitination, causing excessive mitophagy and hepatotoxicity; MCU inhibition (siRNA or Ru360) attenuates VDAC1 dimerization, excessive mitophagy, and hepatocyte death. Co-immunoprecipitation, VDAC1 oligomerization assay, siRNA knockdown, MCU heterozygous knockout mice, mitophagy flux assay Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 36642847
2025 VSTM2L forms a complex with VDAC1 and hexokinase 2 (HK2), enhancing their binding affinity and preventing VDAC1 oligomerization, thereby inhibiting ferroptosis and maintaining mitochondrial homeostasis in prostate cancer cells. Co-immunoprecipitation, VDAC1 oligomerization assay, siRNA knockdown, in vitro and in vivo ferroptosis assays Nature communications Medium 39880844
2018 Zinc and p53 disrupt mitochondrial binding of HK2 to VDAC1 in prostate cancer cells by phosphorylating VDAC1, a process mediated through Akt inhibition and GSK3β activation. Mitochondrial fractionation, co-immunoprecipitation of HK2-VDAC1, VDAC1 phosphorylation western blot, Akt/GSK3β pharmacological inhibition, xenograft model Experimental cell research Medium 30528266
2023 BAP31 directly binds VDAC1 and affects its oligomerization and polyubiquitination; BAP31 knockdown increases lipid peroxidation and facilitates ferroptosis, while BAP31 overexpression inhibits ferroptosis. HNF4A binds the BAP31 promoter and increases its transcription, placing VDAC1 oligomerization downstream of this HNF4A-BAP31 axis. Co-immunoprecipitation, VDAC1 oligomerization assay, ubiquitination assay, siRNA knockdown, lipid peroxidation assay, ChIP for HNF4A-BAP31 promoter interaction Cell death & disease Medium 37296105
2021 VDAC1 promotes cardiomyocyte autophagy in anoxia/reoxygenation injury via the PINK1/Parkin pathway; VDAC1 knockdown inhibits PINK1/Parkin activation and Parkin translocation to mitochondria, reducing autophagic vacuole formation, ROS burst, and mitochondrial dysfunction. siRNA knockdown, autophagic flux assay, Parkin translocation immunofluorescence, ROS measurement, mitochondrial membrane potential assay Cell biology international Low 33675282
2023 Alisol B directly binds VDAC1 at amino acid residues S196 and H184 in the ATP-binding region; mutations at these sites abolish the thermal stabilization effect of Alisol B on VDAC1, and VDAC1 binding mediates Alisol B's ability to decrease mitochondrial ATP production and activate AMPK independently of canonical upstream kinases. Cellular thermal shift assay (CETSA), molecular dynamics, ultrafiltration-LC/MS, site-directed mutagenesis of VDAC1 (S196 and H184 mutations), AMP:ATP ratio measurement Phytomedicine : international journal of phytotherapy and phytopharmacology Medium 38520833
1985 Mitochondrial porin (VDAC) forms large pores permeable to hydrophilic substances up to ~6000 Da, with pore diameter of 1.2–2 nm, and pore conductance is controlled by electric fields and metabolic processes. These properties were established in early electrophysiological characterization. Planar lipid bilayer electrophysiology, molecular sieving assays CRC critical reviews in biochemistry Medium 2415299

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1. Nature cell biology 2372 20098416
2005 Influenza virus PB1-F2 protein induces cell death through mitochondrial ANT3 and VDAC1. PLoS pathogens 296 16201016
2017 Mitochondrial VDAC1: A Key Gatekeeper as Potential Therapeutic Target. Frontiers in physiology 289 28713289
2018 VDAC1, mitochondrial dysfunction, and Alzheimer's disease. Pharmacological research 212 29551631
1985 Porin from bacterial and mitochondrial outer membranes. CRC critical reviews in biochemistry 209 2415299
2020 VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases. Biomolecules 191 33114780
2020 Decision between mitophagy and apoptosis by Parkin via VDAC1 ubiquitination. Proceedings of the National Academy of Sciences of the United States of America 187 32047033
2014 TSPO interacts with VDAC1 and triggers a ROS-mediated inhibition of mitochondrial quality control. Autophagy 181 25470454
2008 Hierarchical involvement of Bak, VDAC1 and Bax in cisplatin-induced cell death. Oncogene 175 18362892
2012 VDAC1: from structure to cancer therapy. Frontiers in oncology 167 23233904
1999 Porin expression in clinical isolates of Klebsiella pneumoniae. Microbiology (Reading, England) 161 10217501
2012 Mediation of the antiapoptotic activity of Bcl-xL protein upon interaction with VDAC1 protein. The Journal of biological chemistry 146 22589539
2017 VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress. Cell stress 143 30542671
1991 Porin interaction with hexokinase and glycerol kinase: metabolic microcompartmentation at the outer mitochondrial membrane. Biochemical medicine and metabolic biology 143 1710914
1987 Mitochondrial porin of Neurospora crassa: cDNA cloning, in vitro expression and import into mitochondria. The EMBO journal 142 2960519
2018 VDAC1 as Pharmacological Target in Cancer and Neurodegeneration: Focus on Its Role in Apoptosis. Frontiers in chemistry 141 29682501
2016 Large-Conductance Transmembrane Porin Made from DNA Origami. ACS nano 140 27504755
2003 VDAC1 is a transplasma membrane NADH-ferricyanide reductase. The Journal of biological chemistry 136 14573604
2016 Novel Compounds Targeting the Mitochondrial Protein VDAC1 Inhibit Apoptosis and Protect against Mitochondrial Dysfunction. The Journal of biological chemistry 131 27738100
2014 Silencing VDAC1 Expression by siRNA Inhibits Cancer Cell Proliferation and Tumor Growth In Vivo. Molecular therapy. Nucleic acids 130 24781191
1987 Porin protein of Neisseria gonorrhoeae: cloning and gene structure. Proceedings of the National Academy of Sciences of the United States of America 125 2825179
2012 Mitochondrial VDAC1: function in cell life and death and a target for cancer therapy. Current medicinal chemistry 117 22204343
2008 Key regions of VDAC1 functioning in apoptosis induction and regulation by hexokinase. Biochimica et biophysica acta 115 19094960
2008 Steroidogenic activity of StAR requires contact with mitochondrial VDAC1 and phosphate carrier protein. The Journal of biological chemistry 109 18250166
2013 The role of calcium in VDAC1 oligomerization and mitochondria-mediated apoptosis. Biochimica et biophysica acta 101 23542128
1989 Osmotic regulation of porin expression: a role for DNA supercoiling. Molecular microbiology 101 2552265
2019 VDAC1 and the TSPO: Expression, Interactions, and Associated Functions in Health and Disease States. International journal of molecular sciences 93 31288390
2015 Antifungal drug itraconazole targets VDAC1 to modulate the AMPK/mTOR signaling axis in endothelial cells. Proceedings of the National Academy of Sciences of the United States of America 89 26655341
1997 The Oms66 (p66) protein is a Borrelia burgdorferi porin. Infection and immunity 88 9284133
2011 Structure-based analysis of VDAC1 protein: defining oligomer contact sites. The Journal of biological chemistry 78 22117062
2009 Nek1 regulates cell death and mitochondrial membrane permeability through phosphorylation of VDAC1. Cell cycle (Georgetown, Tex.) 78 19158487
2013 Oligomerization of the mitochondrial protein VDAC1: from structure to function and cancer therapy. Progress in molecular biology and translational science 77 23663973
2012 Is the mitochondrial outermembrane protein VDAC1 therapeutic target for Alzheimer's disease? Biochimica et biophysica acta 73 22995655
1983 Isolation and characterization of chain-terminating nonsense mutations in a porin regulator gene, envZ. Journal of bacteriology 73 6311806
2016 The porin VDAC2 is the mitochondrial platform for Bax retrotranslocation. Scientific reports 71 27620692
2016 VDAC1-interacting anion transport inhibitors inhibit VDAC1 oligomerization and apoptosis. Biochimica et biophysica acta 70 27064145
2014 Genomic analyses of bacterial porin-cytochrome gene clusters. Frontiers in microbiology 68 25505896
2015 Vorinostat synergizes with EGFR inhibitors in NSCLC cells by increasing ROS via up-regulation of the major mitochondrial porin VDAC1 and modulation of the c-Myc-NRF2-KEAP1 pathway. Free radical biology & medicine 64 26409771
2023 Hypoxia-induced GPCPD1 depalmitoylation triggers mitophagy via regulating PRKN-mediated ubiquitination of VDAC1. Autophagy 63 36803235
2019 Porin Associates with Tom22 to Regulate the Mitochondrial Protein Gate Assembly. Molecular cell 61 30738703
1998 Identification and characterization of two quiescent porin genes, nmpC and ompN, in Escherichia coli BE. Journal of bacteriology 61 9642192
2013 Reduced VDAC1 protects against Alzheimer's disease, mitochondria, and synaptic deficiencies. Journal of Alzheimer's disease : JAD 60 23948905
2017 VDAC1 as a Player in Mitochondria-Mediated Apoptosis and Target for Modulating Apoptosis. Current medicinal chemistry 56 28618997
2023 MCU Upregulation Overactivates Mitophagy by Promoting VDAC1 Dimerization and Ubiquitination in the Hepatotoxicity of Cadmium. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 51 36642847
2010 The complexities of porin genetic regulation. Journal of molecular microbiology and biotechnology 51 20068355
1995 Isolation and characterization of a conserved porin protein from Helicobacter pylori. Journal of bacteriology 51 7559328
2023 Porin-independent accumulation in Pseudomonas enables antibiotic discovery. Nature 50 37993720
2015 A New Fungal Diterpene Induces VDAC1-dependent Apoptosis in Bax/Bak-deficient Cells. The Journal of biological chemistry 50 26253170
2010 Drosophila Porin/VDAC affects mitochondrial morphology. PloS one 50 20949033
2000 Extramitochondrial porin: facts and hypotheses. Journal of bioenergetics and biomembranes 50 11768765
2023 Site-specific ubiquitination of VDAC1 restricts its oligomerization and mitochondrial DNA release in liver fibrosis. Experimental & molecular medicine 49 36658227
2018 Inhibition of VDAC1 Protects Against Glutamate-Induced Oxytosis and Mitochondrial Fragmentation in Hippocampal HT22 Cells. Cellular and molecular neurobiology 48 30421242
2023 HNF4A-BAP31-VDAC1 axis synchronously regulates cell proliferation and ferroptosis in gastric cancer. Cell death & disease 47 37296105
2000 Characterization and functional analysis of PorB, a Chlamydia porin and neutralizing target. Molecular microbiology 47 11115112
1993 Purification and characterization of protein H, the major porin of Pasteurella multocida. Journal of bacteriology 46 7677992
2010 VDAC1 cysteine residues: topology and function in channel activity and apoptosis. The Biochemical journal 45 20192921
1998 Neisseria gonorrhoeae porin modulates phagosome maturation. The Journal of biological chemistry 45 9857075
2008 Expression and porin activity of P28 and OMP-1F during intracellular Ehrlichia chaffeensis development. Journal of bacteriology 44 18359808
1997 New findings concerning vertebrate porin. Die Naturwissenschaften 44 9433706
2021 Structural basis of complex formation between mitochondrial anion channel VDAC1 and Hexokinase-II. Communications biology 43 34083717
1990 Interaction of mitochondrial porin with cytosolic proteins. Experientia 43 1689254
2016 MicroRNA-7 downregulates the oncogene VDAC1 to influence hepatocellular carcinoma proliferation and metastasis. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 41 26831666
2020 VDAC1 in the diseased myocardium and the effect of VDAC1-interacting compound on atrial fibrosis induced by hyperaldosteronism. Scientific reports 37 33328613
2019 A VDAC1-Derived N-Terminal Peptide Inhibits Mutant SOD1-VDAC1 Interactions and Toxicity in the SOD1 Model of ALS. Frontiers in cellular neuroscience 36 31474832
2020 The TLK1/Nek1 axis contributes to mitochondrial integrity and apoptosis prevention via phosphorylation of VDAC1. Cell cycle (Georgetown, Tex.) 35 31914854
2012 Alternative folding pathways of the major porin OprF of Pseudomonas aeruginosa. The FEBS journal 35 22240095
2010 Structures of the OmpF porin crystallized in the presence of foscholine-12. Protein science : a publication of the Protein Society 35 20196071
2019 Metabolic Reprograming Via Silencing of Mitochondrial VDAC1 Expression Encourages Differentiation of Cancer Cells. Molecular therapy. Nucleic acids 33 31195298
2018 Post-translational modifications of VDAC1 and VDAC2 cysteines from rat liver mitochondria. Biochimica et biophysica acta. Bioenergetics 33 29890122
1992 Polyphosphate-selective porin OprO of Pseudomonas aeruginosa: expression, purification and sequence. Molecular microbiology 33 1406271
2011 Effects of amino acid supplementation on porin expression and ToxR levels in Vibrio cholerae. Infection and immunity 32 22144480
2025 VSTM2L protects prostate cancer cells against ferroptosis via inhibiting VDAC1 oligomerization and maintaining mitochondria homeostasis. Nature communications 30 39880844
2018 Zinc and p53 disrupt mitochondrial binding of HK2 by phosphorylating VDAC1. Experimental cell research 30 30528266
1998 Role of Pasteurella multocida porin on cytokine expression and release by murine splenocytes. Veterinary immunology and immunopathology 30 9880114
2022 Human erythroid differentiation requires VDAC1-mediated mitochondrial clearance. Haematologica 29 33406813
2020 Low abundance of NDUFV2 and NDUFS4 subunits of the hydrophilic complex I domain and VDAC1 predicts mammalian longevity. Redox biology 29 32353747
2018 Fosfomycin Permeation through the Outer Membrane Porin OmpF. Biophysical journal 29 30616836
2012 Increased expression of VDAC1 sensitizes carcinoma cells to apoptosis induced by DNA cross-linking agents. Biochemical pharmacology 29 22285227
2009 Downregulation of mitochondrial porin inhibits cell growth and alters respiratory phenotype in Trypanosoma brucei. Eukaryotic cell 29 19617393
2022 Targeting the Mitochondrial Protein VDAC1 as a Potential Therapeutic Strategy in ALS. International journal of molecular sciences 28 36077343
2024 Inhibition of VDAC1 oligomerization blocks cysteine deprivation-induced ferroptosis via mitochondrial ROS suppression. Cell death & disease 27 39521767
2020 The Mitochondrial Protein VDAC1 at the Crossroads of Cancer Cell Metabolism: The Epigenetic Link. Cancers 27 32331482
2018 yVDAC2, the second mitochondrial porin isoform of Saccharomyces cerevisiae. Biochimica et biophysica acta. Bioenergetics 27 29408701
2021 VDAC1 promotes cardiomyocyte autophagy in anoxia/reoxygenation injury via the PINK1/Parkin pathway. Cell biology international 26 33675282
2018 Porin Deficiency in Carbapenem-Resistant Enterobacter aerogenes Strains. Microbial drug resistance (Larchmont, N.Y.) 26 29653477
2009 Development of novel cell surface display in Corynebacterium glutamicum using porin. Applied microbiology and biotechnology 26 19430772
2004 Extracellular secretion of the Borrelia burgdorferi Oms28 porin and Bgp, a glycosaminoglycan binding protein. Infection and immunity 26 15501754
2022 VDAC1 balances mitophagy and apoptosis in leafhopper upon arbovirus infection. Autophagy 25 36409297
2018 Porin proteins have critical functions in mitochondrial phospholipid metabolism in yeast. The Journal of biological chemistry 25 30237174
1991 Cloning and sequencing of the structural gene for the porin protein of Bordetella pertussis. Molecular microbiology 25 1658537
2021 PGC1α Promotes Cisplatin Resistance in Ovarian Cancer by Regulating the HSP70/HK2/VDAC1 Signaling Pathway. International journal of molecular sciences 24 33802591
2020 A unique porin meditates iron-selective transport through cyanobacterial outer membranes. Environmental microbiology 24 33196124
2017 Mitochondrial VDAC1-based peptides: Attacking oncogenic properties in glioblastoma. Oncotarget 24 28412744
2021 VDAC1 Silencing in Cancer Cells Leads to Metabolic Reprogramming That Modulates Tumor Microenvironment. Cancers 23 34200480
2019 VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer. Oncology letters 23 31452730
2017 Investigating asymmetric salt profiles for nanopore DNA sequencing with biological porin MspA. PloS one 23 28749972
2023 Alisol B regulates AMPK/mTOR/SREBPs via directly targeting VDAC1 to alleviate hyperlipidemia. Phytomedicine : international journal of phytotherapy and phytopharmacology 21 38520833
2022 Mitochondrial Dysfunction in Spinocerebellar Ataxia Type 3 Is Linked to VDAC1 Deubiquitination. International journal of molecular sciences 21 35682609
2014 Purification of VDAC1 from rat liver mitochondria. Cold Spring Harbor protocols 21 24371315
2019 Multifaceted roles of porin in mitochondrial protein and lipid transport. Biochemical Society transactions 20 31670371

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