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    Vdac1 voltage-dependent anion channel 1 [ Rattus norvegicus (Norway rat) ]

    Gene ID: 83529, updated on 9-Dec-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    UBA52 Attunes VDAC1-Mediated Mitochondrial Dysfunction and Dopaminergic Neuronal Death.

    UBA52 Attunes VDAC1-Mediated Mitochondrial Dysfunction and Dopaminergic Neuronal Death.
    Tiwari S, Singh A, Gupta P, K A, Singh S.

    03/7/2023
    Inhibition of VDAC1 Rescues Abeta 1-42-Induced Mitochondrial Dysfunction and Ferroptosis via Activation of AMPK and Wnt/beta-Catenin Pathways.

    Inhibition of VDAC1 Rescues Aβ (1-42)-Induced Mitochondrial Dysfunction and Ferroptosis via Activation of AMPK and Wnt/β-Catenin Pathways.
    Zhou X, Tang X, Li T, Li D, Gong Z, Zhang X, Li Y, Zhu J, Wang Y, Zhang B., Free PMC Article

    03/1/2023
    VDAC1 regulates neuronal cell loss after retinal trauma injury by a mitochondria-independent pathway.

    VDAC1 regulates neuronal cell loss after retinal trauma injury by a mitochondria-independent pathway.
    de Sousa E, Móvio MI, de Lima-Vasconcellos TH, Dos Santos GB, Dos Santos Gomes T, Walter LT, da Silva DA, Rodrigues T, Cerchiaro G, Kihara AH., Free PMC Article

    05/7/2022
    VDAC1 promotes cardiomyocyte autophagy in anoxia/reoxygenation injury via the PINK1/Parkin pathway.

    VDAC1 promotes cardiomyocyte autophagy in anoxia/reoxygenation injury via the PINK1/Parkin pathway.
    Yang X, Zhou Y, Liang H, Meng Y, Liu H, Zhou Y, Huang C, An B, Mao H, Liao Z.

    12/11/2021
    VDAC1 in the diseased myocardium and the effect of VDAC1-interacting compound on atrial fibrosis induced by hyperaldosteronism.

    VDAC1 in the diseased myocardium and the effect of VDAC1-interacting compound on atrial fibrosis induced by hyperaldosteronism.
    Klapper-Goldstein H, Verma A, Elyagon S, Gillis R, Murninkas M, Pittala S, Paul A, Shoshan-Barmatz V, Etzion Y., Free PMC Article

    05/8/2021
    Knockout of VDAC1 in H9c2 Cells Promotes Oxidative Stress-Induced Cell Apoptosis through Decreased Mitochondrial Hexokinase II Binding and Enhanced Glycolytic Stress.

    Knockout of VDAC1 in H9c2 Cells Promotes Oxidative Stress-Induced Cell Apoptosis through Decreased Mitochondrial Hexokinase II Binding and Enhanced Glycolytic Stress.
    Yang M, Sun J, Stowe DF, Tajkhorshid E, Kwok WM, Camara AKS., Free PMC Article

    02/2/2021
    MiR-183-5p protects rat hearts against myocardial ischemia/reperfusion injury through targeting VDAC1.

    MiR-183-5p protects rat hearts against myocardial ischemia/reperfusion injury through targeting VDAC1.
    Lin D, Cui B, Ma J, Ren J.

    11/21/2020
    VDAC1 is essential for neurite maintenance and the inhibition of its oligomerization protects spinal cord from demyelination and facilitates locomotor function recovery after spinal cord injury.

    VDAC1 is essential for neurite maintenance and the inhibition of its oligomerization protects spinal cord from demyelination and facilitates locomotor function recovery after spinal cord injury.
    Paschon V, Morena BC, Correia FF, Beltrame GR, Dos Santos GB, Cristante AF, Kihara AH., Free PMC Article

    11/21/2020
    Authors demonstrated that hydrogen-rich saline (HRS) reduced OGD/RP-mediated neuronal loss by stimulating the expression of Bcl-2, which suppressed the activity of VDAC1.

    Hydrogen-rich saline protects rat from oxygen glucose deprivation and reperusion-induced apoptosis through VDAC1 via Bcl-2.
    Mo XY, Li XM, She CS, Lu XQ, Xiao CG, Wang SH, Huang GQ.

    05/30/2020
    Taken together, peroxynitrite produced during cardiac ischemia and reperfusion injury can nitrate tyrosine residues of two key mitochondrial membrane proteins involved in bioenergetics and energy transfer via binding to hexokinase 2 to contribute to mitochondrial and cellular dysfunction.

    Peroxynitrite nitrates adenine nucleotide translocase and voltage-dependent anion channel 1 and alters their interactions and association with hexokinase II in mitochondria.
    Yang M, Xu Y, Heisner JS, Sun J, Stowe DF, Kwok WM, Camara AKS., Free PMC Article

    08/17/2019
    Our research suggests that the protective effect of the WDR26 isoform, MIP2, on the cardiomyocytes against oxidative stress is partly associated with its interaction with VDAC1 and thus inhibiting its expression

    WDR26/MIP2 interacts with VDAC1 and regulates VDAC1 expression levels in H9c2 cells.
    Jiang L, Wang H, Chen G, Feng Y, Zou J, Liu M, Liu K, Wang N, Zhang H, Wang K, Xiao X.

    05/11/2019
    Results identified apoptosis-related gene VDAC1 as a direct target of miR-675 and involved in the regulation of high glucose-induced apoptosis by the H19/miR-675 axis.

    lncRNA H19/miR-675 axis regulates cardiomyocyte apoptosis by targeting VDAC1 in diabetic cardiomyopathy.
    Li X, Wang H, Yao B, Xu W, Chen J, Zhou X., Free PMC Article

    05/5/2018
    this study describes novel drug candidates with a defined mechanism of action that involves inhibition of VDAC1 oligomerization, apoptosis, and mitochondrial dysfunction. The compounds VBIT-3 and VBIT-4 offer a therapeutic strategy for treating different diseases associated with enhanced apoptosis and point to VDAC1 as a promising target for therapeutic intervention.

    Novel Compounds Targeting the Mitochondrial Protein VDAC1 Inhibit Apoptosis and Protect against Mitochondrial Dysfunction.
    Ben-Hail D, Begas-Shvartz R, Shalev M, Shteinfer-Kuzmine A, Gruzman A, Reina S, De Pinto V, Shoshan-Barmatz V., Free PMC Article

    05/27/2017
    VDAC1-interacting anion transport inhibitors inhibited apoptosis via direct interaction with VDAC1 to inhibit its oligomerization and subsequent Cyto c release and apoptosis.

    VDAC1-interacting anion transport inhibitors inhibit VDAC1 oligomerization and apoptosis.
    Ben-Hail D, Shoshan-Barmatz V.

    09/10/2016
    Tubulin tail sequences and post-translational modifications regulate closure of mitochondrial voltage-dependent anion channel, VDAC.

    Tubulin tail sequences and post-translational modifications regulate closure of mitochondrial voltage-dependent anion channel (VDAC).
    Sheldon KL, Gurnev PA, Bezrukov SM, Sackett DL., Free PMC Article

    02/6/2016
    The data obtained argue against VDAC1 and in favor of Cyb5R3 involvement in the activation of redox cyclers in the outer mitochondrial membrane.

    External mitochondrial NADH-dependent reductase of redox cyclers: VDAC1 or Cyb5R3?
    Nikiforova AB, Saris NE, Kruglov AG.

    06/6/2015
    Results indicate that mitochondrial function associated with VDAC1 is decreased in sporadic and experimental Parkinson's disease, and this decrease is associated with alpha-synuclein accumulation and aggregation

    Abnormal alpha-synuclein reduces nigral voltage-dependent anion channel 1 in sporadic and experimental Parkinson's disease.
    Chu Y, Goldman JG, Kelly L, He Y, Waliczek T, Kordower JH.

    03/21/2015
    VDAC1 has a role in alpha-synuclein-induced dopaminergic neuron toxicity in rats

    Voltage-dependent anion channel involved in the α-synuclein-induced dopaminergic neuron toxicity in rats.
    Lu L, Zhang C, Cai Q, Lu Q, Duan C, Zhu Y, Yang H.

    09/14/2013
    Multiple spots on 2D gel representing VDAC1 protein forms with different isoelectric points.

    Relationship between expression of voltage-dependent anion channel (VDAC) isoforms and type of hexokinase binding sites on brain mitochondria.
    Poleti MD, Tesch AC, Crepaldi CR, Souza GH, Eberlin MN, de Cerqueira César M, Poleti MD, Tesch AC, Crepaldi CR, Souza GH, Eberlin MN, de Cerqueira César M.

    09/17/2012
    there are two possible mechanisms triggered by MAP4: stabilization of MT networks; DYNLT1 modulation, which is connected with VDAC1, and inhibition of hypoxia-induced mitochondrial permeabilization

    MAP4 mechanism that stabilizes mitochondrial permeability transition in hypoxia: microtubule enhancement and DYNLT1 interaction with VDAC1.
    Fang YD, Xu X, Dang YM, Zhang YM, Zhang JP, Hu JY, Zhang Q, Dai X, Teng M, Zhang DX, Huang YS., Free PMC Article

    07/21/2012
    Dissection of VDAC1 dimerization/oligomerization as presented here provides structural insight into the oligomeric status of cellular VDAC1 under physiological and apoptotic conditions.

    Structure-based analysis of VDAC1 protein: defining oligomer contact sites.
    Geula S, Naveed H, Liang J, Shoshan-Barmatz V., Free PMC Article

    03/10/2012
    Co-immunoprecipitation experiments have identified VDAC1 as an interacting partner with Bax in both healthy and apopotic neurons solubilized with digitonin.

    Identification of Bax-voltage-dependent anion channel 1 complexes in digitonin-solubilized cerebellar granule neurons.
    Huckabee DB, Jekabsons MB., Free PMC Article

    01/14/2012
    Up-regulation of VDAC1 and down-regulation of VDAC2 may participate in hippocampal neuron injury induced by zinc deficiency.

    Effects of intracellular zinc depletion on the expression of VDAC in cultured hippocampal neurons.
    Lu H, Pang W, Hu YD, Yang HP, Huang CY, Jiang YG.

    09/17/2011
    Results describe the expression of voltage-dependent anion channel isoforms in rat, bovine, and chicken brain mitochondria, and suggest that the nature of hexokinase binding site is not determined by the expression of a single VDAC isoform.

    Relationship between expression of voltage-dependent anion channel (VDAC) isoforms and type of hexokinase binding sites on brain mitochondria.
    Poleti MD, Tesch AC, Crepaldi CR, Souza GH, Eberlin MN, de Cerqueira César M, Poleti MD, Tesch AC, Crepaldi CR, Souza GH, Eberlin MN, de Cerqueira César M.

    07/19/2010
    As with wild-type VDAC1, overexpression of either the wild-type or mutated VDAC1 dimeric fusion protein induced apoptotic cell death.

    Dominant-negative VDAC1 mutants reveal oligomeric VDAC1 to be the active unit in mitochondria-mediated apoptosis.
    Mader A, Abu-Hamad S, Arbel N, Gutiérrez-Aguilar M, Shoshan-Barmatz V.

    07/5/2010
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