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Voltage-dependent anion channel 1

VDAC1, Voltage-Dependent Anion Channel 1, VDAC, POR1
This gene encodes a voltage-dependent anion channel protein that is a major component of the outer mitochondrial membrane. The encoded protein facilitates the exchange of metabolites and ions across the outer mitochondrial membrane and may regulate mitochondrial functions. This protein also forms channels in the plasma membrane and may be involved in transmembrane electron transport. Alternate splicing results in multiple transcript variants. Multiple pseudogenes of this gene are found on chromosomes 1, 2 3, 6, 9, 12, X and Y.[provided by RefSeq, Sep 2010] (from NCBI)
Top mentioned proteins: CAN, bcl-2, V1a, ACID, Hexokinase
Papers using VDAC1 antibodies
Mitochondrial and Nuclear Genomic Responses to Loss of LRPPRC Expression*
Mootha Vamsi K. et al., In The Journal of Biological Chemistry, 2008
... Antibodies including CO2, NDUFB8, SDHB, UQCRC2, ATP5A, and VDAC1 were purchased from Mitosciences (Eugene, OR) ...
Bioinformatics enrichment tools: paths toward the comprehensive functional analysis of large gene lists
Martelli Fabio, In PLoS ONE, 2008
... Antibody for VDAC1 (ab15895) (1∶500) was from Abcam.
The mitochondrial permeability transition, release of cytochrome c and cell death. Correlation with the duration of pore openings in situ.
Koch Karl-Wilhelm, In PLoS ONE, 2000
... Sigma; the monoclonal anti-CyP-D antibody was from Calbiochem (San Diego, CA); the rabbit polyclonal anti VDAC1 antibody was from Abcam, (Cambridge, UK); the goat ...
ARL4, an ARF-like Protein That Is Developmentally Regulated and Localized to Nuclei and Nucleoli
Aspenstrom Pontus, In PLoS ONE, 1999
... ATPase, Bax (Santa Cruz Biotechnology, Santa Cruz, CA, USA), VDAC (Cell Signaling Technology, Danvers, MA, USA), ...
Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L)
Youle Richard J. et al., In The Journal of Cell Biology, 1995
... Human VDAC-1 (a gift from Michael Forte, Vollum Institute, Oregon Health Sciences University, Portland, OR) was cloned into the DsRed vector (CLONTECH Laboratories, Inc.) ...
Papers on VDAC1
TSPO: kaleidoscopic 18-kDa amid biochemical pharmacology, control and targeting of mitochondria.
Campanella et al., London, United Kingdom. In Biochem J, Feb 2016
It interacts and forms complexes with other mitochondrial proteins such as the voltage-dependent anion channel (VDAC) via which signalling and regulatory transduction of these core cellular events may be influenced.
Role of hexokinase and VDAC in neurological disorders.
de Cerqueira César et al., Pirassununga, Brazil. In Curr Mol Pharmacol, Feb 2016
A key feature of brain bioenergetics is hexokinase (HK) binding to the outer mitochondrial membrane through the voltage dependent anion channel (VDAC).
VDAC3 as a sensor of oxidative state of the intermembrane space of mitochondria: the putative role of cysteine residue modifications.
De Pinto et al., Catania, Italy. In Oncotarget, Feb 2016
UNASSIGNED: Voltage-Dependent Anion selective Channels (VDAC) are pore-forming mitochondrial outer membrane proteins.
VDAC-2: Mitochondrial outer membrane regulator masquerading as a channel?
Mahalakshmi et al., Bhopāl, India. In Febs J, Jan 2016
Although VDAC-1 has an established role in apoptosis and cell homeostasis, the role of VDAC-2 has been controversial.
Deletion of Mitochondrial Porin Alleviates Stress Sensitivity in the Yeast Model of Shwachman-Diamond Syndrome.
Jensen et al., Bangkok, Thailand. In J Genet Genomics, Jan 2016
Prior disruption of POR1, encoding the mitochondrial voltage dependent anion channel (VDAC), abrogated the effects of SDO1 deletion and substantially restored resistance to environmental stressors and protected against damage to mtDNA.
Quercetin Attenuates Chronic Ethanol-Induced Hepatic Mitochondrial Damage through Enhanced Mitophagy.
Yao et al., Wuhan, China. In Nutrients, Dec 2015
Moreover, quercetin blocked chronic ethanol-induced mitophagy suppression as denoted by mitophagosomes-lysosome fusion and mitophagy-related regulator elements, including LC3II, Parkin, p62 and voltage-dependent anion channel 1 (VDAC1), paralleling with increased FoxO3a nuclear translocation.
Polyphenols as mitochondria-targeted anticancer drugs.
Lewandowska et al., Łódź, Poland. In Cancer Lett, Nov 2015
(2013) according to their molecular mode of action into: hexokinase inhibitors; mimickers of the Bcl-2 homology-3 (BH3) domains; thiol redox inhibitors; deregulators of voltage-dependent anionic channel (VDAC)/adenine nucleotide translocase (ANT) complex; electron redox chain-targeting agents; lipophilic cations targeting the mitochondrial inner membrane; tricarboxylic acid cycle-targeting agents; and mitochondrial DNA-targeting agents.
Molecular Targets of Cannabidiol in Neurological Disorders.
Whalley et al., Reading, United Kingdom. In Neurotherapeutics, Oct 2015
Of interest and after excluding unlikely and implausible targets, the remaining molecular targets of CBD with plausible evidence for involvement in therapeutic effects in neurological disorders (e.g., voltage-dependent anion channel 1, G protein-coupled receptor 55, CaV3.x, etc.) are associated with either the regulation of, or responses to changes in, intracellular calcium levels.
TSPO is a REDOX regulator of cell mitophagy.
Campanella et al., London, United Kingdom. In Biochem Soc Trans, Sep 2015
This review focuses on the current understanding of this pathway and focuses on the interplay with reactive oxygen species (ROS) and the voltage-dependent anion channel (VDAC), to which TSPO binds, in the regulation of cell mitophagy and hence homoeostasis of the mitochondrial network as a whole.
Sequential fractionation and isolation of subcellular proteins from tissue or cultured cells.
Schulz et al., Edmonton, Canada. In Methodsx, 2014
simple to replicate or adjust; this method does not require expensive reagents or use of commercial kits•The protocol can be applied to tissue samples or cultured cells without changing buffer components•Yields purified fractions of cytosolic, membrane bound and nuclear proteins, with the proper distribution of the appropriate subcellular markers: GAPDH, VDAC, SERCA2 and lamin A/C.
Structural basis for membrane binding specificity of the Bin/Amphiphysin/Rvs (BAR) domain of Arfaptin-2 determined by Arl1 GTPase.
Wakatsuki et al., Tsukuba, Japan. In J Biol Chem, 2012
The Arl1.Arfaptin-2 BAR structure suggests that one of the two Arl1 molecules competes with Rac1, which binds to the concave face of the Arfaptin-2 BAR homodimer and may hinder its membrane association.
Mediation of the antiapoptotic activity of Bcl-xL protein upon interaction with VDAC1 protein.
Shoshan-Barmatz et al., Beersheba, Israel. In J Biol Chem, 2012
Interfering with Bcl-xL binding to the mitochondria by VDAC1-based peptides may serve to induce apoptosis in cancer cells.
Structure-based analysis of VDAC1: N-terminus location, translocation, channel gating and association with anti-apoptotic proteins.
Shoshan-Barmatz et al., Beersheba, Israel. In Biochem J, 2012
A single cysteine-residue-bearing VDAC1 demonstrates that the N-terminal region lies inside the channel pore.
Peripheral benzodiazepine receptor regulates vascular endothelial activations via suppression of the voltage-dependent anion channel-1.
Jeon et al., Taejŏn, South Korea. In Febs Lett, 2012
PBR can inhibit endothelial activation through inhibition of mitochondrial ROS and/or VDAC-1 expression in endothelial cells
Lipid dynamics and protein-lipid interactions in 2D crystals formed with the β-barrel integral membrane protein VDAC1.
Griffin et al., Cambridge, United States. In J Am Chem Soc, 2012
analysis of lipid dynamics and protein-lipid interactions in 2D crystals formed with the beta-barrel integral membrane protein VDAC1
PKCε promotes oncogenic functions of ATF2 in the nucleus while blocking its apoptotic function at mitochondria.
Ronai et al., Los Angeles, United States. In Cell, 2012
Genotoxic stress attenuates PKCε effect on ATF2; enables ATF2 nuclear export and localization at the mitochondria, where it perturbs the HK1-VDAC1 complex; increases mitochondrial permeability; and promotes apoptosis.
PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1.
Springer et al., Tübingen, Germany. In Nat Cell Biol, 2010
Data identified VDAC1 (voltage-dependent anion channel 1) as a target for Parkin-mediated Lys 27 poly-ubiquitylation and mitophagy.
Solution structure of the integral human membrane protein VDAC-1 in detergent micelles.
Wagner et al., Boston, United States. In Science, 2008
study presents NMR solution structure of recombinant VDAC-1 reconstituted in detergent micelles
RAS-RAF-MEK-dependent oxidative cell death involving voltage-dependent anion channels.
Stockwell et al., New York City, United States. In Nature, 2007
RNA-interference-mediated knockdown of VDAC2 or VDAC3 caused resistance to erastin, implicating these two VDAC isoforms in the mechanism of action of erastin.
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death.
Molkentin et al., Cincinnati, United States. In Nat Cell Biol, 2007
Vdacs are dispensable for both MPT and Bcl-2 family member-driven cell death.
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