VDAC1 Antibody - #DF6140

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Product: VDAC1 Antibody
Catalog: DF6140
Description: Rabbit polyclonal antibody to VDAC1
Application: WB IHC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 31kDa; 31kD(Calculated).
Uniprot: P21796
RRID: AB_2838107

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 100ul $280 In stock
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MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Zebrafish(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
VDAC1 Antibody detects endogenous levels of total VDAC1.
RRID:
AB_2838107
Cite Format: Affinity Biosciences Cat# DF6140, RRID:AB_2838107.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

N2441; OMP2; POR1; hVDAC1; MGC111064; Mitochondrial Porin; Outer mitochondrial membrane protein porin 1; Plasmalemmal porin; Porin 31HL; Porin 31HM; VDAC; VDAC-1; Vdac1; VDAC1_HUMAN; Voltage dependent anion channel 1; Voltage dependent anion selective channel protein 1; Voltage-dependent anion-selective channel protein 1; YNL055C; YNL2441C;

Immunogens

Immunogen:
Uniprot:

P21796(VDAC1_HUMAN) >>Visit HPA database.

Gene(ID):
VDAC1(7416)
Expression:
P21796 VDAC1_HUMAN:

Heart, liver and skeletal muscle.

Description:
Voltage-dependent anion channel (VDAC), ubiquitously expressed and located in the outer mitochondrial membrane, is generally thought to be the primary means by which metabolites diffuse in and out of the mitochondria (1). In addition, this channel plays a role in apoptotic signaling. The change in mitochondrial permeability characteristic of apoptosis is mediated by Bcl-2 family proteins, which bind to VDAC, altering the channel kinetics (2). Homodimerization of VDAC may be a mechanism for changing mitochondrial permeability and supporting release of cytochrome c (3). In mammalian cells, there are three VDAC isoforms, VDAC1, which is the most widely expressed isoform, as well as VDAC2 and VDAC3 (4,5).
Sequence:
MAVPPTYADLGKSARDVFTKGYGFGLIKLDLKTKSENGLEFTSSGSANTETTKVTGSLETKYRWTEYGLTFTEKWNTDNTLGTEITVEDQLARGLKLTFDSSFSPNTGKKNAKIKTGYKREHINLGCDMDFDIAGPSIRGALVLGYEGWLAGYQMNFETAKSRVTQSNFAVGYKTDEFQLHTNVNDGTEFGGSIYQKVNKKLETAVNLAWTAGNSNTRFGIAAKYQIDPDACFSAKVNNSSLIGLGYTQTLKPGIKLTLSALLDGKNVNAGGHKLGLGLEFQA

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Xenopus
100
Zebrafish
100
Chicken
100
Rabbit
100
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P21796 As Substrate

Site PTM Type Enzyme
A2 Acetylation
K12 Acetylation
K12 Ubiquitination
S13 Phosphorylation
T19 Phosphorylation
K20 Acetylation
K20 Ubiquitination
Y22 Phosphorylation
K28 Acetylation
K28 Ubiquitination
K34 Acetylation
K34 Ubiquitination
S43 Phosphorylation
S44 Phosphorylation
S46 Phosphorylation
K53 Ubiquitination
S57 Phosphorylation
K61 Acetylation
K61 Ubiquitination
Y62 Phosphorylation
T65 Phosphorylation
Y67 Phosphorylation
T98 Phosphorylation
S101 Phosphorylation
S102 Phosphorylation
S104 Phosphorylation
T107 Phosphorylation
K109 Acetylation
K109 Sumoylation
K109 Ubiquitination
K110 Ubiquitination
K119 Acetylation
K161 Ubiquitination
R163 Methylation
T165 Phosphorylation
S167 Phosphorylation
Y173 Phosphorylation
K174 Acetylation
K174 Methylation
S193 Phosphorylation Q96PY6 (NEK1)
Y195 Phosphorylation
K197 Ubiquitination
T204 Phosphorylation
S215 Phosphorylation
K224 Acetylation
K224 Ubiquitination
Y225 Phosphorylation
C232 S-Nitrosylation
S234 Phosphorylation
K236 Acetylation
S240 Phosphorylation
S241 Phosphorylation
Y247 Phosphorylation
T250 Phosphorylation
K252 Acetylation
K252 Ubiquitination
S260 Phosphorylation
K266 Acetylation
K266 Ubiquitination
K274 Acetylation
K274 Sumoylation
K274 Ubiquitination

Research Backgrounds

Function:

Forms a channel through the mitochondrial outer membrane and also the plasma membrane. The channel at the outer mitochondrial membrane allows diffusion of small hydrophilic molecules; in the plasma membrane it is involved in cell volume regulation and apoptosis. It adopts an open conformation at low or zero membrane potential and a closed conformation at potentials above 30-40 mV. The open state has a weak anion selectivity whereas the closed state is cation-selective. May participate in the formation of the permeability transition pore complex (PTPC) responsible for the release of mitochondrial products that triggers apoptosis.

PTMs:

Phosphorylation at Ser-193 by NEK1 promotes the open conformational state preventing excessive mitochondrial membrane permeability and subsequent apoptotic cell death after injury. Phosphorylation by the AKT-GSK3B axis stabilizes the protein probably by preventing ubiquitin-mediated proteasomal degradation.

Ubiquitinated by PRKN during mitophagy, leading to its degradation and enhancement of mitophagy. Deubiquitinated by USP30.

Subcellular Location:

Mitochondrion outer membrane>Multi-pass membrane protein. Cell membrane>Multi-pass membrane protein. Membrane raft>Multi-pass membrane protein.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Heart, liver and skeletal muscle.

Subunit Structure:

Interacts with hexokinases including HK1. The HK1-VDAC1 complex interacts with ATF2. Interacts with BCL2L1. Interacts with BAK1. Interacts with RTL10/BOP (via BH3 domain). Interacts with amyloid-beta and APP; induces VDAC1 dephosphorylation. Component of the mitochondrial permeability transition pore complex (mPTPC), at least composed of SPG7, VDAC1 and PPIF. Interacts with SPG7, NIPSNAP2 and SLC25A30.

(Microbial infection) Interacts with influenza A virus PB1-F2 protein.

Family&Domains:

Consists mainly of a membrane-spanning beta-barrel formed by 19 beta-strands. The helical N-terminus folds back into the pore opening and plays a role in voltage-gated channel activity.

Belongs to the eukaryotic mitochondrial porin family.

Research Fields

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Environmental Information Processing > Signal transduction > Calcium signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cGMP-PKG signaling pathway.   (View pathway)

· Human Diseases > Neurodegenerative diseases > Parkinson's disease.

· Human Diseases > Neurodegenerative diseases > Huntington's disease.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Digestive system > Cholesterol metabolism.

References

1). Synthesis of hydroxycinnamic acid derivatives as mitochondria-targeted antioxidants and cytotoxic agents. Acta Pharmaceutica Sinica B, 2017 (PubMed: 28119815) [IF=14.5]

Application: WB    Species: Human    Sample:

Figure 7 Detection of cyt c release from energized mitochondria suspensions (2 mg protein/mL). (A) In the presence of 10 μmol/L MitoHCAs. a: control; b: MitoCaA; c: MitoFA; d: Mitop-CoA; e: MitoCA. (B) a: control; b: 1 μmol/L MitoCaA; c: 20 μmol/L MitoCaA +1 μmol/L CsA; d: 20 μmol/L MitoCaA. The blots shown are representative of three independent experiments demonstrating similar results. (C) In the presence of the various concentrations of MitoCaA. (D) In the presence of MitoHCAs, CaA and butylTPP (10 μmol/L) with or without Ca2+. The quantitative assays were performed by the dithionite-reduction method. The values represent mean±SEM of three independent experiments. ***P
2). Emodin targets mitochondrial cyclophilin D to induce apoptosis in HepG2 cells. BIOMEDICINE & PHARMACOTHERAPY, 2017 (PubMed: 28363167) [IF=7.5]

Application: WB    Species: human    Sample:

Fig. 2. Effects of CsA on emodin-induced apoptosis. The cells were treated with emodin for 48 h in the presence or absence of CsA (5mM), then assays were performed. (A) Analysis of apoptosis by nuclear condensation. The Hoechst 33342 staining showed typical apoptotic morphology changes after emodin treatment. The images were acquired by inverted fluorescence microscopy. (B) Analysis of apoptosis by Annexin V/PI double-staining assay. (C) Determination of Cyto-C level in mitochondria and cytosol by western blots. b-actin and VDAC1 were used as internal control.
3). Walnut-Derived Peptide Enhances Mitophagy via JNK-Mediated PINK1 Activation to Reduce Oxidative Stress in HT-22 Cells. JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY, 2022 (PubMed: 35187930) [IF=6.1]
4). Ginsenoside CK improves skeletal muscle insulin resistance by activating DRP1/PINK1-mediated mitophagy. Food & Function, 2023 (PubMed: 36562271) [IF=6.1]
5). Silibinin Therapy Improves Cholangiocarcinoma Outcomes by Regulating ERK/Mitochondrial Pathway. Frontiers in Pharmacology, 2022 (PubMed: 35401195) [IF=5.6]

Application: WB    Species: Mice    Sample: cholangiocarcinoma cell

FIGURE 4 Silibinin induced apoptosis of cholangiocarcinoma cells through the ERK/Cytochrome c pathway. (A). Expression of upstream proteins of the mitochondrial apoptosis pathway, as detected by western blotting. Cells were treated with IC50 and 2*IC50 concentrations of silibinin for 48 h (B). Cytochrome C expression in different parts after mitochondrial isolation. (C). The quantification results of western blotting. Data are shown as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, significantly different compared to the control group.
6). Single-walled carbon nanohorn aggregates promotes mitochondrial dysfunction-induced apoptosis in hepatoblastoma cells by targeting SIRT3. INTERNATIONAL JOURNAL OF ONCOLOGY, 2018 (PubMed: 29956732) [IF=5.2]

Application: WB    Species: mouse    Sample: L02 cells

Figure 3.| Treatment with SWNHs alters the expression of mitochondrial apoptotic pathway-associated proteins in vitro. (A) HepG2 and (B) L02 cells were incubated with different concentrations of SWNHs in 6-well plates for 48 h. The changes in the expression and the relative quantification of proteins in (C) HepG2 cells or (D) L02 cells were identified by western blotting. SW0, SW10, SW20, SW30, SW40 and SW50 correspond to the concentrations of SWNHs: 0, 0.21, 0.42, 0.64, 0.85 and 0.96 µg/cm2, respectively. Data are presented as the mean ± standard deviation (n=3). *P<0.05 compared with the SW0 group. AceCS2, acyl-CoA synthetase short chain family member 1; SCNN1A, sodium channel epithelial 1α subunit; SIRT3, sirtuin 3; SWNH, single-walled carbon nanohorn; VDAC1, voltage-dependent anion channel 1.
7). Titanium dioxide nanoparticles induce mitochondria-associated apoptosis in HepG2 cells. RSC Advances, 2018 (PubMed: 35548213) [IF=3.9]
8). Mechanism of Baihu Renshen decoction on T2DM rats based on mitochondrial autophagy mediated by PINK1/Parkin. , 2023

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