Mouse Monoclonal VDAC1/Porin antibody - conjugated to HRP. Suitable for WB, ICC/IF and reacts with Rat, Human samples. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human VDAC1.
Preservative: 0.1% Sodium azide
Constituents: 50% Glycerol (glycerin, glycerine), 49% PBS
WB | ICC/IF | |
---|---|---|
Human | Expected | Expected |
Rat | Expected | Expected |
Species | Dilution info | Notes |
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Species Rat, Human | Dilution info Use at an assay dependent concentration. | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Rat, Human | Dilution info Use at an assay dependent concentration. | Notes - |
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Non-selective voltage-gated ion channel that mediates the transport of anions and cations through the mitochondrion outer membrane and plasma membrane (PubMed:10661876, PubMed:11845315, PubMed:18755977, PubMed:30061676, PubMed:8420959). 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 (PubMed:10661876, PubMed:11845315, PubMed:18755977, PubMed:8420959). It adopts an open conformation at low or zero membrane potential and a closed conformation at potentials above 30-40 mV (PubMed:10661876, PubMed:18755977, PubMed:8420959). The open state has a weak anion selectivity whereas the closed state is cation-selective (PubMed:18755977, PubMed:8420959). Binds various signaling molecules, including the sphingolipid ceramide, the phospholipid phosphatidylcholine, and the sterols cholesterol and oxysterol (PubMed:18755977, PubMed:31015432). In depolarized mitochondria, acts downstream of PRKN and PINK1 to promote mitophagy or prevent apoptosis; polyubiquitination by PRKN promotes mitophagy, while monoubiquitination by PRKN decreases mitochondrial calcium influx which ultimately inhibits apoptosis (PubMed:32047033). May participate in the formation of the permeability transition pore complex (PTPC) responsible for the release of mitochondrial products that triggers apoptosis (PubMed:15033708, PubMed:25296756). May mediate ATP export from cells (PubMed:30061676). Part of a complex composed of HSPA9, ITPR1 and VDAC1 that regulates mitochondrial calcium-dependent apoptosis by facilitating calcium transport from the ER lumen to the mitochondria intermembrane space thus providing calcium for the downstream calcium channel MCU that directly releases it into mitochondria matrix (By similarity). Mediates cytochrome c efflux (PubMed:20230784). Catalyzes the scrambling of phospholipids across the outer mitochondrial membrane; the mechanism is unrelated to channel activity and is capable of translocating both anionic and zwitterionic phospholipids.
VDAC, VDAC1, Non-selective voltage-gated ion channel VDAC1, Outer mitochondrial membrane protein porin 1, Plasmalemmal porin, Porin 31HL, Porin 31HM, Voltage-dependent anion-selective channel protein 1, VDAC-1, hVDAC1
Mouse Monoclonal VDAC1/Porin antibody - conjugated to HRP. Suitable for WB, ICC/IF and reacts with Rat, Human samples. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human VDAC1.
Preservative: 0.1% Sodium azide
Constituents: 50% Glycerol (glycerin, glycerine), 49% PBS
Does not cross-react with VDAC2 or VDAC3 (based on KO validation results).
The clone number has been updated from S152B-23 to N152B/23, both clone numbers name the same antibody clone.
VDAC1 also known as Voltage-Dependent Anion Channel 1 or Porin is a channel protein with a mass around 31 kDa. It is located in the outer mitochondrial membrane and is express widely in various tissues. This protein forms a channel that allows the transport of metabolites and ions playing an important role in regulating energy and metabolic exchange between the mitochondria and the rest of the cell. Scientists often study it as a significant focus in cellular bioenergetics and apoptosis research.
VDAC1 acts as a pore-forming unit within the mitochondrial membrane allowing for the passage of small hydrophilic molecules. It is not part of a larger complex but works closely with other proteins to maintain mitochondrial function. VDAC1 regulates the entry and exit of proteins and ions essential for mitochondrial homeostasis and cellular energy production. By controlling the exchange of inorganic phosphate adenine nucleotides and Ca2+ VDAC1 influences both mitochondrial and cellular metabolism.
VDAC1 is involved in apoptosis and energy production pathways. It associates with proteins such as the Bcl-2 family in the apoptosis pathway influencing cell survival and programmed cell death. In energy production VDAC1 works in conjunction with the adenine nucleotide translocase facilitating ATP and ADP exchanges that are critical for maintaining cellular energy levels.
VDAC1 has a connection to cancer and neurodegenerative diseases. Upregulation or dysfunction of VDAC1 is observed in various cancers where it affects mitochondrial apoptosis regulation linked often with Bcl-2 anti-apoptotic proteins. In neurodegenerative diseases like Alzheimer’s alterations in VDAC1 expression and function can disrupt mitochondrial permeability. This interaction can result in disturbed neuronal energy metabolism often associated with amyloid precursor protein and its derivatives.
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