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VDAC/Porin Antibody

based on 3 citations in multiple journalsVDAC/Porin Antibody34.1 4
Catalog #: 3594
SKU-Size Size Price Qty
3594-30T 30 µg
$89.00
3594-100 100 µg
$280.00
More Sizes Get Quote

Product Details

Antibody Target VDAC/Porin
Host Rabbit
Antibody Type Polyclonal
Isotype Rabbit IgG
Immunogen Synthetic peptide surrounding amino acid 189 of human VDAC
Accession # P21796
Gene ID 7416
Appearance Colorless liquid
Concentration 0.5 mg/ml
Formulation 100 µg (0.5 mg/ml) affinity purified rabbit anti-VDAC/Porin polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 0.5% BSA, and 0.01% thimerosal.
Purification Affinity purified
Species Reactivity Human, mouse, rat, bovine, rabbit
Application Western blot, Immunohistochemistry
Positive Control Western Blot: 3T3 cell lysate. IHC: Liver tissue
Application & Usage Western blotting (0.5-4 µg/ml) and Immunohistochemistry (2.5 µg/ml). However, the optimal concentrations should be determined individually. The antibody recognizes ~31 kDa VDAC/Porin from samples of human, mouse, rat, bovine, pig, and rabbit origins.
Handling The antibody solution should be gently mixed before use.
Storage Conditions -20 °C
Shipping Conditions Gel Pack
USAGE For Research Use Only! Not For Use in Humans.

Details

The Voltage-Dependent Anion Channel (VDAC or mitochondrial Porin)I is an outer membrane mitochondrial protein. The VDAC protein is thoμght to form the major pores throμgh which adenine nucleotides are transferred throμgh the outer mitochondrial membrane. VDAC has also been implicated in the formation of the mitochondrial permeability transition pore complex in apoptotic cells. This complex, formed by VDAC, ANT, and CypD is thoμght to allow the mitochondria to undergo metabolic uncoupling and irreversible morphologic changes that ultimately destroy the mitochondria during apoptosis.


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Chourasia et al., Mitophagy defects arising from BNip3 loss promote mammary tumor progression to metastasis.  EMBO Rep., Sep 2015; 16: 1145 - 1163.
Anna Ghelli et al., The cytochrome b p.278Y>C mutation causative of a multisystem disorder enhances superoxide production and alters supramolecular interactions of respiratory chain complexes. Hum. Mol. Genet., Jun 2013; 22: 2141 - 2151.
Bortner, C et al., Osmotic Stress Resistance Imparts Acquipurple Anti-apoptotic Mechanisms in Lymphocytes, J. Biol. Chem., Feb 2012; 287: 6284 - 6295.
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