Adenine Nucleotide Translocase (ANT) monoclonal antibody
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Catalog No. MSA02
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$325.00 - 100 µg w/ Incubation Solution
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Product Specifications
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Applications:
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Western blotting (special protocol using included incubation solution), Immunocytochemistry (heat-induced antigen-retrieval improves signal)
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Species Reactivity:
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human, rat, bovine, mouse, C. elegans
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Host Species:
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mouse
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Isotype:
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IgG1, κ
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Clone ID:
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5F51BB5AG7
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Concentration:
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1.0 mg/mL in Hepes-Buffered Saline (HBS) with 0.02% azide as a preservative.
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Suggested Working Concentration:
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1 µg/mL for Western blotting
10 µg/mL for Immunocytochemistry
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Storage Conditions:
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4°C for both antibody & 100 mL of Incubation Solution (Included)
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Country of Origin:
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USA
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WB Images
(click to enlarge)
Figure 1. Isolated mitochondria from human heart (lane 1), bovine heart (lane 2), rat heart (lane 3), and mouse heart (lane 4) detected with (MSA02) anti-ANT antibody. Extra bands in the mouse sample (lane 4) are due to the reaction of the IgG-specific goat anti-mouse secondary antibody with residual mouse blood in the heart tissue, as it is very difficult to entirely remove the blood from these small organs.
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ICC Images
(click to enlarge)
Figure 2. Mitochondrial localization of ANT visualized by immunocytochemistry using anti-ANT mAb 5F51BB5AG7 (MSA02). Cultured human fibroblasts were fixed, permeabilized, and then labeled with MSA02 followed by a fluorescent goat-anti-mouse IgG.
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Published Studies Using This Product:
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Brouwers et al., 2011. Overexpression of Glyoxalase-I Reduces Hyperglycemia-induced Levels of Advanced Glycation End Products and Oxidative Stress in Diabetic Rats.
Martin et al., 2011. The mitochondrial permeability transition pore regulates nitric oxide-mediated apoptosis of neurons induced by target deprivation.
Suthammarak et al., 2010. Mutations in Mitochondrial Complex III Uniquely Affect Complex I in Caenorhabditis elegans.
Lynn et al., 2010. Transient upregulation of PGC-1alpha diminishes cardiac ischemia tolerance via upregulation of ANT1.
Brys et al., 2010. Disruption of insulin signalling preserves bioenergetic competence of mitochondria in ageing Caenorhabditis elegans.
Li et al., 2010. p53-Induced growth arrest is regulated by the mitochondrial SirT3 deacetylase.
Queiroga et al., 2010. Glutathionylation of adenine nucleotide translocase induced by carbon monoxide prevents mitochondrial membrane permeabilisation and apoptosis.
Martin et al., 2009. The mitochondrial permeability transition pore in motor neurons: involvement in the pathobiology of ALS mice.
Ventura et al., 2009. p53/CEP-1 increases or decreases lifespan, depending on level of mitochondrial bioenergetic stress.
Fu et al., 2009. Quantitative proteomic analysis of mitochondria in aging PS-1 transgenic mice.
Liu et al., 2009. Enzymatically inactive adenylate kinase 4 interacts with mitochondrial ADP/ATP translocase.
Hofer et al., 2009. Bioenergetics and permeability transition pore opening in heart subsarcolemmal and interfibrillar mitochondria: effects of aging and lifelong calorie restriction.
Eliseev et al., 2009. Cyclophilin D interacts with Bcl2 and exerts an anti-apoptotic effect.
Suthammarak et al., 2009. Complex I function is defective in complex IV-deficient Caenorhabditis elegans.
Leung et al., 2008. The mitochondrial phosphate carrier interacts with cyclophilin D and may play a key role in the permeability transition.
Rea et al., 2007. Relationship between mitochondrial electron transport chain dysfunction, development, and life extension in Caenorhabditis elegans.
Chen et al., 2007. Cytotoxic phospholipid oxidation products. Cell death from mitochondrial damage and the intrinsic caspase cascade.
Ventura et al., 2007. Caenorhabditis elegans mitochondrial mutants as an investigative tool to study human neurodegenerative diseases associated with mitochondrial dysfunction.
Barrett et al., 2006. Elk-1 associates with the mitochondrial permeability transition pore complex in neurons.
Murray et al., 2004. Focused proteomics: towards a high throughput monoclonal antibody-based resolution of proteins for diagnosis of mitochondrial diseases.
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