Complex I subunit NDUFB8 monoclonal antibody
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Catalog No. MS105
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$325.00 - 100 µg
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UniProt Number:
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O95169
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Alternate Names:
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NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 8, NADH-ubiquinone oxidoreductase ASHI subunit, Complex I-ASHI, CI-ASHI, NDUFB8
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Structure and Function:
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There are 45 unique subunits of Complex I, and this subunit is 188 AA long. Previously, based on MW and isoelectric point on gels, MS105 was tentatively identified as likely reacting against subunit ND6; mass spectrometry now confirms identification of it as subunit NDUFB8. It is thought that this subunit does not contribute to catalytic functions of Complex I.
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Product Specifications
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Applications:
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Western blotting, Immunohistochemistry, Blue Native Electrophoresis
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Species Reactivity:
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human, bovine, mouse, rat
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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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20E9DH10C12
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Concentration:
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1 mg/mL in Hepes-Buffered Saline (HBS)-Buffered Saline (HBS) with 0.02% azide as a preservative.
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Suggested Working Concentration:
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0.5 µg/mL for Western blotting
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Storage Conditions:
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Store at 4°C. Do not freeze.
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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 (MS105) anti-NDUFB8 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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IHC Images
(click to enlarge)
Figure 2. Skeletal muscle immunohistochemistry using MS114- fixed frozen tissue sections from a patient with a single large deletion of the mtDNA show a mosaic of complex I positive and complex I negative fibers. Image kindly provided by Dr. J. Murphy and D. Turnbull, Mitochondrial Research Group, Newcastle University.
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Published Studies Using This Product:
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Ferreira et al., 2011. Progressive cavitating leukoencephalopathy associated with respiratory chain complex I deficiency and a novel mutation in NDUFS1.
Kemp et al., 2010. Nuclear factors involved in mitochondrial translation cause a subgroup of combined respiratory chain deficiency.
Tuppen et al., 2010. The p.M292T NDUFS2 mutation causes complex I-deficient Leigh syndrome in multiple families.
Thomas et al., 2010. Recombinant human mitochondrial transcription factor A stimulates mitochondrial biogenesis and ATP synthesis, improves motor function after MPTP, reduces oxidative stress and increases survival after endotoxin.
Nadanaciva et al., 2010. High-Content Screening for Compounds That Affect mtDNA-Encoded Protein Levels in Eukaryotic Cells.
Dennerlein et al., 2010. Human ERAL1 is a mitochondrial RNA chaperone involved in the assembly of the 28S small mitochondrial ribosomal subunit.
Wydro et al., 2010. Targeting of the cytosolic poly(A) binding protein PABPC1 to mitochondria causes mitochondrial translation inhibition.
Hangen et al., 2010. A brain-specific isoform of mitochondrial apoptosis-inducing factor: AIF2.
Fogal et al., 2010. Mitochondrial p32 Protein is a Critical Regulator of Tumor Metabolism via Maintenance of Oxidative Phosphorylation.
Folbergrová et al., 2009. Sustained deficiency of mitochondrial complex I activity during long periods of survival after seizures induced in immature rats by homocysteic acid.
Davis et al., 2009. Nitration of the mitochondrial complex I subunit NDUFB8 elicits RIP1- and RIP3-mediated necrosis.
Horvath et al., 2009. Molecular basis of infantile reversible cytochrome c oxidase deficiency myopathy.
Arthur et al., 2009. Parkinson's disease brain mitochondria have impaired respirasome assembly, age-related increases in distribution of oxidative damage to mtDNA and no differences in heteroplasmic mtDNA mutation abundance.
Keeney et al., 2009. Mitochondrial gene therapy augments mitochondrial physiology in a Parkinson's disease cell model.
Iyer et al., 2009. Recombinant mitochondrial transcription factor A with N-terminal mitochondrial transduction domain increases respiration and mitochondrial gene expression.
Son et al., 2009. Redox susceptibility of SOD1 mutants is associated with the differential response to CCS over-expression in vivo.
Potluri et al., 2009. A novel NDUFA1 mutation leads to a progressive mitochondrial complex I-specific neurodegenerative disease.
Nadanaciva et al., 2009. Lateral-flow immunoassay for detecting drug-induced inhibition of mitochondrial DNA replication and mtDNA-encoded protein synthesis.
Khidr et al., 2008. Role of SUV3 helicase in maintaining mitochondrial homeostasis in human cells.
Son et al., 2008. Isolated cytochrome c oxidase deficiency in G93A SOD1 mice overexpressing CCS protein.
Wall et al., 2006. Alterations in oxidative phosphorylation complex proteins in the hearts of transgenic mice that overexpress the p38 MAP kinase activator, MAP kinase kinase 6.
Keeney et al., 2006. Parkinson's disease brain mitochondrial complex I has oxidatively damaged subunits and is functionally impaired and misassembled.
Schilling et al., 2005. Rapid purification and mass spectrometric characterization of mitochondrial NADH dehydrogenase (Complex I) from rodent brain and a dopaminergic neuronal cell line.
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CART
