Complex I subunit GRIM-19 monoclonal antibody
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Catalog No. MS103
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$325.00 - 100 µg
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This antibody can also be purchased as part of a Sample Pack.
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UniProt Number:
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Q9P0J0
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Alternate Names:
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NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 13, NADH-ubiquinone oxidoreductase B16.6 subunit, Complex I-B16.6, CI-B16.6, Gene associated with retinoic-interferon-induced mortality 19 protein, Gene associated with retinoic and IFN-induced mortality 19 protein, GRIM-19, Cell death regulatory protein GRIM-19, NDUFA13, GRIM19, CGI-39, CDA016
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Structure and Function:
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GRIM-19 (Gene associated with Retinoid IFN-induced Mortality) was first described as an apoptotic factor located in the cytosol and nucleus of cells undergoing programmed cell death.
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Disease Associations:
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GRIM-19 defects may be a cause of susceptibility to Hurthle cell thyroid carcinoma. GRIM-19 is also down-regulated in intestinal mucosa in areas involved in Crohn disease and ulcerative colitis.
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Product Specifications
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Applications:
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Western blotting, Immunocytochemistry, In-Cell ELISA, Blue Native Electrophoresis
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Species Reactivity:
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human, mouse, rat, bovine
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Host Species:
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mouse
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Isotype:
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IgG2b, κ
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Clone ID:
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6E1BH7
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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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1 µg/ml for Western blotting
1 µg/ml for Immunocytochemistry
8 µg/mL for In-Cell ELISA (0.8 µg/well)
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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 MS103 anti-GRIM-19 monoclonal antibody.
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ICC Images
(click to enlarge)
Figure 2. Mitochondrial localization of ATP synthase visualized by immunocytochemistry using anti-ATP synthase subunit GRIM-19 mAb 6E1BH7 (MS103). Cultured human fibroblasts were fixed, permeabilized and then labeled with MS103 followed by Alexa® 488 goat-anti-mouse IgG.
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Published Studies Using This Product:
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Gerards et al., 2010. Riboflavin-responsive oxidative phosphorylation complex I deficiency caused by defective ACAD9: new function for an old gene.
Sheftel et al., 2009. Human ind1, an iron-sulfur cluster assembly factor for respiratory complex I.
Leshinsky-Silver et al., 2009. NDUFS4 mutations cause Leigh syndrome with predominant brainstem involvement.
Yahata et al., 2009. Nicotinamide mononucleotide adenylyltransferase expression in mitochondrial matrix delays Wallerian degeneration.
Potluri et al., 2009. A novel NDUFA1 mutation leads to a progressive mitochondrial complex I-specific neurodegenerative disease.
Bielecka et al., 2009. Respiratory chain complexes in healthy and cardiomyopathic hearts.
Minai et al., 2008. Mitochondrial respiratory chain complex assembly and function during human fetal development.
Lebon et al., 2007. A novel mutation of the NDUFS7 gene leads to activation of a cryptic exon and impaired assembly of mitochondrial complex I in a patient with Leigh syndrome.
Li et al., 2007. An assembled complex IV maintains the stability and activity of complex I in mammalian mitochondria.
Mehrabian et al., 2007. The IFN-beta and retinoic acid-induced cell death regulator GRIM-19 is upregulated during focal cerebral ischemia.
Vogel et al., 2007. Identification of mitochondrial complex I assembly intermediates by tracing tagged NDUFS3 demonstrates the entry point of mitochondrial subunits.
Deng et al., 2006. Nuclear suppression of mitochondrial defects in cells without the ND6 subunit.
Ogilvie et al., 2005. A molecular chaperone for mitochondrial complex I assembly is mutated in a progressive encephalopathy.
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CART
