Cytochrome c monoclonal antibody
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Catalog No. MSA06
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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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P99999
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Structure and Function:
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Cytochrome c receives electrons in the respiratory chain from complex III and passes them to complex IV via redox reactions. Cytochrome c also plays a role is apoptosis in that when the mitochondrial membrane permeability is altered due to the suppression or activation of apoptotic factors it is often released into the cytosol. This allows it to bind with Apaf-1, resulting in caspase-9 activation and an increased rate of apoptosis.
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Disease Associations:
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Abnormalities in cytochrome c can cause thrombocytopenia type 4 (THC4), which may result from improper regulation of platelet formation. THC4 is a form of thrombocytopenia, a condition characterized by a deficient number of platelets, but the clinical symptoms are either minor or absent.
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Product Specifications
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Applications:
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Western blotting, Immunocytochemistry, In-Cell ELISA
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Species Reactivity:
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human, bovine, rat, mouse, C. elegans
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Host Species:
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mouse
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Isotype:
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IgG2a, κ
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Clone ID:
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37BA11
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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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0.25-1.0 µg/mL for Western blotting
0.5-2 µg/mL for Immunocytochemistry (heat induced antigen retrieval in 0.1 M Tris-HCl, 5% urea, pH 9.5 for 5 min at 95°C improves signal).
4 µg/mL for In-Cell ELISA (0.4 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), mouse heart (lane 4) detected with (MSA06) anti-Cytochrome c antibody.
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ICC Images
(click to enlarge)
Figure 2. Mitochondrial localization of cytochrome c visualized by immunocytochemistry using anti-cytochrome c mAb (MSA06). Cultured human fibroblasts were fixed permeabilized and then labeled with anti-cytochrome c mAb 37BA11 (MSA06) followed by a fluorescent goat-anti-mouse IgG.
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Published Studies Using This Product:
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Brys et al., 2010. Disruption of insulin signalling preserves bioenergetic competence of mitochondria in ageing Caenorhabditis elegans.
Cataldo et al., 2010. Abnormalities in mitochondrial structure in cells from patients with bipolar disorder.
Perocchi et al., 2010. MICU1 encodes a mitochondrial EF hand protein required for Ca2+ uptake
Liu et al., 2009. Functional analysis of FSP27 protein regions for lipid droplet localization, caspase-dependent apoptosis, and dimerization with CIDEA.
Snyder et al., 2009. Nitric oxide induces cell death by regulating anti-apoptotic BCL-2 family members.
Shroff et al., 2009. BH3 peptides induce mitochondrial fission and cell death independent of BAX/BAK.
Brennan et al., 2009. Deletion of mouse MsrA results in HBO-induced cataract: MsrA repairs mitochondrial cytochrome c.
Srivastava et al., 2009. PGC-1alpha/beta induced expression partially compensates for respiratory chain defects in cells from patients with mitochondrial disorders.
Vempati et al., 2009. Lack of cytochrome c in mouse fibroblasts disrupts assembly/stability of respiratory complexes I and IV.
Ranganathan et al., 2009. Mitochondrial abnormalities in spinal and bulbar muscular atrophy.
Greiss et al., 2008. C. elegans SIR-2.1 translocation is linked to a proapoptotic pathway parallel to cep-1/p53 during DNA damage-induced apoptosis.
Jacobs et al., 2008. SIRT3 interacts with the daf-16 homolog FOXO3a in the mitochondria, as well as increases FOXO3a dependent gene expression.
Yadavilli et al., 2007. Diepoxybutane activates the mitochondrial apoptotic pathway and mediates apoptosis in human lymphoblasts through oxidative stress.
Ma et al., 2007. p66Shc mediates anoikis through RhoA.
Wilson et al., 2007. Pyruvate induces mitochondrial biogenesis by a PGC-1 alpha-independent mechanism.
Ramanujan et al., 2007. Aging process modulates nonlinear dynamics in liver cell metabolism.
Benard et al., 2006. Physiological diversity of mitochondrial oxidative phosphorylation.
Zhu et al., 2006. Phospholipases A2 mediate amyloid-beta peptide-induced mitochondrial dysfunction.
Leshinsky-Silver et al., 2005. Fulminant neurological deterioration in a neonate with Leigh syndrome due to a maternally transmitted missense mutation in the mitochondrial ND3 gene.
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