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Upingbio
SKU:YP-Ab-16276-100UL
CYCS Monoclonal Antibody(4B10)
CYCS Monoclonal Antibody(4B10)
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- Reaction species: Human;Mouse;Rat;Chicken
- Gene Name: CYCS
- Protein name: Cytochrome c
- Molecular weight (DA): 14kD
- Immunogen: Recombinant Protein of CYCS
- Specificity: The antibody detects endogenous CYCS protein.
- Composition: PBS, pH 7.4, containing 0.5%BSA, 0.02% sodium azide as Preservative and 50% Glycerol.
- Source: Monoclonal, Mouse
- Dilution ratio: WB: 1:1000-5000 IHC: 1:500-1000 IF 1:200
- Purification process: The antibody was affinity-purified from mouse ascites by affinity-chromatography using epitope-specific immunogen.
- Storage: -20°C/1 year
- Other Names: CYCS; CYC; Cytochrome c
- Background: This gene encodes a small heme protein that functions as a central component of the electron transport chain in mitochondria. The encoded protein associates with the inner membrane of the mitochondrion where it accepts electrons from cytochrome b and transfers them to the cytochrome oxidase complex. This protein is also involved in initiation of apoptosis. Mutations in this gene are associated with autosomal dominant nonsyndromic thrombocytopenia. Numerous processed pseudogenes of this gene are found throughout the human genome.[provided by RefSeq, Jul 2010],
- Function: disease:Defects in CYCS are the cause of thrombocytopenia type 4 (THC4) [MIM:612004]; also known as autosomal dominant thrombocytopenia type 4. Thrombocytopenia is the presence of relatively few platelets in blood. THC4 is a non-syndromic form of thrombocytopenia. Clinical manifestations of thrombocytopenia are absent or mild. THC4 may be caused by dysregulated platelet formation.,function:Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain.,function:Plays a role in apoptosis. Suppression of the anti-apoptotic members or activation of the pro-apoptotic members of the Bcl-2 family leads to altered mitochondrial membrane perm
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