COX10 antibody

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Description
Converts protoheme IX and farnesyl diphosphate to heme O.
Documents del producto
Product specifications
Category | Primary Antibodies |
Immunogen Target | COX10 homolog, cytochrome c oxidase assembly protein, heme A: farnesyltransferase(yeast) (COX10) |
Host | Rabbit |
Reactivity | Human, Mouse, Rat |
Recommended Dilution | WB: 1:500-1:2000 |
Clonality | polyclonal |
Conjugation | Unconjugated |
Isotype | IgG |
Observed MW | 51 kDa |
Purity | ≥95% as determined by SDS-PAGE |
Purification | Immunogen affinity purified |
Size 1 | 100µg |
Form | liquid |
Tested Applications | ELISA, WB |
Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
UniProt ID | Q12887 |
Gene ID | 1352 |
Alias | Protoheme IX farnesyltransferase, mitochondrial,Heme O synthase,COX10 |
Background | Antibody anti-COX10 |
Status | RUO |
Note | Mol. Weight 51 kDa |
Descripción
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COX11, Cytochrome C Oxidase Copper Chaperone (COX10) Antibody
COX10 Antibody is a Rabbit Polyclonal Antibody against COX10.
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COX11, Cytochrome C Oxidase Copper Chaperone (COX10) Antibody
Cytochrome c oxidase (COX), the terminal component of the mitochondrial respiratory chain, catalyzes the electron transfer from reduced cytochrome c to oxygen. This component is a heteromeric complex consisting of 3 catalytic subunits encoded by mitochondrial genes and multiple structural subunits encoded by nuclear genes. The mitochondrially-encoded subunits function in electron transfer, and the nuclear-encoded subunits may function in the regulation and assembly of the complex. This nuclear gene encodes heme A:farnesyltransferase, which is not a structural subunit but required for the expression of functional COX and functions in the maturation of the heme A prosthetic group of COX. This protein is predicted to contain 7-9 transmembrane domains localized in the mitochondrial inner membrane. A gene mutation, which results in the substitution of a lysine for an asparagine (N204K), is identified to be responsible for cytochrome c oxidase deficiency. In addition, this gene is disrupted in patients with CMT1A (Charcot-Marie-Tooth type 1A) duplication and with HNPP (hereditary neuropathy with liability to pressure palsies) deletion.
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