Product Datasheet  
COX10 Antibody  
Catalog Number: 35579  
Technical:tech@swbio.com  
Information:info@swbio.com  
Description  
  • host_species：  
  • Rabbit
  • Amount：  
  • 100μgμg
  • Swiss-Prot No.：  
  • Swiss-Prot#: Q12887
    NCBI Gene ID: 1352
    Gene Accssion: BC000060
  • Form of Antibody：  
  • Rabbit IgG in pH7.4 PBS, 0.05% NaN3, 40% Glycerol.
  • Storage：  
  • Store at -20˚C
  • Immunogen：  
  • Fusion protein corresponding to a region derived from internal residues of human COX10 homolog, cytochrome c oxidase assembly protein, heme A: farnesyltransferase
  • reactivity：  
  • Hu
  • appl_detail：  
  • Immunohistochemistry: 1:50-1:200
  • other_names：  
  • COX10; COX10 homolog; cytochrome c oxidase assembly protein
  • Purification：  
  • Antigen affinity purification.
  • Specificity：  
  • The antibody detects endogenous levels of total COX10 protein.
  • Applications：  
  • IHC
  • Background：  
  • 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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