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COX10 Polyclonal Antibody

Cat:E-AB-13841
Manual MSDS

Price: $ 399

Price: $ 240

Price: $ 143

Price: $ 73

Size:
200μL 120μL 60μL 20μL
Quantity:
  • Host: Rabbit
  • Reactivity: Human
  • Applications: IHC
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Product Details
Verified Samples Verified Samples in IHC:Human renal cancer
Dilution

IHC 1:50-1:200

Western Blot Operation Guide
Clonality Polyclonal
Immunogen Recombinant protein of human COX10
Abbre COX10
Synonyms 2410004F01Rik;AU042636;COX10;COX10;Cytochrome c oxidase assembly protein;Cytochrome c oxidase subunit X;Heme A farnesyltransferase;Heme O synthase;OTTMUSP00000006085;Protoheme IX farnesyltransferase;mitochondrial;Protoheme IX farnesyltransferase;mitochondrial precursor;RP23-78H18.1
Swissprot
Cellular Localization Mitochondrion membrane.
Concentration 0.4 mg/mL
Buffer PBS with 0.05% sodium azide and 50% glycerol, PH7.4
Purification Method Affinity purification
Research Areas Cancer; Metabolism; Signal Transduction
Conjugation Unconjugated
Storage Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles.
Shipping Biological ice pack at 4 ℃
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.