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COX10 Polyclonal Antibody Store at -20°C

SKU: E-AB-13841-200

  • $ 33995


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COX10 Polyclonal Antibody Store at -20°C

 

SKU # E-AB-13841
Reactivity Human
Host Rabbit
Applications IHC

 

Product Details

Isotype IgG
Host Rabbit
Reactivity Human
Applications IHC
Clonality Polyclonal
Immunogen Recombinant protein of human COX10
Abbre COX10
Synonyms 2410004F01Rik,  AU042636,  COX10,  Cytochrome c oxidase assembly protein,  Cytochrome c oxidase subunit X,  Heme A farnesyltransferase,  Heme O synthase,  OTTMUSP00000006085,  Protoheme IX farnesyltransferase,  mitochond,  mitochondrial
Swissprot
Cellular Localization Mitochondrion membrane.
Concentration 0.4 mg/mL
Buffer Phosphate buffered solution, pH 7.4, containing 0.05% stabilizer and 50% glycerol.
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 The product is shipped with ice pack,upon receipt,store it immediately at the temperature recommended.

 

Related Reagents

Applications Recommended Dilution
IHC 1:50-1:200

 

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.