COX15 Rabbit Polyclonal Antibody

COX15 Rabbit Polyclonal Antibody

Size1:50μl Price1:$118
Size2:100μl Price2:$220
Size3:500μl Price3:$980
SKU: APRab09267 Category: Polyclonal Antibody Tags: , , ,

Datasheet

Summary

Production Name

COX15 Rabbit Polyclonal Antibody

Description

Rabbit Polyclonal Antibody

Host

Rabbit

Application

IHC,ELISA

Reactivity

Human,Mouse,Rat

 

Performance

Conjugation

Unconjugated

Modification

Unmodified

Isotype

IgG

Clonality

Polyclonal

Form

Liquid

Storage

Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.

Buffer

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% New type preservative N.

Purification

Affinity purification

 

Immunogen

Gene Name

COX15

Alternative Names

COX15; Cytochrome c oxidase assembly protein COX15 homolog

Gene ID

1355

SwissProt ID

Q7KZN9

 

Application

Dilution Ratio

IHC 1:100-1:300 ELISA: 1:5000

Molecular Weight

 

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 a protein which is not a structural subunit, but may be essential for the biogenesis of COX formation and may function in the hydroxylation of heme O, according to the yeast mutant studies. This protein is predicted to contain 5 transmembrane domains localized in the mitochondrial inner membrane. Alternative splicing of this gene generates two transcript variants divergingdisease:Defects in COX15 are a cause of cytochrome c oxidase deficiency (COX deficiency) [MIM:220110]. COX deficiency is a clinically heterogeneous disorder. The clinical features range from isolated myopathy to severe multisystem disease with onset from infancy to adulthood.,disease:Defects in COX15 are a cause of Leigh syndrome [MIM:256000]. Leigh syndrome is an early-onset progressive neurodegenerative disorder characterized by delayed onset of symptoms, hypotonia, feeding difficulties, failure to thrive, motor regression and brainstem signs. Diagnosis is confirmed by the presence of focal, bilateral lesions in one or more areas of the central nervous system including the brainstem, thalamus, basal ganglia, cerebellum and spinal cord.,function:May be involved in the biosynthesis of heme A.,pathway:Porphyrin metabolism; heme A biosynthesis; heme A from heme O: step 1/1.,similarity:Belongs to the COX15/ctaA family.,tissue specificity:Predominantly found in tissues characterized by high rates of oxidative phosphorylation (OxPhos), including muscle, heart, and brain.,

 

Research Area

Oxidative phosphorylation;Porphyrin and chlorophyll metabolism;