Rabbit COXI Polyclonal Antibody | anti-COXI antibody

COXI Polyclonal Antibody

Cat. Num. AAA3001433

• Gene Names: mt-Co1; CoxI; COX1
• Reactivity: Human, Mouse, Rat
• Applications: Western Blot
• Purity: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is >95% (by SDS-PAGE).
• Synonyms: COXI; Polyclonal Antibody; COXI Polyclonal Antibody; Cytochrome c oxidase subunit 1; Cytochrome c oxidase subunit I; Cytochrome oxidase subunit 1; mt-Co1; Co1; COX1; anti-COXI antibody

• Host: Rabbit
• Reactivity: Human, Mouse, Rat
• Clonality: Polyclonal
• Isotype: IgG
• Specificity: COXI polyclonal antibody detects endogenous levels of COXI protein.
• Purity/Purification: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is >95% (by SDS-PAGE).
• Form/Format: Rabbit IgG, 1mg/ml in PBS with 0.02% sodium azide, 50% glycerol, pH7.2
• Sequence Length: 514

• Applicable Applications for anti-COXI antibody: Western Blot (WB)
• Application Notes: WB: 1:500-1:2000
• Immunogen: A synthetic peptide corresponding to amino acids 433-445 of Mouse COXI.
• Preparation and Storage: Store at 4 degree C short term.; Aliquot and store at -20 degree C long term.; Avoid freeze-thaw cycles.

Western Blot (WB)

(Western Blot (WB) analysis of COXI pAb at 1:2000 dilutionLane1:The Brain tissue lysate of Mouse (40ug) Lane2:The Skin tissue lysate of Rat (40ug) Lane3:CT26 whole cell lysate (40ug) Lane4:C6 whole cell lysate (40ug) Lane5:Hela whole cell lysate (40ug) Lane6:A375 whole cell lysate (30ug))

Related Product Information for anti-COXI antibody

Cytochrome c oxidase subunit I, COX1 (also designated COI, MTCO1 or oxidative phosphorylation (OxPhos) Complex IV, subunit I) is one of three mitochondrial DNA (mtDNA) encoded subunits (MTCO1-3) of respiratory Complex IV. Cytochrome c oxidase is a hetero-oligomeric enzyme composed of 13 subunits localized to the mitochondrial inner membrane and is the terminal enzyme complex of the electron transport chain. Complex IV catalyzes the reduction of molecular oxygen to water. The energy released is used to transport protons across the mitochondrial inner membrane. The resulting electro-chemical gradient is necessary for the synthesis of ATP. Complex IV contains 13 polypeptides; COX1, COX2 and COX3 (MTCO1-3) make up the catalytic core and are encoded by mtDNA while subunits IV, Va, Vb, VIa, VIb, VIc, VIIa, VIIb, VIIc and VIII are nuclear-encoded.

NCBI and Uniprot Product Information

• NCBI GI #: 34538600
• NCBI GeneID: 17708
• NCBI Accession #: NP_904330.1
• NCBI GenBank Nucleotide #: NP_904330.1
• UniProt Accession #: Q9MD68; P00397
• Molecular Weight: ~ 57kDa
• NCBI Official Full Name: cytochrome c oxidase subunit I (mitochondrion)
• NCBI Official Synonym Full Names: cytochrome c oxidase I, mitochondrial
• NCBI Official Symbol: mt-Co1
• NCBI Official Synonym Symbols: CoxI; COX1
• NCBI Protein Information: cytochrome c oxidase subunit I
• UniProt Protein Name: Cytochrome c oxidase subunit 1
• UniProt Gene Name: mt-Co1
• UniProt Entry Name: Q9MD68_MOUSE

Uniprot Description

COX1: Cytochrome c oxidase is the component of the respiratory chain that catalyzes the reduction of oxygen to water. Subunits 1- 3 form the functional core of the enzyme complex. CO I is the catalytic subunit of the enzyme. Electrons originating in cytochrome c are transferred via the copper A center of subunit 2 and heme A of subunit 1 to the bimetallic center formed by heme A3 and copper B. Defects in MT-CO1 are a cause of Leber hereditary optic neuropathy (LHON). LHON is a maternally inherited disease resulting in acute or subacute loss of central vision, due to optic nerve dysfunction. Cardiac conduction defects and neurological defects have also been described in some patients. LHON results from primary mitochondrial DNA mutations affecting the respiratory chain complexes. MT-CO1 may play a role in the pathogenesis of acquired idiopathic sideroblastic anemia, a disease characterized by inadequate formation of heme and excessive accumulation of iron in mitochondria. Mitochondrial iron overload may be attributable to mutations of mitochondrial DNA because these can cause respiratory chain dysfunction, thereby impairing reduction of ferric iron to ferrous iron. The reduced form of iron is essential to the last step of mitochondrial heme biosynthesis. Defects in MT-CO1 are a cause of mitochondrial complex IV deficiency (MT-C4D); also known as cytochrome c oxidase deficiency. A disorder of the mitochondrial respiratory chain with heterogeneous clinical manifestations, ranging from isolated myopathy to severe multisystem disease affecting several tissues and organs. Features include hypertrophic cardiomyopathy, hepatomegaly and liver dysfunction, hypotonia, muscle weakness, excercise intolerance, developmental delay, delayed motor development and mental retardation. A subset of patients manifest Leigh syndrome. Defects in MT-CO1 are associated with recurrent myoglobinuria mitochondrial (RM-MT). Recurrent myoglobinuria is characterized by recurrent attacks of rhabdomyolysis (necrosis or disintegration of skeletal muscle) associated with muscle pain and weakness, and followed by excretion of myoglobin in the urine. Defects in MT-CO1 are a cause of deafness sensorineural mitochondrial (DFNM). DFNM is a form of non-syndromic deafness with maternal inheritance. Affected individuals manifest progressive, postlingual, sensorineural hearing loss involving high frequencies. Defects in MT-CO1 are a cause of colorectal cancer (CRC). Belongs to the heme-copper respiratory oxidase family.

Protein type: Mitochondrial; Energy Metabolism - oxidative phosphorylation; Membrane protein, multi-pass; Membrane protein, integral; EC 1.9.3.1; Oxidoreductase

Cellular Component: mitochondrial inner membrane; mitochondrial respiratory chain complex IV; mitochondrion

Molecular Function: cytochrome-c oxidase activity

Biological Process: response to oxidative stress