COX15 sirna

COX15 siRNA (Human)

Cat. Num. AAA8208177

• Gene Names: COX15; CEMCOX2
• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: COX15; COX15 siRNA (Human); Cytochrome c oxidase assembly protein COX15 homolog; COX15 sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: COX15 siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 388

• Applicable Applications for COX15 sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human COX15 gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for COX15 sirna

siRNA to inhibit COX15 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 17921987
• NCBI GeneID: 1355
• NCBI Accession #: NP_004367.2
• NCBI GenBank Nucleotide #: NM_004376.5
• UniProt Accession #: Q7KZN9; O60556; O75878; Q5TD00; Q5TD01; Q7Z3Q3; Q9NTN0; A8K6I9
• Molecular Weight: 43,835 Da
• NCBI Official Full Name: cytochrome c oxidase assembly protein COX15 homolog isoform 2
• NCBI Official Synonym Full Names: cytochrome c oxidase assembly homolog 15 (yeast)
• NCBI Official Symbol: COX15
• NCBI Official Synonym Symbols: CEMCOX2
• NCBI Protein Information: cytochrome c oxidase assembly protein COX15 homolog
• UniProt Protein Name: Cytochrome c oxidase assembly protein COX15 homolog
• Protein Family: Cytochrome c oxidase assembly protein
• UniProt Gene Name: COX15
• UniProt Entry Name: COX15_HUMAN

NCBI Description

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 diverging in the 3' region. [provided by RefSeq, Jul 2008]

Uniprot Description

COX15: May be involved in the biosynthesis of heme A. Defects in COX15 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 COX15 are a cause of Leigh syndrome (LS). An early-onset progressive neurodegenerative disorder characterized 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. Clinical features depend on which areas of the central nervous system are involved and include subacute onset of psychomotor retardation, hypotonia, ataxia, weakness, vision loss, eye movement abnormalities, seizures, and dysphagia. Belongs to the COX15/CtaA family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Energy Metabolism - oxidative phosphorylation; Cofactor and Vitamin Metabolism - porphyrin and chlorophyll; Membrane protein, integral; Membrane protein, multi-pass; Mitochondrial

Chromosomal Location of Human Ortholog: 10q24

Cellular Component: mitochondrion; mitochondrial inner membrane; integral to membrane; mitochondrial respiratory chain

Molecular Function: cytochrome-c oxidase activity; oxidoreductase activity, acting on the CH-CH group of donors

Biological Process: respiratory chain complex IV assembly; porphyrin metabolic process; cellular respiration; mitochondrial electron transport, cytochrome c to oxygen; heme a biosynthetic process; respiratory gaseous exchange; heme biosynthetic process

Disease: Leigh Syndrome; Cardioencephalomyopathy, Fatal Infantile, Due To Cytochrome C Oxidase Deficiency 2