COX10 sirna

COX10 siRNA (Human)

Cat. Num. AAA8241017

• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: COX10; COX10 siRNA (Human); Protoheme IX farnesyltransferase mitochondrial; Heme O synthase; COX10 sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: COX10 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: 251

• Applicable Applications for COX10 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 COX10 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 COX10 sirna

siRNA to inhibit COX10 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 17921982
• NCBI GeneID: 1352
• NCBI Accession #: NP_001294.2
• NCBI GenBank Nucleotide #: NM_001303.3
• UniProt Accession #: Q12887; O15334; Q969F7; B2R6U5; B4DJ50
• Molecular Weight: 27,594 Da
• NCBI Official Full Name: protoheme IX farnesyltransferase, mitochondrial
• NCBI Official Synonym Full Names: COX10 heme A:farnesyltransferase cytochrome c oxidase assembly factor
• NCBI Official Symbol: COX10
• NCBI Protein Information: protoheme IX farnesyltransferase, mitochondrial
• UniProt Protein Name: Protoheme IX farnesyltransferase, mitochondrial
• Protein Family: Probable protoheme IX farnesyltransferase
• UniProt Gene Name: COX10
• UniProt Entry Name: COX10_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 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. [provided by RefSeq, Jul 2008]

Uniprot Description

COX10: Converts protoheme IX and farnesyl diphosphate to heme O. Defects in COX10 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 COX10 are a cause of Leigh syndrome (LS). LS is a severe neurological disorder characterized by bilaterally symmetrical necrotic lesions in subcortical brain regions. Belongs to the UbiA prenyltransferase family.

Protein type: EC 2.5.1.-; Cofactor and Vitamin Metabolism - porphyrin and chlorophyll; Energy Metabolism - oxidative phosphorylation; Membrane protein, multi-pass; Membrane protein, integral; Transferase

Chromosomal Location of Human Ortholog: 17p12

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

Molecular Function: cytochrome-c oxidase activity; farnesyltranstransferase activity; protoheme IX farnesyltransferase activity

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

Disease: Leigh Syndrome; Mitochondrial Complex Iv Deficiency