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Cytochrome c oxidase (COX), the terminal component of the mitochondrial respiratory chain, catalyzes the electron transfer from reduced cytochrome c to oxygen. Additionally we are shipping COX10 Antibodies (47) and many more products for this protein.
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On the basis of its pivotal role in regulating cell death upon COX (show COX8A Proteins) dysfunction, CerS6 (show CERS6 Proteins) might potentially represent a novel target for therapeutic intervention in mitochondrial diseases caused by COX (show COX8A Proteins) dysfunction.
ISCU (show ISCU Proteins) and COX10 are target genes of miR (show MLXIP Proteins)-210 related to mitochondrial metabolism
COX 15 mRNA was significantly more abundant in the cerebral tissue of Alzheimer's disease (AD) patients and COX10 and COX15 SNP were significantly less represented in the patient group, suggesting a possible protective role toward the risk for AD
The expression of the AOX (show ACOX1 Proteins), well-tolerated by the cells, compensates for both the growth defect and the pronounced oxidant-sensitivity of COX (show COX8A Proteins)-deficient human cells.
Cytochrome c (show CYCS Proteins) oxidase is decreased significantly in platelets and hippocampus in Alzheimer patients compared to controls.
COX10 has a role in mitochondrial heme A biosynthesis
This study report a cytochrome c (show CYCS Proteins) oxidase (COX (show COX8A Proteins))-deficient patient, clinically affected with Leigh-like disease, with a homozygous mutation in the COX10 start codon.
Geranylgeranyltransferase inhibitor-2147 (GGTI (show PGGT1B Proteins)-2147), an inhibitor of this enzyme prenylation, elicited significant inhibition of glucose-stimulated insulin (show INS Proteins) secretion from INS (show INS Proteins) 832/13 islet cells.
Mice lacking COX10 in skeletal muscle recapitulate the phenotype of progressive mitochondrial myopathies associated with cytochrome c (show CYCS Proteins) oxidase deficiency.
The levels of respiratory complex I were markedly reduced in COX10 knockout clones.
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.
protoheme IX farnesyltransferase, mitochondrial
, heme A:farnesyltransferase
, COX10 homolog, cytochrome c oxidase assembly protein, heme A: farnesyltransferase
, cytochrome c oxidase assembly protein
, cytochrome c oxidase subunit X
, heme A: farnesyltransferase
, heme O synthase