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COX15 homolog, cytochrome c oxidase assembly protein

COX15, Cox15p
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] (from NCBI)
Top mentioned proteins: CAN, SURF1, SCO1, HAD, SCO2
Papers on COX15
Multiple Origins of Eukaryotic cox15 Suggest Horizontal Gene Transfer from Bacteria to Jakobid Mitochondrial DNA.
New
Baldauf et al., Uppsala, Sweden. In Mol Biol Evol, Jan 2016
Of these, the most extreme example to date is the Andalucia godoyi mitochondrial DNA (mtDNA), including a cox15 gene encoding the respiratory enzyme heme A synthase (HAS), which is nuclear-encoded in nearly all other mitochondriate eukaryotes.
Importance of the alternative oxidase (AOX) pathway in regulating cellular redox and ROS homeostasis to optimize photosynthesis during restriction of the cytochrome oxidase pathway in Arabidopsis thaliana.
New
Padmasree et al., Hyderābād, India. In Ann Bot, Sep 2015
By contrast, WT plants showed a significant increase in transcript levels of CSD1, CAT1, sAPX, COX15 and AOX1A in contrast to aox1a mutants.
Identification of B cells participated in the mechanism of postmenopausal women osteoporosis using microarray analysis.
Zhang et al., Jinan, China. In Int J Clin Exp Med, 2014
Functional enrichment analysis indicated that the genes (ITPA, ATIC, UMPS, HPRT1, COX10 and COX15) might participate in metabolic pathways, MAP3K10 and MAP3K9 might participate in the activation of JNKK activity, COX10 and COX15 might involve in mitochondrial electron transport, and ATIC, UMPS and HPRT1 might involve in transferase activity.
Essentiality of respiratory activity for pentose utilization in thermotolerant yeast Kluyveromyces marxianus DMKU 3-1042.
Yamada et al., Ube, Japan. In Antonie Van Leeuwenhoek, 2013
By random integrative mutagenesis with a kanMX4 cassette in Kluyveromyces marxianus DMKU 3-1042, we obtained three mutants of COX15, ATP25 and CYC3 encoding a cytochrome oxidase assembly factor (singleton), a transcription factor required for assembly of the Atp9p subunit of mitochondrial ATP synthase and cytochrome c heme lyase, respectively, as mutants lacking growth capability on xylose and/or arabinose.
Strikingly bacteria-like and gene-rich mitochondrial genomes throughout jakobid protists.
Lang et al., Montréal, Canada. In Genome Biol Evol, 2012
The extra genes are rpl35 (a large subunit mitoribosomal protein) and cox15 (involved in cytochrome oxidase assembly), which are nucleus encoded throughout other eukaryotes.
Structural and thermodynamic characterization of the adrenodoxin-like domain of the electron-transfer protein Etp1 from Schizosaccharomyces pombe.
Bernhardt et al., Berlin, Germany. In J Inorg Biochem, 2011
The protein Etp1 of Schizosaccharomyces pombe consists of an amino-terminal COX15-like domain and a carboxy-terminal ferredoxin-like domain, Etp1(fd), which is cleaved off after mitochondrial import.
Infantile cardioencephalopathy due to a COX15 gene defect: report and review.
Review
Vallance et al., Vancouver, Canada. In Am J Med Genet A, 2011
Subsequent molecular investigations showed compound heterozygosity for two known pathogenic mutations in the COX15 gene.
Analysis of the genes coding for subunit 10 and 15 of cytochrome c oxidase in Alzheimer's disease.
GeneRIF
Finazzi et al., Brescia, Italy. In J Neural Transm, 2009
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 alternative oxidase, a tool for compensating cytochrome c oxidase deficiency in human cells.
Rustin et al., Paris, France. In Physiol Plant, 2009
We used immortalized COX15-deficient skin fibroblasts from a patient who died from an early fatal cardiomyopathy.
Tachyphylaxis effects on postprandial oxidative stress and mitochondrial-related gene expression in overweight subjects after a period of energy restriction.
Martínez et al., Pamplona, Spain. In Eur J Nutr, 2009
The expression of four mitochondrial-related genes, COX15, NDUFS2, MGST2 and TNF-alfa, was measured in peripheral blood mononuclear cells (PBMC) by quantitative RT-PCR.
Mutation analysis of COX18 in 29 patients with isolated cytochrome c oxidase deficiency.
Trevisson et al., Nice, France. In J Hum Genet, 2009
Mutations in SURF1, SCO2, SCO1, COX10, COX15 and in mitochondrial DNA, had been ruled out earlier.
Expression of the alternative oxidase complements cytochrome c oxidase deficiency in human cells.
GeneRIF
Rustin et al., Paris, France. In Embo Mol Med, 2009
The expression of the AOX, well-tolerated by the cells, compensates for both the growth defect and the pronounced oxidant-sensitivity of COX-deficient human cells.
Regulation of the heme A biosynthetic pathway: differential regulation of heme A synthase and heme O synthase in Saccharomyces cerevisiae.
GeneRIF
Hegg et al., East Lansing, United States. In J Biol Chem, 2009
COX10, the physiological partner of COX15, does not share the same regulatory mechanism with COX15
Cells by design: a mini-review of targeting cell engineering using DNA microarrays.
Review
Shiloach et al., Baltimore, United States. In Mol Biotechnol, 2008
In a separate example, a gene encoding a mitochondrial assembly protein (cox15) and a gene encoding a kinase (cdkl3), were found to influence cellular growth.
Enhancement of cell proliferation in various mammalian cell lines by gene insertion of a cyclin-dependent kinase homolog.
GeneRIF
Shiloach et al., Bethesda, United States. In Bmc Biotechnol, 2006
cdkl3 transfected in anchorage-independent (suspension) HeLa cells overexpressed relative to attached cells and lead to elevated proliferation and viability relative to untransfected. Same in two HEK-293 and a CHO cell lines.
Defects in the biosynthesis of mitochondrial heme c and heme a in yeast and mammals.
Review
Barrientos et al., Miami, United States. In Biochim Biophys Acta, 2005
COX10 and COX15 are two genes, initially identified in Saccharomyces cerevisiae that have been found to cause infantile cytochrome c oxidase deficiency in humans.
Functional and genetic studies demonstrate that mutation in the COX15 gene can cause Leigh syndrome.
GeneRIF
Brown et al., In J Med Genet, 2004
A patient with typical clinical and neuroradiological features of Leigh syndrome and cytochrome oxidase deficiency was found to have a mutation in the COX15 gene.
Genetic defects of cytochrome c oxidase assembly.
Review
Houstek et al., Praha, Czech Republic. In Physiol Res, 2003
All these mutations are located in genes encoding COX-specific assembly proteins including SURF1, SCO1, SCO2, COX10, and COX15.
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