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Pathogenicity of two COQ7 mutations and responses to 2,4-dihydroxybenzoate bypass treatment.
Mitochondrial COQ9 is a lipid-binding protein that associates with COQ7 to enable coenzyme Q biosynthesis.
action of clioquinol on several age-dependent neurodegenerative diseases with distinct etiologies might result from a slowing down of the aging process through action of the drug on CLK-1.
The siRNA-mediated knock down leads to an increase in cytoplasmic superoxide dismutase (SOD1) mRNA levels and activity
Clk1 plays a direct role in dopaminergic neuronal survival via regulating the autophagy-lysosome pathway that may contribute to the pathologic development of Parkinson disease.
An enhanced immune response of Mclk1+/- mutant mice is associated with partial protection from fibrosis, cancer and the development of biomarkers of aging
These findings indicate that MCLK1 (also known as Coq7) regulates both coenzyme Q synthesis and distribution within mitochondrial membranes.
Calorie restriction modifies ubiquinone and COQ transcript levels in mouse tissues
the partial resistance to I/R injury suggests that Mclk1(+/)(-) mutants have an enhanced recovery potential following age-dependant vascular accidents, which correlates well with their longer survival
CLK-1 protein has DNA binding activity specific to O(L) region of mitochondrial DNA.
clk-1 deficiency induces apoptosis associated with mitochondrial dysfunction in mouse embryos.
Mclk1 has a role in mitochondrial function, energy metabolism and the aging process
Mclk1 heterozygosity does not necessarily protect against atherosclerosis. Moreover, in the presence of hyperlipidemia and chronic inflammation, Mclk1 heterozygosity is incapable of extending lifespan
Reduction in COQ7 levels gradually prevents the deterioration of mitochondrial function and associated increase of global oxidative stress that is normally observed in Sod2(+/-) mutants.
Loss of ubiquinone biosynthesis is responsible for all phenotypes resulting from loss of CLK-1, including behavioral phenotypes, altered expression of mitochondrial quality control genes, and lifespan.
Nuclear CLK-1 mediates a retrograde signalling pathway that is conserved from Caenorhabditis elegans to humans and is responsive to mitochondrial reactive oxygen species, thus acting as a barometer of oxidative metabolism.
no measurable intrinsic ETC defect exists in clk-1 mitochondria. The data indicate that DMQ(9) specifically inhibits electron transfer from complex I to ubiquinone.
Prolonged life span of Clk mutants cannot be attributed to reduced metabolic rate or an increased activity of the major antioxidant enzymes catalase and SOD.
Complementation of Escherichia coli ubiF mutation by Caenorhabditis elegans CLK-1.
Caenorhabditis elegans clk-1 mutants are sensitive to ubiquinone side-chain length
in maternally resqued animals, the effect of clk-1 mutations on adult lifespan in uncoupled from their effects on development and reproduction
differential fertility of clk-1 mutant nematodes fed Q isoforms may result from changes in Q localization, altered recognition by Q-binding proteins, and/or potential defects in mitochondrial function resulting from the mutant CLK-1 polypeptide itself.
Suppressors of the missense mutation of clk-1 were identified; each mutant suppresses a different subset of phenotypes.
The protein encoded by this gene is similar to a mitochondrial di-iron containing hydroxylase in Saccharomyces cerevisiae that is involved with ubiquinone biosynthesis. Mutations in the yeast gene lead to slower development and longer life span. Alternatively spliced transcript variants have been found for this gene.
COQ7 coenzyme Q, 7 homolog ubiquinone
, coenzyme Q biosynthesis protein 7 homolog
, placental protein KG-20
, timing protein clk-1 homolog
, ubiquinone biosynthesis protein COQ7 homolog
, Coenzyme q (ubiquinone) biosynthetic enzyme (DHPB methyltransferase) 7
, demethyl-Q 7