clk-1 Antibody

1. 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. PMID: 28404998
2. 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. PMID: 25961505
3. 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. PMID: 21745495
4. Complementation of Escherichia coli ubiF mutation by Caenorhabditis elegans CLK-1. PMID: 12753928
5. Caenorhabditis elegans clk-1 mutants are sensitive to ubiquinone side-chain length PMID: 12893826
6. in maternally resqued animals, the effect of clk-1 mutations on adult lifespan in uncoupled from their effects on development and reproduction PMID: 14517217
7. 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. PMID: 14530273
8. Suppressors of the missense mutation of clk-1 were identified; each mutant suppresses a different subset of phenotypes. PMID: 16648490
9. 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. PMID: 18927074

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KEGG: cel:CELE_ZC395.2

STRING: 6239.ZC395.2.2

UniGene: Cel.10672