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Evolutionary conservation of the clk-1-dependent mechanism of longevity: loss of mclk1 increases cellular fitness and lifespan in mice

Inactivation of the Caenorhabditis elegans gene clk-1, which is required for ubiquinone biosynthesis, increases lifespan by an insulin signaling-independent mechanism. We find that homozygous inactivation of mclk1, the mouse ortholog of clk-1, yields ES cells that are protected from oxidative stress...

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Autores principales: Liu, Xingxing, Jiang, Ning, Hughes, Bryan, Bigras, Eve, Shoubridge, Eric, Hekimi, Siegfried
Formato: Artigo
Lenguaje:Inglês
Publicado: Cold Spring Harbor Laboratory Press 2005
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Acceso en línea:https://ncbi.nlm.nih.gov/pmc/articles/PMC1257397/
https://ncbi.nlm.nih.gov/pubmed/16195414
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1101/gad.1352905
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