טוען...
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...
שמור ב:
| Main Authors: | , , , , , |
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| פורמט: | Artigo |
| שפה: | Inglês |
| יצא לאור: |
Cold Spring Harbor Laboratory Press
2005
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| נושאים: | |
| גישה מקוונת: | 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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