|camk1gb ||calcium/calmodulin-dependent protein kinase IGb ||camk1gb appears to link the pineal master clock with the periphery. camk1gb is a rhythmically expressed gene that connects the clock with donwstream physiology of the pineal gland. Knockdown of camk1gb disrupts locomotor activity in the whole larva, even through it is predominantly expressed within the pineal gland [Tovin et al. 2012; http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1003116]. ||Zebrafish |
|tim ||timeless ||TIMELESS (TIM) oscillation are attenuated in the cerebral clock neurons of elderly flies .
Tim01 mutants have nearly a 50% reduced fecundity . ||Fruit fly |
|Prkaa1 ||Protein kinase, AMP-activated, alpha 1 catalytic subunit ||Prkaa1 hosphorylates Cryptochromes and leads to their degradation . ||House mouse |
|Klf10 ||Kruppel-like factor 10 ||Klf10 is circadian, induced by glucose, binds and represses Arntl promoter. Klf10 RNAi caused cellular period shortening (of Arntl- and Per2-luc) . ||House mouse |
|Rgs16 ||Regulator of G-protein signaling 16 ||Rgs16 knockdown have shorter free-running period of locomotors activity rhythm and reduced total activity. Under daytime RF food-anticipatory activity is attenuated and phase-advance of rhythmic Per2 expression in liver and thalamus is diminished . ||House mouse |
|Sirt1 ||sirtuin 1 (silent mating type information regulation 2, homolog) 1 (S. cerevisiae) ||Whole-body deletion of Sirt1 in the adulthood results in mice which are seemingly normal in every way. When mice were given low doses of resveratrol after Sirt1 was disabled, there were no discernible improvement in mitochondrial function or any parameter, while mice with normal Sirt1 function given reservatrol showed dramatic increases in energy, mitochondrial biogenesis and function, AMPK activation and increased NAD+ levels in skeletal muscle. When mice lacking Sirt1 were given low doses of reserveratrol, AMPK was unaffected. When doses were significantly increased in these mice, AMPK was activated in a SIRT1-indepent manner, but still no benefit to mitochondrial function resulted . Sirt1 overexpression mimicks the effect on reservatrol on mitochondrial function, but failed to extend lifespan .
SIRT1 knock-out mouse embryonic fibroblasts (MEFs) have a significant greater replicative capacity in culture. p19ARF levels are significantly reduced in SIRT1 knock-out MEFs .
Sirt1-null mice do not exhibit lifespan extension upon Dietary Restriction .
Sirt1 is required for high-magnitude circadian transcription of several core clock genes. It deacetylates Per2, Arntl and histones of clock-controlled genes .
SIRT1 directly  and indirectly  prevents telomere shortening. ||House mouse |