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- W1985164095 abstract "Abstract Circadian clocks are based on a molecular mechanism regulated at the transcriptional, translational and post-translational levels. Recent experimental data unravel a complex role of the phosphorylations in these clocks. In mammals, several kinases play differential roles in the regulation of circadian rhythmicity. A dysfunction in the phosphorylation of one clock protein could lead to sleep disorders such as the Familial Advanced Sleep Phase Disorder, FASPS. Moreover, several drugs are targeting kinases of the circadian clocks and can be used in cancer chronotherapy or to treat mood disorders. In Drosophila, recent experimental observations also revealed a complex role of the phosphorylations. Because of its high degree of homology with mammals, the Drosophila system is of particular interest. In the circadian clock of cyanobacteria, an atypical regulatory mechanism is based only on three clock proteins (KaiA, KaiB, KaiC) and ATP and is sufficient to produce robust temperature-compensated circadian oscillations of KaiC phosphorylation. This review will show how computational modeling has become a powerful and useful tool in investigating the regulatory mechanism of circadian clocks, but also how models can give rise to testable predictions or reveal unexpected results." @default.
- W1985164095 created "2016-06-24" @default.
- W1985164095 creator A5047890146 @default.
- W1985164095 date "2009-09-01" @default.
- W1985164095 modified "2023-10-16" @default.
- W1985164095 title "Circadian clocks and phosphorylation: Insights from computational modeling" @default.
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