Our circadian clocks can be misaligned by a variety of reasons. Some of us are morning larks, other night owls. Sometimes, mutations to our genes lead to the Familial Advanced Sleep Phase (FASP) condition. People with this mutation sleep and wake very early.
Previous research has suggested that a ‘priming’ kinase is required to ‘switch on’ the FASP site, a key control point that plays an important role in regulating our biological clock.
An international team of researchers, led by Professor David Virshup in the Programme in Cancer and Stem Cell Biology, Duke-NUS Medical School, found that CK1 is the priming kinase.1 CK1 is a well-known kinase, though the discovery of this new key role is novel. The team also uncovered the mechanisms in which these proteins switch on the site. Members from the family of CK1 proteins cooperatively regulate the circadian clock. For example, while CK1D1 accelerates the circadian clock, CK1D2 slows it down.
By shining a light on this key part of how these CK1 proteins work on the circadian clock, we have a better understanding of what we can do when our circadian clock breaks down and problems arise, and the treatments we can develop. Those of us doing shift work or suffering from jet lag look forward to the day that drugs that inhibit CK1 allow us to wake and sleep on time!
Editor’s note: Read full study
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