In:
Science, American Association for the Advancement of Science (AAAS), Vol. 326, No. 5951 ( 2009-10-16), p. 378-379
Abstract:
In mammals, sleeping, feeding, and most other physiological processes are influenced by a circadian system and therefore display daily oscillations. These rhythms are generated by self-sustained and cell-autonomous molecular clocks that exist in virtually all cell types. A “master clock” located in the brain's suprachiasmatic nucleus (SCN) can synchronize these peripheral clocks, but for many organs, feeding-fasting rhythms are the dominant zeitgebers (timing cues) ( 1 , 2 ). On page 437 of this issue, Lamia et al. propose a molecular mechanism through which metabolic cycles may interact with the circadian clockwork circuitry. They show that an enzyme that responds to nutrient availability—adenosine monophosphate–activated protein kinase (AMPK)—directly phosphorylates the core clock protein cryptochrome 1 (CRY1), thereby marking it for degradation ( 3 ).
Type of Medium:
Online Resource
ISSN:
0036-8075
,
1095-9203
DOI:
10.1126/science.1181278
Language:
English
Publisher:
American Association for the Advancement of Science (AAAS)
Publication Date:
2009
detail.hit.zdb_id:
128410-1
detail.hit.zdb_id:
2066996-3
detail.hit.zdb_id:
2060783-0
SSG:
11
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