| Literature DB >> 11163178 |
M K Bunger1, L D Wilsbacher, S M Moran, C Clendenin, L A Radcliffe, J B Hogenesch, M C Simon, J S Takahashi, C A Bradfield.
Abstract
Circadian oscillations in mammalian physiology and behavior are regulated by an endogenous biological clock. Here we show that loss of the PAS protein MOP3 (also known as BMAL1) in mice results in immediate and complete loss of circadian rhythmicity in constant darkness. Additionally, locomotor activity in light-dark (LD) cycles is impaired and activity levels are reduced in Mop3-/- mice. Analysis of Period gene expression in the suprachiasmatic nucleus (SCN) indicates that these behavioral phenotypes arise from loss of circadian function at the molecular level. These results provide genetic evidence that MOP3 is the bona fide heterodimeric partner of mCLOCK. Furthermore, these data demonstrate that MOP3 is a nonredundant and essential component of the circadian pacemaker in mammals.Entities:
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Year: 2000 PMID： 11163178 PMCID： PMC3779439 DOI： 10.1016/s0092-8674(00)00205-1
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582