Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-12-8
pubmed:abstractText
Several genes have been recognized in Drosophila that regulate circadian rhythms. Homologues of these genes have now been found in mice and humans, suggesting a mechanism that is conserved throughout the animal kingdom. For some of these genes and their products, molecular oscillations are produced in certain cells of the Drosophila and mammalian brain. Two genes, period and timeless, are transcribed with a circadian rhythm that is regulated by activities derived from their encoded proteins, PER and TIM. Nuclear localization of these proteins downregulates per and tim transcription by suppressing the activities of two transcription factors, dCLOCK and dBMAL1. Cycles in this feedback regulation are promoted by events that regulate the accumulation, physical interaction, and nuclear translocation of PER and TIM proteins. PER and TIM must physically associate to enter the nucleus and their cytoplasmic interaction is delayed by a kinase encoded by the clock gene, double-time. This kinase directs PER phosphorylation, which leads to PER degradation. Effects of the kinase are blocked once PER is complexed to TIM. These interactions prolong the interval of per and tim transcription by ensuring that PER/TIM complexes from only after TIM has accumulated for several hours.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0079-9963
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-94; discussion 94-5
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Molecular control of circadian behavioral rhythms.
pubmed:affiliation
Laboratory of Genetics, Rockefeller University, New York, New York 10021, USA.
pubmed:publicationType
Journal Article, Review