| pubmed-article:20159956 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20159956 | lifeskim:mentions | umls-concept:C0035143 | lld:lifeskim |
| pubmed-article:20159956 | lifeskim:mentions | umls-concept:C0013138 | lld:lifeskim |
| pubmed-article:20159956 | lifeskim:mentions | umls-concept:C2936272 | lld:lifeskim |
| pubmed-article:20159956 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:20159956 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20159956 | pubmed:dateCreated | 2010-2-17 | lld:pubmed |
| pubmed-article:20159956 | pubmed:abstractText | Transcriptional feedback loops are central to the generation and maintenance of circadian rhythms. In animal systems as well as Neurospora, transcriptional repression is believed to occur by catalytic post-translational events. We report here in the Drosophila model two different mechanisms by which the circadian repressor PERIOD (PER) inhibits CLOCK/CYCLE (CLK/CYC)-mediated transcription. First, PER is recruited to circadian promoters, which leads to the nighttime decrease of CLK/CYC activity. This decrease is proportional to PER levels on DNA, and PER recruitment probably occurs via CLK. Then CLK is released from DNA and sequestered in a strong, approximately 1:1 PER-CLK off-DNA complex. The data indicate that the PER levels bound to CLK change dynamically and are important for repression, first on-DNA and then off-DNA. They also suggest that these mechanisms occur upstream of post-translational events, and that elements of this two-step mechanism likely apply to mammals. | lld:pubmed |
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| pubmed-article:20159956 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:20159956 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20159956 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20159956 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:20159956 | pubmed:issn | 1549-5477 | lld:pubmed |
| pubmed-article:20159956 | pubmed:author | pubmed-author:AbruzziKathar... | lld:pubmed |
| pubmed-article:20159956 | pubmed:author | pubmed-author:RosbashMichae... | lld:pubmed |
| pubmed-article:20159956 | pubmed:author | pubmed-author:MenetJerome... | lld:pubmed |
| pubmed-article:20159956 | pubmed:author | pubmed-author:RodriguezJose... | lld:pubmed |
| pubmed-article:20159956 | pubmed:author | pubmed-author:DesrochersJen... | lld:pubmed |
| pubmed-article:20159956 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20159956 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:20159956 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:20159956 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20159956 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20159956 | pubmed:pagination | 358-67 | lld:pubmed |
| pubmed-article:20159956 | pubmed:dateRevised | 2010-9-28 | lld:pubmed |
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| pubmed-article:20159956 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20159956 | pubmed:articleTitle | Dynamic PER repression mechanisms in the Drosophila circadian clock: from on-DNA to off-DNA. | lld:pubmed |
| pubmed-article:20159956 | pubmed:affiliation | Department of Biology, Howard Hughes Medical Institute, National Center for Behavioral Genomics, Brandeis University, Waltham, Massachusetts 02454, USA. | lld:pubmed |
| pubmed-article:20159956 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20159956 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20159956 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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