| pubmed-article:19305390 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19305390 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:19305390 | lifeskim:mentions | umls-concept:C1704735 | lld:lifeskim |
| pubmed-article:19305390 | lifeskim:mentions | umls-concept:C0257253 | lld:lifeskim |
| pubmed-article:19305390 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19305390 | pubmed:dateCreated | 2009-4-1 | lld:pubmed |
| pubmed-article:19305390 | pubmed:abstractText | The COP9 signalosome (CSN) is a highly conserved protein complex that was originally described as a repressor of light-dependent growth and transcription in Arabidopsis. The most studied CSN function is the regulation of protein degradation, which occurs primarily through the removal of the ubiquitin-like modifier Nedd8 from cullin-based E3 ubiquitin ligases. This activity can regulate transcription-factor stability and, therefore, transcriptional activity. Recent data suggest that the CSN also regulates transcription on the chromatin by mechanisms that are not yet clearly understood. Furthermore, the CSN subunits CSN5 and CSN2 seem to act as transcriptional coactivators and corepressors, respectively. Here, I re-evaluate the mechanisms by which the CSN acts as a transcriptional regulator, and suggest that they could extend beyond the regulation of protein stability. | lld:pubmed |
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| pubmed-article:19305390 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19305390 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19305390 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19305390 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19305390 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:19305390 | pubmed:issn | 1469-3178 | lld:pubmed |
| pubmed-article:19305390 | pubmed:author | pubmed-author:ChamovitzDani... | lld:pubmed |
| pubmed-article:19305390 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19305390 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:19305390 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19305390 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19305390 | pubmed:pagination | 352-8 | lld:pubmed |
| pubmed-article:19305390 | pubmed:dateRevised | 2010-9-23 | lld:pubmed |
| pubmed-article:19305390 | pubmed:meshHeading | pubmed-meshheading:19305390... | lld:pubmed |
| pubmed-article:19305390 | pubmed:meshHeading | pubmed-meshheading:19305390... | lld:pubmed |
| pubmed-article:19305390 | pubmed:meshHeading | pubmed-meshheading:19305390... | lld:pubmed |
| pubmed-article:19305390 | pubmed:meshHeading | pubmed-meshheading:19305390... | lld:pubmed |
| pubmed-article:19305390 | pubmed:meshHeading | pubmed-meshheading:19305390... | lld:pubmed |
| pubmed-article:19305390 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19305390 | pubmed:articleTitle | Revisiting the COP9 signalosome as a transcriptional regulator. | lld:pubmed |
| pubmed-article:19305390 | pubmed:affiliation | Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel. dannyc@tauex.tau.ac.il | lld:pubmed |
| pubmed-article:19305390 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19305390 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:19305390 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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