| pubmed-article:19269369 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19269369 | lifeskim:mentions | umls-concept:C1101610 | lld:lifeskim |
| pubmed-article:19269369 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:19269369 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
| pubmed-article:19269369 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:19269369 | pubmed:dateCreated | 2009-3-9 | lld:pubmed |
| pubmed-article:19269369 | pubmed:abstractText | TRIM-NHL proteins represent a large class of metazoan proteins implicated in development and disease. We demonstrate that a C. elegans TRIM-NHL protein, NHL-2, functions as a cofactor for the microRNA-induced silencing complex (miRISC) and thereby enhances the posttranscriptional repression of several genetically verified microRNA targets, including hbl-1 and let-60/Ras (by the let-7 family of microRNAs) and cog-1 (by the lsy-6 microRNA). NHL-2 is localized to cytoplasmic P-bodies and physically associates with the P-body protein CGH-1 and the core miRISC components ALG-1/2 and AIN-1. nhl-2 and cgh-1 mutations compromise the repression of microRNA targets in vivo but do not affect microRNA biogenesis, indicating a role for an NHL-2:CGH-1 complex in the effector phase of miRISC activity. We propose that the NHL-2:CGH-1 complex functions in association with mature miRISC to modulate the efficacy of microRNA:target interactions in response to physiological and developmental signals, thereby ensuring the robustness of genetic regulatory pathways regulated by microRNAs. | lld:pubmed |
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| pubmed-article:19269369 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19269369 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19269369 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19269369 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:19269369 | pubmed:issn | 1097-4172 | lld:pubmed |
| pubmed-article:19269369 | pubmed:author | pubmed-author:BlackwellT... | lld:pubmed |
| pubmed-article:19269369 | pubmed:author | pubmed-author:AmbrosVictorV | lld:pubmed |
| pubmed-article:19269369 | pubmed:author | pubmed-author:HammellChrist... | lld:pubmed |
| pubmed-article:19269369 | pubmed:author | pubmed-author:BoagPeter RPR | lld:pubmed |
| pubmed-article:19269369 | pubmed:author | pubmed-author:LubinIsabella... | lld:pubmed |
| pubmed-article:19269369 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19269369 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:19269369 | pubmed:volume | 136 | lld:pubmed |
| pubmed-article:19269369 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19269369 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19269369 | pubmed:pagination | 926-38 | lld:pubmed |
| pubmed-article:19269369 | pubmed:dateRevised | 2010-9-23 | lld:pubmed |
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| pubmed-article:19269369 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19269369 | pubmed:articleTitle | nhl-2 Modulates microRNA activity in Caenorhabditis elegans. | lld:pubmed |
| pubmed-article:19269369 | pubmed:affiliation | University of Massachusetts Medical School, Worcester, 01605, USA. | lld:pubmed |
| pubmed-article:19269369 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19269369 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19269369 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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