pubmed-article:16227573 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C0024660 | lld:lifeskim |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C0013485 | lld:lifeskim |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C1101610 | lld:lifeskim |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C1518294 | lld:lifeskim |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C1423887 | lld:lifeskim |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C2346626 | lld:lifeskim |
pubmed-article:16227573 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:16227573 | pubmed:issue | 21 | lld:pubmed |
pubmed-article:16227573 | pubmed:dateCreated | 2005-10-17 | lld:pubmed |
pubmed-article:16227573 | pubmed:abstractText | Vertebrate genomes each encode hundreds of micro-RNAs (miRNAs), yet for few of these miRNAs is there empirical evidence as to which mRNA(s) they regulate. Here we report the identification of human lin-28 mRNA as a regulatory target of human miR-125b and its homolog miR-125a. Studies of miR-125b function in mouse P19 embryonal carcinoma cells induced to develop into neurons suggest a role for this regulatory miRNA in mammalian neuronal differentiation, since its increased concentration in these cells contributes to lin-28 downregulation. Within the lin-28 3' untranslated region (UTR) are two conserved miRNA responsive elements (miREs) that mediate repression by miR-125b and miR-125a. Simultaneous deletion of both miREs renders the lin-28 3' UTR almost completely insensitive to these miRNAs, indicating that these two miREs are the principal elements in the lin-28 3' UTR that respond to miR-125. At the 3' end of each element is an adenosine residue that makes a significant contribution to function irrespective of its complementarity to the 5'-terminal nucleotide of miR-125. By contrast to most earlier reports of gene repression by other miRNAs that are imperfectly complementary to their targets, lin-28 downregulation by miR-125 involves reductions in both translational efficiency and mRNA abundance. The decrease in the mRNA concentration is achieved by a posttranscriptional mechanism that is independent of the inhibitory effect on translation. | lld:pubmed |
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pubmed-article:16227573 | pubmed:language | eng | lld:pubmed |
pubmed-article:16227573 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16227573 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16227573 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16227573 | pubmed:month | Nov | lld:pubmed |
pubmed-article:16227573 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:16227573 | pubmed:author | pubmed-author:BelascoJoel... | lld:pubmed |
pubmed-article:16227573 | pubmed:author | pubmed-author:WuLigangL | lld:pubmed |
pubmed-article:16227573 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16227573 | pubmed:volume | 25 | lld:pubmed |
pubmed-article:16227573 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16227573 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16227573 | pubmed:pagination | 9198-208 | lld:pubmed |
pubmed-article:16227573 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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