pubmed-article:17401374 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17401374 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
pubmed-article:17401374 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:17401374 | lifeskim:mentions | umls-concept:C1101610 | lld:lifeskim |
pubmed-article:17401374 | lifeskim:mentions | umls-concept:C1415068 | lld:lifeskim |
pubmed-article:17401374 | lifeskim:mentions | umls-concept:C1416584 | lld:lifeskim |
pubmed-article:17401374 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
pubmed-article:17401374 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:17401374 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:17401374 | pubmed:dateCreated | 2007-4-6 | lld:pubmed |
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pubmed-article:17401374 | pubmed:abstractText | MicroRNAs (miRNAs) are endogenous noncoding RNAs, about 22 nucleotides in length, that mediate post-transcriptional gene silencing by annealing to inexactly complementary sequences in the 3'-untranslated regions of target mRNAs. Our current understanding of the functions of miRNAs relies mainly on their tissue-specific or developmental stage-dependent expression and their evolutionary conservation, and therefore is primarily limited to their involvement in developmental regulation and oncogenesis. Of more than 300 miRNAs that have been identified, miR-1 and miR-133 are considered to be muscle specific. Here we show that miR-1 is overexpressed in individuals with coronary artery disease, and that when overexpressed in normal or infarcted rat hearts, it exacerbates arrhythmogenesis. Elimination of miR-1 by an antisense inhibitor in infarcted rat hearts relieved arrhythmogenesis. miR-1 overexpression slowed conduction and depolarized the cytoplasmic membrane by post-transcriptionally repressing KCNJ2 (which encodes the K(+) channel subunit Kir2.1) and GJA1 (which encodes connexin 43), and this likely accounts at least in part for its arrhythmogenic potential. Thus, miR-1 may have important pathophysiological functions in the heart, and is a potential antiarrhythmic target. | lld:pubmed |
pubmed-article:17401374 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17401374 | pubmed:language | eng | lld:pubmed |
pubmed-article:17401374 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17401374 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17401374 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17401374 | pubmed:month | Apr | lld:pubmed |
pubmed-article:17401374 | pubmed:issn | 1078-8956 | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:ZhangYingY | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:WangZhiguoZ | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:LiBaoxinB | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:LuYanjieY | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:WangHuizhenH | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:YangBaofengB | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:LinHuixianH | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:XuChaoqianC | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:ChenGuohaoG | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:XiaoJieningJ | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:LuoXiaobinX | lld:pubmed |
pubmed-article:17401374 | pubmed:author | pubmed-author:BaiYunlongY | lld:pubmed |
pubmed-article:17401374 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17401374 | pubmed:volume | 13 | lld:pubmed |
pubmed-article:17401374 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17401374 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17401374 | pubmed:pagination | 486-91 | lld:pubmed |
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pubmed-article:17401374 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17401374 | pubmed:articleTitle | The muscle-specific microRNA miR-1 regulates cardiac arrhythmogenic potential by targeting GJA1 and KCNJ2. | lld:pubmed |
pubmed-article:17401374 | pubmed:affiliation | Department of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), Harbin Medical University, Harbin, Heilongjiang 150086, China. yangbf@ems.hrbmu.edu.cn | lld:pubmed |
pubmed-article:17401374 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17401374 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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