| pubmed-article:11795949 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11795949 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:11795949 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:11795949 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:11795949 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:11795949 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:11795949 | lifeskim:mentions | umls-concept:C1710265 | lld:lifeskim |
| pubmed-article:11795949 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:11795949 | pubmed:dateCreated | 2002-1-17 | lld:pubmed |
| pubmed-article:11795949 | pubmed:abstractText | Recent studies using mice with genetically engineered gap junction protein connexin (Cx) genes have provided evidence that reduced gap-junctional coupling in ventricular cardiomyocytes predisposes to ventricular arrhythmia. However, the pathological processes of arrhythmogenesis due to abnormalities in gap junctions are poorly understood. We have postulated a hypothesis that dysfunction of gap junctions at the single-cell level may affect synchronization of calcium transients among cardiomyocytes. To examine this hypothesis, we developed a novel system in which gap-junctional intercellular communication in primary neonatal rat cardiomyocytes was inhibited by a mutated (Delta130-137) Cx43 fused with enhanced green fluorescent protein (Cx43-EGFP), and calcium transients were imaged in real time while the mutated Cx43-EGFP-expressing cardiomyocytes were identified. The mutated Cx43-EGFP inhibited dye coupling not only in the liver epithelial cell line IAR 20 but also in primary neonatal rat cardiomyocytes in a dominant-negative manner, whereas wild-type Cx43-EGFP made functional gap junctions in otherwise communication-deficient HeLa cells. The mutated Cx43-EGFP induced desynchronization of calcium transients among cardiomyocytes with significantly higher frequency than wild-type Cx43-EGFP. These results suggest that dysfunction of gap-junctional intercellular communication at the single-cell level could hamper synchronous beating among cardiomyocytes as a result of desynchronization of calcium transients. | lld:pubmed |
| pubmed-article:11795949 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11795949 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11795949 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11795949 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11795949 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11795949 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11795949 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11795949 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11795949 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11795949 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11795949 | pubmed:issn | 0014-4827 | lld:pubmed |
| pubmed-article:11795949 | pubmed:author | pubmed-author:OyamadaYumiko... | lld:pubmed |
| pubmed-article:11795949 | pubmed:author | pubmed-author:ZhouWuxiongW | lld:pubmed |
| pubmed-article:11795949 | pubmed:author | pubmed-author:OyamadaHideto... | lld:pubmed |
| pubmed-article:11795949 | pubmed:author | pubmed-author:TakamatsuTets... | lld:pubmed |
| pubmed-article:11795949 | pubmed:author | pubmed-author:OyamadaMasahi... | lld:pubmed |
| pubmed-article:11795949 | pubmed:copyrightInfo | Copyright 2001 Elsevier Science. | lld:pubmed |
| pubmed-article:11795949 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11795949 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11795949 | pubmed:volume | 273 | lld:pubmed |
| pubmed-article:11795949 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11795949 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11795949 | pubmed:pagination | 85-94 | lld:pubmed |
| pubmed-article:11795949 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:11795949 | pubmed:meshHeading | pubmed-meshheading:11795949... | lld:pubmed |
| pubmed-article:11795949 | pubmed:meshHeading | pubmed-meshheading:11795949... | lld:pubmed |
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| pubmed-article:11795949 | pubmed:meshHeading | pubmed-meshheading:11795949... | lld:pubmed |
| pubmed-article:11795949 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11795949 | pubmed:articleTitle | Dominant-negative connexin43-EGFP inhibits calcium-transient synchronization of primary neonatal rat cardiomyocytes. | lld:pubmed |
| pubmed-article:11795949 | pubmed:affiliation | Department of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan. | lld:pubmed |
| pubmed-article:11795949 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11795949 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:11795949 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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