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pubmed-article:11007485 | lifeskim:mentions | umls-concept:C1522565 | lld:lifeskim |
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pubmed-article:11007485 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:11007485 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:11007485 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
pubmed-article:11007485 | lifeskim:mentions | umls-concept:C0243067 | lld:lifeskim |
pubmed-article:11007485 | lifeskim:mentions | umls-concept:C0457405 | lld:lifeskim |
pubmed-article:11007485 | lifeskim:mentions | umls-concept:C2700061 | lld:lifeskim |
pubmed-article:11007485 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
pubmed-article:11007485 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:11007485 | pubmed:dateCreated | 2000-10-4 | lld:pubmed |
pubmed-article:11007485 | pubmed:abstractText | HF-1 b, an SP1 -related transcription factor, is preferentially expressed in the cardiac conduction system and ventricular myocytes in the heart. Mice deficient for HF-1 b survive to term and exhibit normal cardiac structure and function but display sudden cardiac death and a complete penetrance of conduction system defects, including spontaneous ventricular tachycardia and a high incidence of AV block. Continuous electrocardiographic recordings clearly documented cardiac arrhythmogenesis as the cause of death. Single-cell analysis revealed an anatomic substrate for arrhythmogenesis, including a decrease and mislocalization of connexins and a marked increase in action potential heterogeneity. Two independent markers reveal defects in the formation of ventricular Purkinje fibers. These studies identify a novel genetic pathway for sudden cardiac death via defects in the transition between ventricular and conduction system cell lineages. | lld:pubmed |
pubmed-article:11007485 | pubmed:language | eng | lld:pubmed |
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pubmed-article:11007485 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11007485 | pubmed:month | Sep | lld:pubmed |
pubmed-article:11007485 | pubmed:issn | 0092-8674 | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:ClarkR BRB | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:FellG SGS | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:FiserAA | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:ChienK RKR | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:KondoRR | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:GilesW RWR | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:WollertK CKC | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:GourdieR GRG | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:KubalakS WSW | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:BrownA BAB | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:MinamisawaSS | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:Ruiz-LozanoPP | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:RahmeM MMM | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:NormanL WLW | lld:pubmed |
pubmed-article:11007485 | pubmed:author | pubmed-author:Nguyên-TrânV... | lld:pubmed |
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pubmed-article:11007485 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11007485 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11007485 | pubmed:volume | 102 | lld:pubmed |
pubmed-article:11007485 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11007485 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11007485 | pubmed:pagination | 671-82 | lld:pubmed |
pubmed-article:11007485 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:11007485 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:11007485 | pubmed:articleTitle | A novel genetic pathway for sudden cardiac death via defects in the transition between ventricular and conduction system cell lineages. | lld:pubmed |
pubmed-article:11007485 | pubmed:affiliation | UCSD-Salk Program in Molecular Medicine and the UCSD Institute of Molecular Medicine, University of California, San Diego, La Jolla 92093, USA. | lld:pubmed |
pubmed-article:11007485 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11007485 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11007485 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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