pubmed-article:19684871 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19684871 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
pubmed-article:19684871 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:19684871 | lifeskim:mentions | umls-concept:C0037492 | lld:lifeskim |
pubmed-article:19684871 | lifeskim:mentions | umls-concept:C0039082 | lld:lifeskim |
pubmed-article:19684871 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
pubmed-article:19684871 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:19684871 | pubmed:dateCreated | 2009-10-7 | lld:pubmed |
pubmed-article:19684871 | pubmed:abstractText | Long-QT syndrome (LQTS) is an inherited disorder associated with sudden cardiac death. The cytoskeletal protein syntrophin-alpha(1) (SNTA1) is known to interact with the cardiac sodium channel (hNa(v)1.5), and we hypothesized that SNTA1 mutations might cause phenotypic LQTS in patients with genotypically normal hNa(v)1.5 by secondarily disturbing sodium channel function. | lld:pubmed |
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pubmed-article:19684871 | pubmed:language | eng | lld:pubmed |
pubmed-article:19684871 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19684871 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:19684871 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19684871 | pubmed:month | Aug | lld:pubmed |
pubmed-article:19684871 | pubmed:issn | 1941-3084 | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:ChengJieJ | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:ShimizuWataru... | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:MossArthur... | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:VattaMatteoM | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:TowbinJeffrey... | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:QiMingM | lld:pubmed |
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pubmed-article:19684871 | pubmed:author | pubmed-author:MohapatraBhag... | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:YutaoXiX | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:GeruWuW | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:PurevjavEnkhs... | lld:pubmed |
pubmed-article:19684871 | pubmed:author | pubmed-author:SamaniKavehK | lld:pubmed |
pubmed-article:19684871 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19684871 | pubmed:volume | 1 | lld:pubmed |
pubmed-article:19684871 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19684871 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19684871 | pubmed:pagination | 193-201 | lld:pubmed |
pubmed-article:19684871 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:19684871 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:19684871 | pubmed:articleTitle | alpha-1-syntrophin mutation and the long-QT syndrome: a disease of sodium channel disruption. | lld:pubmed |
pubmed-article:19684871 | pubmed:affiliation | Electrophysiology Research Laboratory, Texas Heart Institute/St. Luke's Episcopal Hospital, Houston, Texas, USA. | lld:pubmed |