| pubmed-article:11369778 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11369778 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:11369778 | lifeskim:mentions | umls-concept:C0018801 | lld:lifeskim |
| pubmed-article:11369778 | lifeskim:mentions | umls-concept:C0003811 | lld:lifeskim |
| pubmed-article:11369778 | lifeskim:mentions | umls-concept:C0037492 | lld:lifeskim |
| pubmed-article:11369778 | lifeskim:mentions | umls-concept:C1414672 | lld:lifeskim |
| pubmed-article:11369778 | pubmed:issue | 30 | lld:pubmed |
| pubmed-article:11369778 | pubmed:dateCreated | 2001-7-23 | lld:pubmed |
| pubmed-article:11369778 | pubmed:abstractText | We investigated the cellular and molecular mechanisms underlying arrhythmias in heart failure. A genetically engineered mouse lacking the expression of the muscle LIM protein (MLP-/-) was used in this study as a model of heart failure. We used electrocardiography and patch clamp techniques to examine the electrophysiological properties of MLP-/- hearts. We found that MLP-/- myocytes had smaller Na+ currents with altered voltage dependencies of activation and inactivation and slower rates of inactivation than control myocytes. These changes in Na+ currents contributed to longer action potentials and to a higher probability of early afterdepolarizations in MLP-/- than in control myocytes. Western blot analysis suggested that the smaller Na+ current in MLP-/- myocytes resulted from a reduction in Na+ channel protein. Interestingly, the blots also revealed that the alpha-subunit of the Na+ channel from the MLP-/- heart had a lower average molecular weight than in the control heart. Treating control myocytes with the sialidase neuraminidase mimicked the changes in voltage dependence and rate of inactivation of Na+ currents observed in MLP-/- myocytes. Neuraminidase had no effect on MLP-/- cells thus suggesting that Na+ channels in these cells were sialic acid-deficient. We conclude that deficient glycosylation of Na+ channel contributes to Na+ current-dependent arrhythmogenesis in heart failure. | lld:pubmed |
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| pubmed-article:11369778 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11369778 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11369778 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11369778 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11369778 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11369778 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11369778 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11369778 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11369778 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:11369778 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:11369778 | pubmed:author | pubmed-author:LedererW JWJ | lld:pubmed |
| pubmed-article:11369778 | pubmed:author | pubmed-author:SantanaL FLF | lld:pubmed |
| pubmed-article:11369778 | pubmed:author | pubmed-author:RockmanH AHA | lld:pubmed |
| pubmed-article:11369778 | pubmed:author | pubmed-author:BaroD JDJ | lld:pubmed |
| pubmed-article:11369778 | pubmed:author | pubmed-author:Ufret-Vincent... | lld:pubmed |
| pubmed-article:11369778 | pubmed:author | pubmed-author:QuinonesL ELE | lld:pubmed |
| pubmed-article:11369778 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11369778 | pubmed:day | 27 | lld:pubmed |
| pubmed-article:11369778 | pubmed:volume | 276 | lld:pubmed |
| pubmed-article:11369778 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11369778 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11369778 | pubmed:pagination | 28197-203 | lld:pubmed |
| pubmed-article:11369778 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:11369778 | pubmed:meshHeading | pubmed-meshheading:11369778... | lld:pubmed |
| pubmed-article:11369778 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11369778 | pubmed:articleTitle | Role of sodium channel deglycosylation in the genesis of cardiac arrhythmias in heart failure. | lld:pubmed |
| pubmed-article:11369778 | pubmed:affiliation | Institute of Neurobiology, University of Puerto Rico, San Juan, Puerto Rico 00901, USA. | lld:pubmed |
| pubmed-article:11369778 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11369778 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11369778 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| entrez-gene:13009 | entrezgene:pubmed | pubmed-article:11369778 | lld:entrezgene |
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