| pubmed-article:17446472 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C0019904 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C1621574 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C2348693 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
| pubmed-article:17446472 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:17446472 | pubmed:dateCreated | 2007-4-20 | lld:pubmed |
| pubmed-article:17446472 | pubmed:abstractText | Mice with homozygous overexpression of the Na+-Ca2+ exchanger (NCX) exhibit threefold levels of NCX expression and an increased Ca2+ extrusion rate. To investigate how Ca2+ homeostasis is maintained in this model, we have characterized Ca2+ influx under these conditions. We find that L-type Ca2+ currents (I(Ca)) inactivate slower due to a reduction of Ca2+-dependent inactivation. Additionally, NCX-overexpressing animals exhibit a prolongation of the action potential (AP). We conclude that transsarcolemmal Ca2+ fluxes in NCX-overexpressing myocytes are balanced by an increase in Ca2+ influx via (a) slowed inactivation of I(Ca) and (b) a prolongation of the AP to compensate for increased Ca2+ efflux. | lld:pubmed |
| pubmed-article:17446472 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17446472 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17446472 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17446472 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17446472 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17446472 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17446472 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17446472 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17446472 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:17446472 | pubmed:issn | 0077-8923 | lld:pubmed |
| pubmed-article:17446472 | pubmed:author | pubmed-author:PhilipsonKenn... | lld:pubmed |
| pubmed-article:17446472 | pubmed:author | pubmed-author:GoldhaberJosh... | lld:pubmed |
| pubmed-article:17446472 | pubmed:author | pubmed-author:PottChristian... | lld:pubmed |
| pubmed-article:17446472 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17446472 | pubmed:volume | 1099 | lld:pubmed |
| pubmed-article:17446472 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17446472 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17446472 | pubmed:pagination | 310-4 | lld:pubmed |
| pubmed-article:17446472 | pubmed:dateRevised | 2007-12-3 | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:meshHeading | pubmed-meshheading:17446472... | lld:pubmed |
| pubmed-article:17446472 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17446472 | pubmed:articleTitle | Homozygous overexpression of the Na+-Ca2+ exchanger in mice: evidence for increased transsarcolemmal Ca2+ fluxes. | lld:pubmed |
| pubmed-article:17446472 | pubmed:affiliation | Department of Physiology, David Geffen School of Medicine at UCLA, 675 Charles E. Young Dr. South, Los Angeles, CA 90095, USA. | lld:pubmed |
| pubmed-article:17446472 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17446472 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17446472 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17446472 | lld:pubmed |
