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rdf:type |
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lifeskim:mentions |
umls-concept:C0018787,
umls-concept:C0020564,
umls-concept:C0205314,
umls-concept:C0225828,
umls-concept:C0442732,
umls-concept:C0449432,
umls-concept:C0679622,
umls-concept:C0684215,
umls-concept:C1179435,
umls-concept:C1524073,
umls-concept:C1548799,
umls-concept:C1566772,
umls-concept:C1705248
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pubmed:issue |
5
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pubmed:dateCreated |
2007-5-15
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pubmed:abstractText |
The intercalated disc (ID) of cardiac myocytes is emerging as a crucial structure in the heart. Loss of ID proteins like N-cadherin causes lethal cardiac abnormalities, and mutations in ID proteins cause human cardiomyopathy. A comprehensive screen for novel mechanisms in failing hearts demonstrated that expression of the lysosomal integral membrane protein 2 (LIMP-2) is increased in cardiac hypertrophy and heart failure in both rat and human myocardium. Complete loss of LIMP-2 in genetically engineered mice did not affect cardiac development; however, these LIMP-2 null mice failed to mount a hypertrophic response to increased blood pressure but developed cardiomyopathy. Disturbed cadherin localization in these hearts suggested that LIMP-2 has important functions outside lysosomes. Indeed, we also find LIMP-2 in the ID, where it associates with cadherin. RNAi-mediated knockdown of LIMP-2 decreases the binding of phosphorylated beta-catenin to cadherin, whereas overexpression of LIMP-2 has the opposite effect. Collectively, our data show that LIMP-2 is crucial to mount the adaptive hypertrophic response to cardiac loading. We demonstrate a novel role for LIMP-2 as an important mediator of the ID.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-10025662,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-10093046,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-10662767,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-10972294,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-11063735,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-11716909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-11950881,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-11972068,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-12554098,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-12620969,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-12628346,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-14993121,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-15284191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-15520318,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-16103240,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-16399138,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-16452123,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-16567567,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-16608515,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-16901941,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-8582267,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-8746204,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-8858175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-9015265,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-91593,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-9281442,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17485520-9478926
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1007
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pubmed:author |
pubmed-author:BertrandAnne TAT,
pubmed-author:DebetsJacques JJJ,
pubmed-author:DuistersRudy FRF,
pubmed-author:HøydalMorten AMA,
pubmed-author:HeymansStephaneS,
pubmed-author:JanssenBen JBJ,
pubmed-author:KubbenNardN,
pubmed-author:LeendersJoost JJJ,
pubmed-author:PintoYigal MYM,
pubmed-author:SaftigPaulP,
pubmed-author:SchellingsMark WMW,
pubmed-author:SchroenBlancheB,
pubmed-author:SchwakeMichaelM,
pubmed-author:van ErkArieA,
pubmed-author:van LeeuwenRick ERE,
pubmed-author:van LoonMirjamM
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pubmed:issnType |
Print
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pubmed:day |
14
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pubmed:volume |
204
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1227-35
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:17485520-Animals,
pubmed-meshheading:17485520-Antigens, CD36,
pubmed-meshheading:17485520-Aortic Valve Stenosis,
pubmed-meshheading:17485520-Cadherins,
pubmed-meshheading:17485520-Cardiomyopathy, Dilated,
pubmed-meshheading:17485520-DNA Primers,
pubmed-meshheading:17485520-Gene Expression Profiling,
pubmed-meshheading:17485520-Gene Expression Regulation,
pubmed-meshheading:17485520-Humans,
pubmed-meshheading:17485520-Hypertension,
pubmed-meshheading:17485520-Lysosome-Associated Membrane Glycoproteins,
pubmed-meshheading:17485520-Mice,
pubmed-meshheading:17485520-Mice, Knockout,
pubmed-meshheading:17485520-Myocytes, Cardiac,
pubmed-meshheading:17485520-RNA Interference,
pubmed-meshheading:17485520-Rats,
pubmed-meshheading:17485520-Rats, Sprague-Dawley,
pubmed-meshheading:17485520-beta Catenin
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pubmed:year |
2007
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pubmed:articleTitle |
Lysosomal integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte hypertrophy.
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pubmed:affiliation |
Department of Experimental and Molecular Cardiology, University of Maastricht, Maastricht, Netherlands.
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