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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2009-11-6
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pubmed:abstractText |
Genetic mutations in a number of putative glycosyltransferases lead to the loss of glycosylation of dystroglycan and loss of its laminin-binding activity in genetic forms of human muscular dystrophy. Human patients and glycosylation defective myd mice develop cardiomyopathy with loss of dystroglycan matrix receptor function in both striated and smooth muscle.
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pubmed:grant |
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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 |
Nov
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pubmed:issn |
1524-4571
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
6
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pubmed:volume |
105
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
984-93
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pubmed:dateRevised |
2011-5-5
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pubmed:meshHeading |
pubmed-meshheading:19797173-Animals,
pubmed-meshheading:19797173-Cardiomyopathies,
pubmed-meshheading:19797173-Cell Membrane,
pubmed-meshheading:19797173-Dystroglycans,
pubmed-meshheading:19797173-Glycosylation,
pubmed-meshheading:19797173-Glycosyltransferases,
pubmed-meshheading:19797173-Heart Ventricles,
pubmed-meshheading:19797173-Humans,
pubmed-meshheading:19797173-Mice,
pubmed-meshheading:19797173-Mice, Transgenic,
pubmed-meshheading:19797173-Muscle, Skeletal,
pubmed-meshheading:19797173-Muscle, Smooth,
pubmed-meshheading:19797173-Muscular Dystrophies,
pubmed-meshheading:19797173-Mutation,
pubmed-meshheading:19797173-Myocardium,
pubmed-meshheading:19797173-Myocytes, Cardiac
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pubmed:year |
2009
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pubmed:articleTitle |
Dystroglycan matrix receptor function in cardiac myocytes is important for limiting activity-induced myocardial damage.
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pubmed:affiliation |
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-0622, USA. dmichele@umich.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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