rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2011-1-24
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pubmed:abstractText |
Genetic studies have shown that many slow cardiac myosin regulatory light chain 2 (MYL2) gene mutations can cause hypertrophic cardiomyopathy, which is one of the most common causes of heart failure (HF). But until now there has been no pathological or histological evidence that MYL2 may be associated with HF development. Recent microarray studies indicated that myosin heavy chain expression changed in the pathological process of HF. Because MYL2 is a regulatory component of myosin heavy polypeptide, the role of MYL2 protein in HF needs to be studied.
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pubmed:commentsCorrections |
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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 |
Jan
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pubmed:issn |
1932-8737
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pubmed:author |
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pubmed:copyrightInfo |
Copyright © 2010 Wiley Periodicals, Inc.
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pubmed:issnType |
Electronic
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pubmed:volume |
34
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
30-4
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pubmed:meshHeading |
pubmed-meshheading:21259275-Adolescent,
pubmed-meshheading:21259275-Adult,
pubmed-meshheading:21259275-Aged,
pubmed-meshheading:21259275-Blotting, Western,
pubmed-meshheading:21259275-Case-Control Studies,
pubmed-meshheading:21259275-Chronic Disease,
pubmed-meshheading:21259275-Down-Regulation,
pubmed-meshheading:21259275-Female,
pubmed-meshheading:21259275-Heart Failure,
pubmed-meshheading:21259275-Humans,
pubmed-meshheading:21259275-Immunohistochemistry,
pubmed-meshheading:21259275-Male,
pubmed-meshheading:21259275-Middle Aged,
pubmed-meshheading:21259275-Myocardium,
pubmed-meshheading:21259275-Myosin Light Chains,
pubmed-meshheading:21259275-Severity of Illness Index
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pubmed:year |
2011
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pubmed:articleTitle |
Slow cardiac myosin regulatory light chain 2 (MYL2) was down-expressed in chronic heart failure patients.
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pubmed:affiliation |
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
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pubmed:publicationType |
Journal Article,
Comment
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