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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2002-5-28
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pubmed:abstractText |
Chronic rejection in cardiac allografts depletes vascular smooth muscle (VSM) alpha-actin from the coronary arterial smooth muscle bed while promoting its abnormal accumulation in cardiomyocytes and myofibroblasts. The objective was to determine if the newly discovered TEF1, MSY1, Puralpha and Purbeta VSM alpha-actin transcriptional reprogramming proteins (TRPs) were associated with development of chronic rejection histopathology in accepted murine cardiac allografts.
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pubmed:grant |
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Genetic Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nsep1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Elongation Factor 1,
http://linkedlifedata.com/resource/pubmed/chemical/Pura protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Purb protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0008-6363
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
539-48
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12031699-Actins,
pubmed-meshheading:12031699-Animals,
pubmed-meshheading:12031699-Chronic Disease,
pubmed-meshheading:12031699-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:12031699-DNA,
pubmed-meshheading:12031699-DNA-Binding Proteins,
pubmed-meshheading:12031699-Female,
pubmed-meshheading:12031699-Fibrosis,
pubmed-meshheading:12031699-Gene Expression,
pubmed-meshheading:12031699-Genes, Regulator,
pubmed-meshheading:12031699-Genetic Markers,
pubmed-meshheading:12031699-Graft Rejection,
pubmed-meshheading:12031699-Heart Transplantation,
pubmed-meshheading:12031699-Mice,
pubmed-meshheading:12031699-Mice, Inbred C57BL,
pubmed-meshheading:12031699-Mice, Inbred DBA,
pubmed-meshheading:12031699-Mice, Inbred Strains,
pubmed-meshheading:12031699-Models, Animal,
pubmed-meshheading:12031699-Muscle, Smooth, Vascular,
pubmed-meshheading:12031699-Myocardium,
pubmed-meshheading:12031699-Nerve Tissue Proteins,
pubmed-meshheading:12031699-Peptide Elongation Factor 1,
pubmed-meshheading:12031699-Time Factors,
pubmed-meshheading:12031699-Transcription, Genetic,
pubmed-meshheading:12031699-Transcription Factors,
pubmed-meshheading:12031699-Transplantation, Homologous
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pubmed:year |
2002
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pubmed:articleTitle |
Reprogramming of vascular smooth muscle alpha-actin gene expression as an early indicator of dysfunctional remodeling following heart transplant.
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pubmed:affiliation |
Department of Physiology and Cell Biology and the Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University College of Medicine and Public Health, Columbus, OH 43210, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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