16129800

Source:http://linkedlifedata.com/resource/pubmed/id/16129800

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0018270, umls-concept:C0018787, umls-concept:C0033095, umls-concept:C0033414, umls-concept:C0162638, umls-concept:C0302600, umls-concept:C0333959
pubmed:issue	10
pubmed:dateCreated	2005-9-7
pubmed:abstractText	The Jun family of activator protein 1 (AP-1) transcription factors (c-Jun, JunB, and JunD) is involved in fundamental biological processes such as proliferation, apoptosis, tumor angiogenesis, and hypertrophy. The role of individual AP-1 transcription factors in the stressed heart is not clear. In the present study we analyzed the role of JunD in survival, hypertrophy, and angiogenesis in the pressure-overloaded mouse heart after thoracic aortic constriction.
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/0147763
pubmed:citationSubset	AIM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A
pubmed:status	MEDLINE
pubmed:month	Sep
pubmed:issn	1524-4539
pubmed:author	pubmed-author:DrexlerHelmutH, pubmed-author:Hilfiker-KleinerDeniseD, pubmed-author:HilfikerAndresA, pubmed-author:KaminskiKarolK, pubmed-author:MichelKimK, pubmed-author:ParkJoon-KeunJK, pubmed-author:QuintAnjaA, pubmed-author:SchaeferArndA, pubmed-author:WeitzmanJonathan BJB, pubmed-author:YanivMosheM
pubmed:issnType	Electronic
pubmed:day	6
pubmed:volume	112
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	1470-7
pubmed:dateRevised	2006-11-15
pubmed:meshHeading	pubmed-meshheading:16129800-Adult, pubmed-meshheading:16129800-Animals, pubmed-meshheading:16129800-Apoptosis, pubmed-meshheading:16129800-Capillaries, pubmed-meshheading:16129800-Cardiomegaly, pubmed-meshheading:16129800-Cardiomyopathy, Dilated, pubmed-meshheading:16129800-Humans, pubmed-meshheading:16129800-Lac Operon, pubmed-meshheading:16129800-Male, pubmed-meshheading:16129800-Mice, pubmed-meshheading:16129800-Mice, Inbred Strains, pubmed-meshheading:16129800-Mice, Knockout, pubmed-meshheading:16129800-Mice, Transgenic, pubmed-meshheading:16129800-Middle Aged, pubmed-meshheading:16129800-Myocytes, Cardiac, pubmed-meshheading:16129800-Neovascularization, Pathologic, pubmed-meshheading:16129800-Phenotype, pubmed-meshheading:16129800-Proto-Oncogene Proteins c-jun, pubmed-meshheading:16129800-Tumor Suppressor Protein p53, pubmed-meshheading:16129800-Vascular Endothelial Growth Factor A, pubmed-meshheading:16129800-Ventricular Pressure
pubmed:year	2005
pubmed:articleTitle	Lack of JunD promotes pressure overload-induced apoptosis, hypertrophic growth, and angiogenesis in the heart.
pubmed:affiliation	Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany. hilfiker.denise@mh-hannover.de
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't