Linked Life Data

11375269

Source:http://linkedlifedata.com/resource/pubmed/id/11375269

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2001-5-25
pubmed:abstractText
Expression of adenoviral E1A in cardiomyocytes results in the activation of DNA synthesis followed by apoptosis. In contrast, expression of simian virus 40 large T antigen induces sustained cardiomyocyte proliferation. Previous studies have shown that T antigen binds to 2 proapoptotic proteins in cardiomyocytes, namely the p53 tumor suppressor and p193 (a new member of the BH3-only proapoptosis subfamily). Structure-function analyses identified a p193 C-terminal truncation mutant that encodes prosurvival activity. This mutant was used to test the role of p193 in E1A-induced cardiomyocyte apoptosis. E1A induced apoptosis in cardiomyocytes derived from differentiating embryonic stem cells. Expression of the prosurvival p193 mutant alone or a mutant p53 alone did not block E1A-induced apoptosis. In contrast, combinatorial expression of mutant p193 and mutant p53 blocked E1A-induced apoptosis, resulting in a proliferative response indistinguishable from that seen with T antigen. These results confirm the hypothesis that there are 2 proapoptotic pathways, encoded by p53 and p193, respectively, which restrict cardiomyocyte cell cycle activity in differentiating embryonic stem cell cultures. Furthermore, these results explain in molecular terms the phenotypic differences of E1A versus T-antigen gene transfer in cardiomyocytes.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
25
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1004-11
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11375269-3T3 Cells, pubmed-meshheading:11375269-Adenovirus E1A Proteins, pubmed-meshheading:11375269-Animals, pubmed-meshheading:11375269-Antigens, Viral, Tumor, pubmed-meshheading:11375269-Apoptosis, pubmed-meshheading:11375269-BH3 Interacting Domain Death Agonist Protein, pubmed-meshheading:11375269-Carrier Proteins, pubmed-meshheading:11375269-Cell Cycle, pubmed-meshheading:11375269-Cell Cycle Proteins, pubmed-meshheading:11375269-Cell Division, pubmed-meshheading:11375269-Cell Line, pubmed-meshheading:11375269-Cell Survival, pubmed-meshheading:11375269-Colony-Forming Units Assay, pubmed-meshheading:11375269-Gene Transfer Techniques, pubmed-meshheading:11375269-Mice, pubmed-meshheading:11375269-Mutation, pubmed-meshheading:11375269-Myocardium, pubmed-meshheading:11375269-Nuclear Proteins, pubmed-meshheading:11375269-Regeneration, pubmed-meshheading:11375269-Retinoblastoma-Like Protein p107, pubmed-meshheading:11375269-Signal Transduction, pubmed-meshheading:11375269-Stem Cells, pubmed-meshheading:11375269-Structure-Activity Relationship, pubmed-meshheading:11375269-Tumor Suppressor Protein p53
pubmed:year
2001
pubmed:articleTitle
Coexpression of mutant p53 and p193 renders embryonic stem cell-derived cardiomyocytes responsive to the growth-promoting activities of adenoviral E1A.
pubmed:affiliation
Wells Center for Pediatric Research and Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, IN, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.