Linked Life Data

11956070

Source:http://linkedlifedata.com/resource/pubmed/id/11956070

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2002-4-16
pubmed:abstractText
Apoptosis is a critical early cellular event in the development of polycystic kidney disease (PKD) in humans and mice. In the SBM transgenic model of PKD, both apoptosis and proliferation are c-myc driven and are independent of p53 and Bcl-2 pathways. On the basis of recent evidence implicating the FasL/Fas pathway in c-myc-induced apoptosis, we investigated the potential interaction of these pathways in vivo. We first evaluated the expression of FasL in renal tissues of SBM mice. This analysis showed that the level of FasL expression was elevated 3-4-fold in the SBM kidneys, indicating a potential autocrine suicidal mechanism. We next crossed the SBM mice with gld mice mutated in FasL. The progenies had comparable renal epithelial apoptotic and proliferation rates and a cystic phenotype in all SBM genotypes irrespective of the FasL genotype. Our study proves that c-myc-induced apoptosis can be independent of the FasL/Fas pathway in vivo and implicates the existence of a novel c-myc-driven apoptotic pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
62
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2210-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
c-myc-induced apoptosis in polycystic kidney disease is independent of FasL/Fas interaction.
pubmed:affiliation
Institut de Recherches Cliniques de Montréal, Faculté de Médecine de l'Université de Montréal, Montréal, Québec, H2W 1R7 Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't