Linked Life Data

9846183

Source:http://linkedlifedata.com/resource/pubmed/id/9846183

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1998-12-30
pubmed:abstractText
The v-Rel oncoprotein must be continuously expressed to prevent the apoptosis of transformed lymphoid cells, and also inhibits TNF alpha-induced cell death. A tetracycline-regulated cell system was used to characterize the functions necessary for the anti-apoptotic activity of Rel proteins. v-Rel mutants defective for DNA binding or transactivation showed no protective effect. Similarly, whereas the transcription-competent c-Rel and RelA proteins inhibited TNF alpha-induced cytolysis, the transactivation-negative p50/NF-kappa B1 did not. Importantly, this study is the first to show that c-Rel can also confer significant protection from Fas-mediated cell death. Since the TNFR1- and Fas-signaling pathways involve some intermediates that are common and others that are unique to each pathway, these findings indicate that c-Rel may regulate the expression of genes that function to antagonize either or both death-signaling pathways.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1350-9047
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
963-72
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Rel blocks both anti-Fas- and TNF alpha-induced apoptosis and an intact Rel transactivation domain is essential for this effect.
pubmed:affiliation
Center for Advanced Biotechnology and Medicine, Piscataway, New Jersey 08854-5638, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't