Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-10-5
pubmed:abstractText
E1A oncogene expression increases mammalian cell susceptibility to lysis by cytolytic lymphocytes (CLs) at a stage in this intercellular interaction that is independent of cell surface recognition events. Since CLs can induce either apoptotic or necrotic cell death, we asked whether E1A sensitization to injury-induced apoptosis is sufficient to explain E1A-induced cytolytic susceptibility. Mouse, rat, hamster, and human cells that were rendered cytolytic susceptible by E1A were also sensitized to CL-induced and chemically induced apoptosis. In contrast, E1A-positive cells were no more susceptible to injury-induced necrosis than E1A-negative cells. Similar to induction of cytolytic susceptibility and in contrast to other E1A activities, cellular sensitization to chemically induced apoptosis depended on high-level E1A oncoprotein expression. Loss of both cytolytic susceptibility and sensitization to chemically induced apoptosis was coselected during in vivo selection of E1A-positive sarcoma cells for increased tumorigenicity. Furthermore, E1A mutant proteins that cannot bind the cellular transcriptional coactivator, p300, and that fail to induce cytolytic susceptibility also failed to sensitize cells to injury-induced apoptosis. These data indicate that E1A induces susceptibility to killer cell-induced lysis through sensitization of cells to injury-induced apoptosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-4827
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
251
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
414-23
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10471326-3T3 Cells, pubmed-meshheading:10471326-Adenovirus E1A Proteins, pubmed-meshheading:10471326-Adenoviruses, Human, pubmed-meshheading:10471326-Animals, pubmed-meshheading:10471326-Anti-Bacterial Agents, pubmed-meshheading:10471326-Apoptosis, pubmed-meshheading:10471326-Cell Death, pubmed-meshheading:10471326-Cell Transformation, Viral, pubmed-meshheading:10471326-Cricetinae, pubmed-meshheading:10471326-Cytotoxicity, Immunologic, pubmed-meshheading:10471326-Depsipeptides, pubmed-meshheading:10471326-E1A-Associated p300 Protein, pubmed-meshheading:10471326-Humans, pubmed-meshheading:10471326-Killer Cells, Natural, pubmed-meshheading:10471326-Mice, pubmed-meshheading:10471326-Mutation, pubmed-meshheading:10471326-Necrosis, pubmed-meshheading:10471326-Nuclear Proteins, pubmed-meshheading:10471326-Peptides, pubmed-meshheading:10471326-Rats, pubmed-meshheading:10471326-Sarcoma, Experimental, pubmed-meshheading:10471326-Trans-Activators
pubmed:year
1999
pubmed:articleTitle
E1A oncogene induction of cellular susceptibility to killing by cytolytic lymphocytes through target cell sensitization to apoptotic injury.
pubmed:affiliation
College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.