ArticleJournal of virology1991
The amino-terminal portion of CD1 of the adenovirus E1A proteins is required to induce susceptibility to tumor necrosis factor cytolysis in adenovirus-infected mouse cells.
Article in Journal of virology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Biographical Feature: William S. M. Wold, Ph.D., 1944-2021.Journal of virology · 2021Article
- Role of Bax in death of uninfected retinal cells during murine cytomegalovirus retinitis.Investigative ophthalmology & visual science · 2014Article
- Human adenovirus type 37 and the BALB/c mouse: progress toward a restricted adenovirus keratitis model (an American Ophthalmological Society thesis).Transactions of the American Ophthalmological Society · 2006Article
- The human papillomavirus 16 E6 protein can either protect or further sensitize cells to TNF: effect of dose.Cell death and differentiation · 2005Article
- Induction of caspase-dependent apoptosis in cultured rat oligodendrocytes by murine coronavirus is mediated during cell entry and does not require virus replication.Journal of virology · 2003Article
- The adenovirus e3 promoter is sensitive to activation signals in human T cells.Journal of virology · 2003Article
- Role of the E1A Rb-binding domain in repression of the NF-kappa B-dependent defense against tumor necrosis factor-alpha.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- New hope for an AIDS vaccine.Nature reviews. Immunology · 2002Review
- Review
- Induction of p53-independent apoptosis by the adenovirus E4orf4 protein requires binding to the Balpha subunit of protein phosphatase 2A.Journal of virology · 2000Article
- The role of mouse adenovirus type 1 early region 1A in acute and persistent infections in mice.Journal of virology · 1998Article
- Database of mutations within the adenovirus 5 E1A oncogene.Nucleic acids research · 1998Article
- Induction of TNF-sensitive cellular phenotype by c-Myc involves p53 and impaired NF-kappaB activation.The EMBO journal · 1997Article
- The activity of cytosolic phospholipase A2 is required for the lysis of adenovirus-infected cells by tumor necrosis factor.Journal of virology · 1996Article
- Role of p300-family proteins in E1A oncogene induction of cytolytic susceptibility and tumor cell rejection.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- The adenovirus E3-14.7K protein and the E3-10.4K/14.5K complex of proteins, which independently inhibit tumor necrosis factor (TNF)-induced apoptosis, also independently inhibit TNF-induced release of arachidonic acid.Journal of virology · 1996Article
- The adenovirus death protein (E3-11.6K) is required at very late stages of infection for efficient cell lysis and release of adenovirus from infected cells.Journal of virology · 1996Article
- Induction of susceptibility to tumor necrosis factor by E1A is dependent on binding to either p300 or p105-Rb and induction of DNA synthesis.Journal of virology · 1996Article
- Prolonged survival of pancreatic islet allografts mediated by adenovirus immunoregulatory transgenes.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- c-Myc induces cellular susceptibility to the cytotoxic action of TNF-alpha.The EMBO journal · 1994Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous work by our laboratory and others has shown that mouse cells normally resistant to tumor necrosis factor can be made sensitive to the cytokine by the expression of adenovirus E1A. The E1A gene can be introduced by either infection or transfection, and either of the two major E1A proteins, 289R or 243R, can induce this sensitivity. The E1A proteins are multifunctional and modular, with specific domains associated with specific functions. Here, we report that the CD1 domain of E1A is required to induce susceptibility to tumor necrosis factor cytolysis in adenovirus-infected mouse C3HA fibroblasts. Amino acids C terminal to residue 60 and N terminal to residue 36 are not necessary for this function. This conclusion is based on 51Cr-release assays for cytolysis in cells infected with adenovirus mutants with deletions in various portions of E1A. These E1A mutants are all in an H5dl309 background and therefore they lack the tumor necrosis factor protection function provided by the 14.7-kilodalton (14.7K) protein encoded by region E3. Western blot (immunoblot) analysis indicated that most of the mutant E1A proteins were stable in infected C3HA cells, although with certain large deletions the E1A proteins were unstable. The region between residues 36 and 60 is included within but does not precisely correlate with domains in E1A that have been implicated in nuclear localization, enhancer repression, cellular immortalization, cell transformation in cooperation with ras, induction of cellular DNA synthesis and proliferation, induction of DNA degradation, and binding to the 300K protein and the 105K retinoblastoma protein.
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