ArticleJournal of virology1996
Induction of susceptibility to tumor necrosis factor by E1A is dependent on binding to either p300 or p105-Rb and induction of DNA synthesis.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 77 citations in OpenAlex.
- Adenovirus E1B-55K interferes with cellular IκB kinase complex subunit proteins.Frontiers in immunology · 2025Article
- E1A oncogene expression inhibits PTHrP P3 promoter activity and sensitizes human prostate cancer cells to TNF-induced apoptosis.International urology and nephrology · 2010Article
- Potent anti-tumor effects of a dual specific oncolytic adenovirus expressing apoptin in vitro and in vivo.Molecular cancer · 2010Article
- Intrinsic structural disorder in adenovirus E1A: a viral molecular hub linking multiple diverse processes.Journal of virology · 2008Review
- Involvement of Bcl-X(L) deamidation in E1A-mediated cisplatin sensitization of ovarian cancer cells.Oncogene · 2006Article
- The human papillomavirus 16 E6 protein can either protect or further sensitize cells to TNF: effect of dose.Cell death and differentiation · 2005Article
- Regulation of the activity of p38 mitogen-activated protein kinase by Akt in cancer and adenoviral protein E1A-mediated sensitization to apoptosis.Molecular and cellular biology · 2003Article
- E1A sensitizes cells to tumor necrosis factor alpha by downregulating c-FLIP S.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
- Ceramide does not act as a general second messenger for ultraviolet-induced apoptosis.Oncogene · 2002Article
- Review
- Replication-selective oncolytic adenoviruses: virotherapy aimed at genetic targets in cancer.Oncogene · 2000Review
- Induction of p53-independent apoptosis by the adenovirus E4orf4 protein requires binding to the Balpha subunit of protein phosphatase 2A.Journal of virology · 2000Article
- Article
- Replication-selective adenoviruses as oncolytic agents.The Journal of clinical investigation · 2000Review
- Suppression of E1A-mediated transformation by the p50E4F transcription factor.Molecular and cellular biology · 1999Article
- Adenovirus E3-10.4K/14.5K protein complex inhibits tumor necrosis factor-induced translocation of cytosolic phospholipase A2 to membranes.Journal of virology · 1997Article
- Altered susceptibility to tumor necrosis factor alpha-induced apoptosis of mouse cells expressing polyomavirus middle and small T antigens.Journal of virology · 1997Article
- The activity of cytosolic phospholipase A2 is required for the lysis of adenovirus-infected cells by tumor necrosis factor.Journal of virology · 1996Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The introduction of the adenovirus early region 1A (E1A) gene products into normal cells sensitizes these cells to the cytotoxic effects of tumor necrosis factor (TNF). Previous studies have shown that the region of E1A responsible for susceptibility is CR1, a conserved region within E1A which binds the cellular proteins p300 and p105-Rb at nonoverlapping sites. Binding of these and other cellular proteins by E1A results in the induction of E1A-associated activities such as transformation, immortalization, DNA synthesis, and apoptosis. To investigate the mechanism by which E1A induces susceptibility to TNF, the NIH 3T3 mouse fibroblast cell line was infected with viruses containing mutations within E1A which abrogate binding of some or all of the cellular proteins to E1A. The results show that TNF susceptibility is induced by E1A binding to either p300 or p105-Rb. E1A mutants that bind neither p300 nor p105-Rb do not induce susceptibility to TNF. Experiments with stable cell lines created by transfection with either wild-type or mutant E1A lead to these same conclusions. In addition, a correlation between induction of DNA synthesis and induction of TNF sensitivity is seen. Only viruses which induce DNA synthesis can induce TNF sensitivity. Those viruses which do not induce DNA synthesis also do not induce TNF sensitivity. These data suggest that the mechanisms underlying induction of susceptibility to TNF by E1A are intimately connected to E1A's capacity to override cell cycle controls.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.