ArticleProceedings of the National Academy of Sciences of the United States of America2002
Role of the E1A Rb-binding domain in repression of the NF-kappa B-dependent defense against tumor necrosis factor-alpha.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. 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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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Overview of the Trending Enteric Viruses and Their Pathogenesis in Intestinal Epithelial Cell Infection.Biomedicines · 2024Review
- Human adenovirus oncolytic properties and the inhibitory role of E4 orf4 and E4 orf6/7 on endogenously activated NF-κB.Biochemistry and biophysics reports · 2024Article
- Oncolytic Adenovirus, a New Treatment Strategy for Prostate Cancer.Biomedicines · 2022Review
- PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling.Nature communications · 2022Article
- Molecular mimicry of NF-κB by vaccinia virus protein enables selective inhibition of antiviral responses.Nature microbiology · 2022Article
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- Pathogenesis of Hypervirulent Fowl Adenovirus Serotype 4: The Contributions of Viral and Host Factors.Viruses · 2019Review
- E1A oncogene induced sensitization to NK cell induced apoptosis requires PIDD and Caspase-2.Cell death discovery · 2019Article
- A parapoxviral virion protein targets the retinoblastoma protein to inhibit NF-κB signaling.PLoS pathogens · 2017Article
- Expression of adenoviral E1A throws the PIDD switch.Cell death & disease · 2017Article
- Mechanisms of pathogenesis of emerging adenoviruses.F1000Research · 2017Review
- The Importance of Physiologically Relevant Cell Lines for Studying Virus-Host Interactions.Viruses · 2016Review
- The E1B19K-deleted oncolytic adenovirus mutant AdΔ19K sensitizes pancreatic cancer cells to drug-induced DNA-damage by down-regulating Claspin and Mre11.Oncotarget · 2016Article
- The RB tumor suppressor at the intersection of proliferation and immunity: relevance to disease immune evasion and immunotherapy.Cell cycle (Georgetown, Tex.) · 2015Review
- Herpes simplex virus 1 E3 ubiquitin ligase ICP0 protein inhibits tumor necrosis factor alpha-induced NF-κB activation by interacting with p65/RelA and p50/NF-κB1.Journal of virology · 2013Article
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- Nuclear factor-kappaB activation in neonatal mouse lung protects against lipopolysaccharide-induced inflammation.American journal of respiratory and critical care medicine · 2007Article
- Macrophages kill human papillomavirus type 16 E6-expressing tumor cells by tumor necrosis factor alpha- and nitric oxide-dependent mechanisms.Journal of virology · 2005Article
- Expression of an E1A/E7 chimeric protein sensitizes tumor cells to killing by activated macrophages but not NK cells.Journal of virology · 2004Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The adenoviral E1A oncogene sensitizes mammalian cells to tumor necrosis factor-alpha (TNF-alpha), in part by repressing the nuclear factor-kappa B (NF-kappa B)-dependent defense against this cytokine. Other E1A activities involve binding to either p300/cyclic AMP response element-binding protein (CBP) or retinoblastoma (Rb)-family proteins, but the roles of E1A interactions with these transcriptional regulators in sensitizing cells to TNF-alpha are unclear. E1A expression did not block upstream events in TNF-alpha-induced activation of NF-kappa B in NIH 3T3 cells, including degradation of I kappa B-alpha, nuclear translocation of NF-kappa B subunits, and their dimeric binding to kappa B sequences in the nucleus. However, E1A markedly repressed NF-kappa B-dependent transcription and sensitized cells to TNF-alpha induced apoptosis. These E1A effects were selective for kappa B-dependent transcription and for the function of the NF-kappa B p65/RelA subunit. A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis. In contrast, mutations that eliminate E1A binding to p300/CBP (coactivators of p65/RelA) did not affect either E1A activity. These data suggest that E1A-Rb-binding blocks the NF-kappa B-dependent activation response to TNF-alpha by altering the function of p65/RelA at a stage after formation of the transcription factor-enhancer complex. These observations also open questions about the general role of Rb-family proteins in modulation of NF-kappa B-dependent transcription.
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