ArticleJournal of virology1997
Adenovirus E3-10.4K/14.5K protein complex inhibits tumor necrosis factor-induced translocation of cytosolic phospholipase A2 to membranes.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- miRNAs and Leukotrienes in Respiratory Syncytial Virus Infection.Frontiers in pediatrics · 2021Review
- CD36 protein is involved in store-operated calcium flux, phospholipase A2 activation, and production of prostaglandin E2.The Journal of biological chemistry · 2011Article
- Inhibition of Jak1-dependent signal transduction in airway epithelial cells infected with adenovirus.American journal of respiratory cell and molecular biology · 2007Article
- Transposon-assisted cloning and traceless mutagenesis of adenoviruses: Development of a novel vector based on species D.Journal of virology · 2006Article
- Mechanism for removal of tumor necrosis factor receptor 1 from the cell surface by the adenovirus RIDalpha/beta complex.Journal of virology · 2005Article
- Inhibition of tumor necrosis factor (TNF) signal transduction by the adenovirus group C RID complex involves downregulation of surface levels of TNF receptor 1.Journal of virology · 2004Article
- Adenovirus E3-6.7K protein is required in conjunction with the E3-RID protein complex for the internalization and degradation of TRAIL receptor 2.Journal of virology · 2004Article
- Distinct domains in the adenovirus E3 RIDalpha protein are required for degradation of Fas and the epidermal growth factor receptor.Journal of virology · 2003Article
- Adenovirus RIDbeta subunit contains a tyrosine residue that is critical for RID-mediated receptor internalization and inhibition of Fas- and TRAIL-induced apoptosis.Journal of virology · 2002Article
- Adenovirus E3-6.7K maintains calcium homeostasis and prevents apoptosis and arachidonic acid release.Journal of virology · 2002Article
- Molecular and epidemiological analyses of human adenovirus type 7 strains isolated from the 1995 nationwide outbreak in Japan.Journal of clinical microbiology · 2002Article
- Poliovirus protein 3A inhibits tumor necrosis factor (TNF)-induced apoptosis by eliminating the TNF receptor from the cell surface.Journal of virology · 2001Article
- Inhibition of TRAIL-induced apoptosis and forced internalization of TRAIL receptor 1 by adenovirus proteins.Journal of virology · 2001Article
- The genome of turkey herpesvirus.Journal of virology · 2001Article
- Replication-selective oncolytic adenoviruses: virotherapy aimed at genetic targets in cancer.Oncogene · 2000Review
- The genome of a very virulent Marek's disease virus.Journal of virology · 2000Article
- Replication-selective adenoviruses as oncolytic agents.The Journal of clinical investigation · 2000Review
- New developments in phospholipase A2.Lipids · 1999Review
- Ectopic expression of hepatitis C virus core protein differentially regulates nuclear transcription factors.Journal of virology · 1998Article
- Efficient, repeated adenovirus-mediated gene transfer in mice lacking both tumor necrosis factor alpha and lymphotoxin alpha.Journal of virology · 1998Article
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Authors and funding
6 authors.
Funding
Abstract
We have reported that three adenovirus (Ad) proteins, named E3-10.4K/14.5K, E3-14.7K, and E1B-19K, independently inhibit tumor necrosis factor (TNF)-induced apoptosis in Ad-infected cells. E3-10.4K/14.5K and E3-14.7K also inhibit TNF-induced release of arachidonic acid (AA). TNF-induced apoptosis and AA release are thought to require TNF-activation of the 85-kDa cytosolic phospholipase A2 (cPLA2). cPLA2 normally exists in a latent form in the cytosol; it is activated by phosphorylation by mitogen-activated protein kinase, and in the presence of agents that mobilize intracellular Ca2+, cPLA2 translocates to membranes where it cleaves AA from membrane phospholipids. We now report that TNF induces translocation of cPLA2 from the cytosol to membranes in Ad-infected human A549 cells and that E3-10.4K/14.5K but not E3-14.7K or E1B-19K is required to inhibit TNF-induced translocation of cPLA2. Ad infection also inhibited TNF-induced release of AA. Under the same conditions, Ad infection did not inhibit TNF-induced phosphorylation of cPLA2 or TNF activation of NFkappaB. Ad infection also inhibited cPLA2 translocation in response to the Ca2+ ionophore A23187 and to cycloheximide, but this inhibition did not require E3-10.4K/14.5K. Ad infection did not inhibit cPLA2 translocation in response to interleukin-1beta or platelet-derived growth factor. We propose that E3-10.4K/14.5K inhibits TNF-induced AA release and apoptosis by directly or indirectly inhibiting TNF-induced translocation of cPLA2 from the cytosol to membranes. AA formed by cPLA2 can be metabolized to prostaglandins, leukotrienes, and lipoxyns, molecules that amplify inflammation. E3-10.4K/14.5K probably functions in Ad infections to inhibit both TNF-induced apoptosis and inflammation.
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