http://www.cnr.it/ontology/cnr/individuo/prodotto/ID4649
Herpes Simplex virus disrupts NF-kB regulation by blocking its recruitment on the IkBa promoter and directing the factor on viral genes. (Articolo in rivista)
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- Herpes Simplex virus disrupts NF-kB regulation by blocking its recruitment on the IkBa promoter and directing the factor on viral genes. (Articolo in rivista) (literal)
- Anno
- 2006-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1074/jbc.M512366200 (literal)
- Alternative label
Amici C.(1)*; Rossi A.(2)*; Costanzo A.(3)*; Ciafre S.(2); Marinari M.(3); Balsamo M.(1); Levrero M.(4); Santoro M.G.(1,2) (2006)
Herpes Simplex virus disrupts NF-kB regulation by blocking its recruitment on the IkBa promoter and directing the factor on viral genes.
in The Journal of biological chemistry (Print)
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- Amici C.(1)*; Rossi A.(2)*; Costanzo A.(3)*; Ciafre S.(2); Marinari M.(3); Balsamo M.(1); Levrero M.(4); Santoro M.G.(1,2) (literal)
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- **These authors contributed equally
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- 1-Department of Biology University of Rome Tor Vergata, Via della Ricerca Scientifica, 00133 Rome, Italy;
2- Institute of Neurobiology and Molecular Medicine, CNR, 00133 Rome, Italy;
3-Department of Dermatology University of Rome Tor Vergata, Via della Ricerca Scientifica, 00133 Rome, Italy;
4- Department of Internal Medicine, University of Rome La Sapienza, 00185 Rome, Italy.
* These authors contributed equally to this work. (literal)
- Titolo
- Herpes Simplex virus disrupts NF-kB regulation by blocking its recruitment on the IkBa promoter and directing the factor on viral genes. (literal)
- Abstract
- Herpes simplex viruses (HSVs) are able to hijack the host-cell IkappaB kinase (IKK)/NF-kappaB pathway, which regulates critical cell functions from apoptosis to inflammatory responses; however, the molecular mechanisms involved and the outcome of the signaling dysregulation on the host-virus interaction are mostly unknown. Here we show that in human keratinocytes HSV-1 attains a sophisticated control of the IKK/NF-kappaB pathway, inducing two distinct temporally controlled waves of IKK activity and disrupting the NF-kappaB autoregulatory mechanism. Using chromatin immunoprecipitation we demonstrate that dysregulation of the NF-kappaB-response is mediated by a virus-induced block of NF-kappaB recruitment to the promoter of the IkappaBalpha gene, encoding the main NF-kappaB-inhibitor. We also show that HSV-1 redirects NF-kappaB recruitment to the promoter of ICP0, an immediate-early viral gene with a key role in promoting virus replication. The results reveal a new level of control of cellular functions by invading viruses and suggest that persistent NF-kappaB activation in HSV-1-infected cells, rather than being a host response to the virus, may play a positive role in promoting efficient viral replication. (literal)
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