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Título : Regulation of Inducible Nitric Oxide Synthase Expression by Viral A238L-Mediated Inhibition of p65/RelA Acetylation and p300 Transactivation
Autor : Granja, Aitor G.; Sabina, Prado; Salas, María Luisa; Fresno, Manuel; Revilla Novella, Yolanda
Palabras clave : Nitric-oxide synthase
A238L virus protein
Fecha de publicación : 2006
Editor: American Society for Microbiology
Citación : Journal of Virology, p. 10487-10496, Vol. 80, No. 21
Resumen: Uncontrolled generation of nitric oxide (NO) by inducible nitric-oxide synthase (iNOS) can cause damage to host cells and inflammation, two undesirable events for virus spreading. African swine fever virus (ASFV) infection regulates iNOS-induced gene expression through the synthesis of the A238L virus protein. We here explored the role of A238L, an NF-B and NFAT inhibitor, in the regulation of iNOS transcription in macrophages. NO production and iNOS mRNA and protein levels as well as iNOS promoter activity after lipopolysaccharide (LPS)-gamma interferon (IFN-) treatment were down-regulated both during ASFV infection and in Raw 264.7 cells stably expressing the viral protein. Overexpression of p300, but not of a histone acetyltransferase (HAT) defective mutant, reverted the A238L-mediated inhibition of both basal and LPS-IFN--induced iNOS promoter activity. Following stimulation with LPS-IFN-, p65 and p300 interaction was abolished in Raw-A238L cells. Expression of A238L also inhibited p65/relA and p300 binding to the distal NF-B sequence of the iNOS promoter together with p65 acetylation. Finally, A238L abrogated p300 transactivation mediated by a GAL4-p300 construction. These results provide evidence for an unique viral mechanism involved in transcriptional regulation of iNOS gene expression
Versión del editor: http://dx.doi.org/10.1128/JVI.00862-06
URI : http://hdl.handle.net/10261/8027
DOI: 10.1128/JVI.00862-06
ISSN: 0022-538X (print)
1098-5514 (online)
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