Hepatitis B Virus e Antigen Physically Associates With Receptor-Interacting Serine/Threonine Protein Kinase 2 and Regulates IL-6 Gene Expression.

Détails

Ressource 1Télécharger: serval:BIB_98603AB7AD12.P001 (271.45 [Ko])
Etat: Public
Version: de l'auteur
Licence: Non spécifiée
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ID Serval
serval:BIB_98603AB7AD12
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Hepatitis B Virus e Antigen Physically Associates With Receptor-Interacting Serine/Threonine Protein Kinase 2 and Regulates IL-6 Gene Expression.
Périodique
Journal of Infectious Diseases
Auteur(s)
Wu S., Kanda T., Imazeki F., Nakamoto S., Tanaka T., Arai M., Roger T., Shirasawa H., Nomura F., Yokosuka O.
ISSN
1537-6613 (Electronic)
ISSN-L
0022-1899
Statut éditorial
Publié
Date de publication
2012
Volume
206
Numéro
3
Pages
415-420
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
We previously reported that hepatitis B virus (HBV) e antigen (HBeAg) inhibits production of interleukin 6 by suppressing NF-κB activation. NF-κB is known to be activated through receptor-interacting serine/threonine protein kinase 2 (RIPK2), and we examined the mechanisms of interleukin 6 regulation by HBeAg. HBeAg inhibits RIPK2 expression and interacts with RIPK2, which may represent 2 mechanisms through which HBeAg blocks nucleotide-binding oligomerization domain-containing protein 1 ligand-induced NF-κB activation in HepG2 cells. Our findings identified novel molecular mechanisms whereby HBeAg modulates intracellular signaling pathways by targeting RIPK2, supporting the concept that HBeAg could impair both innate and adaptive immune responses to promote chronic HBV infection.
Pubmed
Web of science
Open Access
Oui
Création de la notice
18/08/2012 10:58
Dernière modification de la notice
25/09/2019 7:10
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