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Dengue virus disrupts Daxx and NF-κB interaction to induce CD137-mediated apoptosis.
Dengue virus disrupts Daxx and NF-κB interaction to induce CD137-mediated apoptosis.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2014 Aug 08; Vol. 450 (4), pp. 1485-91. Date of Electronic Publication: 2014 Jul 11. - Publication Year :
- 2014
-
Abstract
- Dengue virus (DENV) is a positive-strand RNA virus of the Flavivirus family with 4 different serotypes. Clinical manifestations of DENV infection include dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. Following DENV infection, apoptosis of hepatic cells is observed both in vitro and in vivo. However, the molecular mechanisms revealing how viral components affect cellular apoptosis remain unclear. In the present study, the role of death domain-associated protein 6 (Daxx) in DENV-mediated apoptosis was characterized by RNA interference and overexpression studies, and the anti-apoptotic function of Daxx during DENV infection was identified. Furthermore, the viral component, DENV capsid protein (DENV C), interacted with Daxx to disrupt interaction between Daxx and NF-κB. The liberated NF-κB activated the promoter of CD137, which is a member of the TNF family, and is previously shown to induce apoptosis during DENV infection. In summary, DENV C disrupts Daxx and NF-κB interaction to induce CD137-mediated apoptosis during DENV infection.<br /> (Copyright © 2014 Elsevier Inc. All rights reserved.)
- Subjects :
- Base Sequence
Co-Repressor Proteins
DNA Primers
Hep G2 Cells
Humans
Molecular Chaperones
Polymerase Chain Reaction
Protein Binding
Adaptor Proteins, Signal Transducing metabolism
Apoptosis physiology
Dengue Virus physiology
NF-kappa B metabolism
Nuclear Proteins metabolism
Tumor Necrosis Factor Receptor Superfamily, Member 9 physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 450
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 25019989
- Full Text :
- https://doi.org/10.1016/j.bbrc.2014.07.016