IKK{epsilon} modulates RSV-induced NF-{kappa}B-dependent gene transcription
- Department of Pediatrics, University of Texas Medical Branch, Galveston, TX (United States)
- Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX (United States)
Respiratory syncytial virus (RSV), a negative-strand RNA virus, is the most common cause of epidemic respiratory disease in infants and young children. RSV infection of airway epithelial cells induces the expression of immune/inflammatory genes through the activation of a subset of transcription factors, including Nuclear Factor-{kappa}B (NF-{kappa}B). In this study we have investigated the role of the non canonical I{kappa}B kinase (IKK){epsilon} in modulating RSV-induced NF-{kappa}B activation. Our results show that inhibition of IKK{epsilon} activation results in significant impairment of viral-induced NF-{kappa}B-dependent gene expression, through a reduction in NF-{kappa}B transcriptional activity, without changes in nuclear translocation or DNA-binding activity. Absence of IKK{epsilon} results in a significant decrease of RSV-induced NF-{kappa}B phosphorylation on serine 536, a post-translational modification important for RSV-induced NF-{kappa}B-dependent gene expression, known to regulate NF-{kappa}B transcriptional activity without affecting nuclear translocation. This study identifies a novel mechanism by which IKK{epsilon} regulates viral-induced cellular signaling.
- OSTI ID:
- 21486910
- Journal Information:
- Virology, Journal Name: Virology Journal Issue: 2 Vol. 408; ISSN VIRLAX; ISSN 0042-6822
- Country of Publication:
- United States
- Language:
- English
Similar Records
Respiratory syncytial virus M2-1 protein induces the activation of nuclear factor kappa B
Ikkepsilon regulates viral-induced interferon regulatory factor-3 activation via a redox-sensitive pathway
Related Subjects
AGE GROUPS
ANIMALS
CHEMICAL REACTIONS
CHILDREN
DISEASES
DNA
GENES
INFANTS
INFLAMMATION
MAMMALS
MAN
MICROORGANISMS
NUCLEIC ACIDS
ORGANIC COMPOUNDS
PARASITES
PATHOLOGICAL CHANGES
PHOSPHORYLATION
PRIMATES
PROTEINS
RESPIRATORY SYSTEM DISEASES
RNA
SYMPTOMS
TRANSCRIPTION
TRANSCRIPTION FACTORS
TRANSLOCATION
VERTEBRATES
VIRUSES