Document Detail

IKKε modulates RSV-induced NF-κB-dependent gene transcription.
MedLine Citation:
PMID:  20961594     Owner:  NLM     Status:  MEDLINE    
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-κB (NF-κB). In this study we have investigated the role of the non canonical IκB kinase (IKK)ε in modulating RSV-induced NF-κB activation. Our results show that inhibition of IKKε activation results in significant impairment of viral-induced NF-κB-dependent gene expression, through a reduction in NF-κB transcriptional activity, without changes in nuclear translocation or DNA-binding activity. Absence of IKKε results in a significant decrease of RSV-induced NF-κB phosphorylation on serine 536, a post-translational modification important for RSV-induced NF-κB-dependent gene expression, known to regulate NF-κB transcriptional activity without affecting nuclear translocation. This study identifies a novel mechanism by which IKKε regulates viral-induced cellular signaling.
Xiaoyong Bao; Hemalatha Indukuri; Tianshuang Liu; Sui-Ling Liao; Bing Tian; Allan R Brasier; Roberto P Garofalo; Antonella Casola
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-18
Journal Detail:
Title:  Virology     Volume:  408     ISSN:  1096-0341     ISO Abbreviation:  Virology     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-08     Completed Date:  2010-12-06     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  0110674     Medline TA:  Virology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  224-31     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Department of Pediatrics, University of Texas Medical Branch, Galveston, TX, USA.
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MeSH Terms
Cell Line
I-kappa B Kinase / deficiency,  genetics,  metabolism*
Interleukin-8 / biosynthesis,  genetics
Mice, Knockout
NF-kappa B / metabolism*
RNA Interference
Respiratory Syncytial Virus Infections / genetics,  metabolism,  virology
Respiratory Syncytial Viruses / pathogenicity*
Transcription Factor RelA / metabolism
Transcription, Genetic*
Grant Support
06676//PHS HHS; P01 062885//PHS HHS; P01 AI062885/AI/NIAID NIH HHS; P01 AI062885-050003/AI/NIAID NIH HHS
Reg. No./Substance:
0/IL8 protein, human; 0/Interleukin-8; 0/NF-kappa B; 0/RELA protein, human; 0/Transcription Factor RelA; EC B Kinase

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