Journal article
KLF6 and iNOS regulates apoptosis during respiratory syncytial virus infection
Cellular immunology, Vol.283(1-2), pp.1-7
05/2013
Handle:
https://hdl.handle.net/2376/103402
PMCID: PMC3744625
PMID: 23831683
Abstract
•Transactivation of iNOS gene by KLF6 during respiratory syncytial virus infection.•KLF6 is required for optimal apoptosis during respiratory syncytial virus infection.•iNOS/nitric oxide promotes apoptosis during respiratory syncytial virus infection.
Human respiratory syncytial virus (RSV) is a highly pathogenic lung-tropic virus that causes severe respiratory diseases. Enzymatic activity of inducible nitric oxide (iNOS) is required for NO generation. Although NO contributes to exaggerated lung disease during RSV infection, the role of NO in apoptosis during infection is not known. In addition, host trans-activator(s) required for iNOS gene expression during RSV infection is unknown. In the current study we have uncovered the mechanism of iNOS gene induction by identifying kruppel-like factor 6 (KLF6) as a critical transcription factor required for iNOS gene expression during RSV infection. Furthermore, we have also uncovered the role of iNOS as a critical host factor regulating apoptosis during RSV infection.
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Details
- Title
- KLF6 and iNOS regulates apoptosis during respiratory syncytial virus infection
- Creators
- Victoria MgbemenaJesus SegoviaTe-Hung ChangSantanu Bose
- Publication Details
- Cellular immunology, Vol.283(1-2), pp.1-7
- Academic Unit
- Veterinary Microbiology and Pathology, Department of
- Publisher
- Elsevier Inc
- Identifiers
- 99900546797801842
- Language
- English
- Resource Type
- Journal article