Journal
CELLULAR IMMUNOLOGY
Volume 283, Issue 1-2, Pages 1-7Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2013.06.002
Keywords
Respiratory syncytial virus; Nitric oxide; Apoptosis; Transcription factor; Kruppel-like factor 6; Inducible nitric oxide synthase
Categories
Funding
- NIH [AI083387]
- Center for Innovation in Prevention and Treatment of Airway Diseases (CIPTAD)
- San Antonio Vaccine Center
- NIH NIDCR [DE14318]
- Translational Science Training (TST) Across Disciplines program at UT Health Science Center San Antonio
- CTSA [8UL1 TR000149, UL1RR025767]
- NATIONAL CANCER INSTITUTE [P30CA054174] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR001120, UL1TR000149] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [UL1RR025767] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI083387] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [T32DE014318] Funding Source: NIH RePORTER
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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. (C) 2013 Elsevier Inc. All rights reserved.
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