View : 33 Download: 0
Activation of c-Myb transcription factor is critical for PMA-induced lysozyme expression in airway epithelial cells
- Activation of c-Myb transcription factor is critical for PMA-induced lysozyme expression in airway epithelial cells
- Moon U.Y.; Bae J.H.; Kim C.-H.; Kim H.J.; Kang J.W.; Yoon J.-H.
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- Journal of Cellular Biochemistry
- vol. 111, no. 2, pp. 476 - 487
- SCI; SCIE; SCOPUS
- Lysozyme is a major component of airway epithelial secretions, acts as cationic anti-microbial protein for innate immunity. Although lysozyme plays an important role in airway defense and is a key component of airway secretions under inflammatory conditions, little is understood about the regulation of its expression and the associated signaling pathway. We wanted to examine whether Phorbol 12-myristate 13-acetate (PMA), one of PKC activators, treatment of the airway epithelial cell line NCI-H292 increases lysozyme gene expression. In this study, we sought to determine which signal molecules are involved in PMA-induced lysozyme gene expression. We found that PKC and mitogen-activating protein/ERK2 kinase are essential for PMA-induced lysozyme expression and also mediate the PMA-induced activation of c-Myb protein. We identified a proximal region of the lysozyme promoter essential for promoter activity containing c-Myb transcription factor binding site. Additionally, by site-directed promoter mutagenesis, we identified that c-Myb preferred the CAA motif of the -85/-73 region of the lysozyme promoter. Finally, we showed that overexpression of c-Myb without PMA treatment increased the lysozyme promoter activity and protein expression. From these results, we conclude that PMA induces overexpression of lysozyme via ERK1/2 MAP kinase-c-Myb signaling pathways in NCI-H292 cells. © 2010 Wiley-Liss, Inc.
- Appears in Collections:
- 의과대학 > 의학과 > Journal papers
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.