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Induction of nuclear factor-κB activation through TAK1 and NIK by diesel exhaust particles in L2 cell lines

Authors
 Young-Pil Yun  ;  Jin-Deok Joo  ;  Joo-Yong Lee  ;  Hae-Yun Nam  ;  Young-Hoon Kim  ;  Kweon-Haeng Lee  ;  Cheol-Soo Lim  ;  Hyung-Jung Kim  ;  Yong-Gul Lim  ;  Young Lim 
Citation
 TOXICOLOGY LETTERS, Vol.155(2) : 337-342, 2005 
Journal Title
TOXICOLOGY LETTERS
ISSN
 0378-4274 
Issue Date
2005
MeSH
Animals ; Cell Line ; Epithelial Cells/drug effects* ; Epithelial Cells/enzymology ; Epithelial Cells/metabolism ; MAP Kinase Kinase Kinases/metabolism* ; NF-kappa B/metabolism* ; Particle Size ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism* ; Rats ; Signal Transduction/drug effects* ; Vehicle Emissions/analysis ; Vehicle Emissions/toxicity*
Keywords
DEP ; NF-κB ; TAK1 ; NIK ; L2 cells
Abstract
Diesel exhaust particles (DEPs) are known to induce allergic responses in airway epithelial cells, such as the production of various cytokines via nuclear factor-kappa B (NF-κB). However, the intracellular signal transduction pathways underlying this phenomenon have not been fully examined. This study showed that DEP induced NF-κB activity via transforming growth factor-β activated kinase 1 (TAK1) and NF-κB-inducing kinase (NIK) in L2 rat lung epithelial cells. DEP induced the NF-kB dependent reporter activity approximately two- to three-fold in L2 cells. However, this effect was abolished by the expression of the dominant negative forms of TAK1 or NIK. Furthermore, it was shown that DEP induced TAK1 phosphorylation in the L2 cells. These results suggest that TAK1 and NIK are important mediators of DEP-induced NF-κB activation.
Full Text
http://www.sciencedirect.com/science/article/pii/S0378427404005016
DOI
10.1016/j.toxlet.2004.10.010
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Hyung Jung(김형중) ORCID logo https://orcid.org/0000-0003-2498-0683
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/151245
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