These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Induction of nuclear factor-kappaB activation through TAK1 and NIK by diesel exhaust particles in L2 cell lines.
    Author: Yun YP, Joo JD, Lee JY, Nam HY, Kim YH, Lee KH, Lim CS, Kim HJ, Lim YG, Lim Y.
    Journal: Toxicol Lett; 2005 Feb 15; 155(2):337-42. PubMed ID: 15603929.
    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-kappaB). However, the intracellular signal transduction pathways underlying this phenomenon have not been fully examined. This study showed that DEP induced NF-kappaB activity via transforming growth factor-beta activated kinase 1 (TAK1) and NF-kappaB-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-kappaB activation.
    [Abstract] [Full Text] [Related] [New Search]