Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 한중수 | - |
dc.date.accessioned | 2017-10-19T01:37:25Z | - |
dc.date.available | 2017-10-19T01:37:25Z | - |
dc.date.issued | 2015-12 | - |
dc.identifier.citation | EUROPEAN JOURNAL OF INFLAMMATION, v. 13, NO 3, Page. 183-195 | en_US |
dc.identifier.issn | 1721-727X | - |
dc.identifier.uri | http://journals.sagepub.com/doi/10.1177/1721727X15619185 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/30105 | - |
dc.description.abstract | The purpose of this study was to identify the mechanism of lipopolysaccharide (LPS)-induced expression of tumor necrosis factor (TNF)-alpha in BEAS-2B. Toll-like receptor (TLR)4-specific siRNA was found to completely abolish the LPS-induced expression of MyD88 and TNF-alpha. There was enhanced binding of MyD88 with IRAK1 following LPS treatment, and MyD88- or IRAK1-specific siRNAs decreased the expression of TNF-alpha. In addition, IRAK1 siRNA downregulated the phosphorylation of PKC alpha, demonstrating that PKC alpha is a downstream effector of IRAK1. Inhibition of PKC alpha completely blocked the activation of AKT, whereas inhibition of AKT with a PI3K inhibitor prevented the LPS-induced expression of TNF-alpha. We found that AKT activated JNK, which then stimulated phosphorylation of I kappa-B alpha, resulting in NF-kappa B activation. As expected, inhibition of NF-kappa B completely inhibited the expression of TNF-alpha. Taken together, our results suggest that LPS induces TNF-alpha expression by activating NF-kappa B via the PKC/PI3K/AKT/JNK pathway, which is in turn dependent on MyD88/IRAK1. | en_US |
dc.description.sponsorship | This study was supported by the National Research Foundation of Korea (NRF), funded by the Mid-Career Researcher Program (NRF-2010-0026844), the Korea government (MEST) (NRF-2013R1A2A2A03067895), and Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2013R1A1A2061420). | en_US |
dc.language.iso | en | en_US |
dc.publisher | BIOLIFE SAS | en_US |
dc.subject | IRAK1 | en_US |
dc.subject | JNK | en_US |
dc.subject | NF-kappa B | en_US |
dc.subject | TLR4 | en_US |
dc.subject | TNF-alpha | en_US |
dc.title | TLR4-mediated IRAK1 activation induces TNF-alpha expression via JNK-dependent NF-kappa B activation in human bronchial epithelial cells | en_US |
dc.type | Article | en_US |
dc.relation.no | 3 | - |
dc.relation.volume | 13 | - |
dc.identifier.doi | 10.1177/1721727X15619185 | - |
dc.relation.page | 183-195 | - |
dc.relation.journal | EUROPEAN JOURNAL OF INFLAMMATION | - |
dc.contributor.googleauthor | Park, Sae Hoon | - |
dc.contributor.googleauthor | Choi, Hye-Jin | - |
dc.contributor.googleauthor | Lee, So Young | - |
dc.contributor.googleauthor | Han, Joong-Soo | - |
dc.relation.code | 2015011355 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jshan | - |
dc.identifier.orcid | http://orcid.org/0000-0002-0875-6158 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.