| First Author | Ohba T | Year | 2012 |
| Journal | FEBS J | Volume | 279 |
| Issue | 2 | Pages | 211-22 |
| PubMed ID | 22059479 | Mgi Jnum | J:192069 |
| Mgi Id | MGI:5463873 | Doi | 10.1111/j.1742-4658.2011.08416.x |
| Citation | Ohba T, et al. (2012) Identification of interleukin-1 receptor-associated kinase 1 as a critical component that induces post-transcriptional activation of IkappaB-zeta. FEBS J 279(2):211-22 |
| abstractText | IkappaB-zeta, an essential inflammatory regulator, is specifically induced by Toll-like receptor ligands or interleukin (IL)-1beta by post-transcriptional activation mediated via a 165-nucleotide element in IkappaB-zeta mRNA. Here, we analyzed the Toll-like receptor-IL-1 receptor signaling components involved in the post-transcriptional regulation of IkappaB-zeta with mutated estrogen receptor [ER(T2)] fusion proteins. Upon 4-hydroxytamoxifen treatment, the ER(T2) fusion proteins with IL-1 receptor-associated kinase (IRAK)1 and IRAK4 elicited specific activation of a reporter gene for the post-transcriptional regulation of IkappaB-zeta. The tumor necrosis factor receptor-associated factor (TRAF)6-ER(T2) protein activated nuclear factor-kappaB, but not post-transcriptional regulation, indicating that activation of IRAK1/4, but not of TRAF6, is sufficient to activate the 165-nucleotide element-mediated post-transcriptional mechanism. Interestingly, the post-transcriptional mechanism was not activated in TRAF6-deficient cells, indicating an essential role for TRAF6. Thus, the signaling pathway leading to nuclear factor-kappaB activation and the post-transcriptional activation bifurcates at IRAK1, suggesting a new pathway activated by IRAK1. |
