Alternative Title転写因子Spi-BによるInterferon-α4遺伝子の転写活性化メカニズム
Periodical titleBiochemical and biophysical research communications
Note (General)Plasmacytoid dendritic cells (pDCs) are characterized by an exclusive expression of nucleic acid sensing Toll-like receptor 7 (TLR7) and TLR9, and production of high amounts of type I interferon (IFN) in response to TLR7/9 signaling. This function is crucial for both antiviral immunity and the pathogenesis of autoimmune diseases. An Ets family transcription factor, i.e., Spi-B (which is highly expressed in pDCs) is required for TLR7/9 signal-induced type I IFN production and can transactivate IFN-α promoter in synergy with IFN regulatory factor-7 (IRF-7). Herein, we analyzed how Spi-B contributes to the transactivation of the Ifna4 promoter. We performed deletion and/or mutational analyses of the Ifna4 promoter and an electrophoretic mobility shift assay (EMSA) and observed an Spi-B binding site in close proximity to the IRF-7 binding site. The EMSA results also showed that the binding of Spi-B to the double-stranded DNA probe potentiated the recruitment of IRF-7 to its binding site. We also observed that the association of Spi-B with transcriptional coactivator p300 was required for the Spi-B-induced synergistic enhancement of the Ifna4 promoter activity by Spi-B. These results clarify the molecular mechanism of action of Spi-B in the transcriptional activation of the Ifna4 promoter.
This is the Publisher's Version of the following article: The mechanism of action of Spi-B in the transcriptional activation of the interferon-α4 gene; Biochemical and biophysical research communications; Volume 525 Issue 2 (2020) Pages:477-482; doi: 10.1016/j.bbrc.2020.02.101, which has been published in final form at https://doi.org/10.1016/j.bbrc.2020.02.101.
Collection (particular)国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
Date Accepted (W3CDTF)2020-08-11T22:41:34+09:00
Data Provider (Database)国立国会図書館 : 国立国会図書館デジタルコレクション