| First Author | Zhu L | Year | 2014 |
| Journal | FEBS Lett | Volume | 588 |
| Issue | 23 | Pages | 4513-9 |
| PubMed ID | 25447538 | Mgi Jnum | J:216947 |
| Mgi Id | MGI:5610067 | Doi | 10.1016/j.febslet.2014.10.025 |
| Citation | Zhu L, et al. (2014) The transcription factor GFI1 negatively regulates NLRP3 inflammasome activation in macrophages. FEBS Lett 588(23):4513-4519 |
| abstractText | Interleukin-1beta (IL-1beta) secretion downstream of Toll-like receptor (TLR) activation is tightly controlled at the transcriptional and post-translational levels. NLRP3 inflammasome is involved in the maturation of pro-IL-1beta, with NLRP3 expression identified as the limiting factor for inflammasome activation. Previously, we had demonstrated that the zinc-finger protein GFI1 inhibits pro-IL-1beta transcription. Here, we show that GFI1 inhibits NLRP3 inflammasome activation and IL-1beta secretion in macrophages. GFI1 suppressed Nlrp3 transcription via two mechanisms: (1) by binding to the Gli-responsive element 1 (GRE1) in the Nlrp3 promoter; and (2) by antagonizing the nuclear factor-kappaB (NF-kappaB) transcriptional activity. Thus, GFI1 negatively regulates TLR-mediated IL-1beta production at both transcriptional and post-translational levels. |
