LPS-induced mortality in CD11c-Cre A20 (fl/fl) mice was characterized by increased serum levels of IL-2, IL-10, IL-12, IFN-γ, and TNF. Upon LPS stimulation, the activation of NF-κB and ERK-NFATc3 pathways were enhanced in A20-deficient DCs, resulting in an increased production of IL-2, IL-12, and TNF both in vitro and in vivo.

2016年8月22日 · 结论：a20能够抑制肺泡巨噬细胞nfκb活性及tnfα、il1β分泌，进而抑制肺泡巨噬细胞炎症反应活性〖bp（〗，由此推测能够减轻急性呼吸窘迫综合征（ards）炎症反应。

2017年7月20日 · The A20 group exhibited significantly up-regulated A20 expression compared to the NS, LPS, and LPS-C1 groups, and down-regulated NF-κB p65 and NF-κB p-P65 expression compared to the LPS and LPS-C1 groups, indicating that the high protein expression of A20 can inhibit the expression of NF-κB p65 and NF-κB p-P65 to some extent, thus ...

The ubiquitin-editing enzyme A20 is known to inhibit the NF-κB transcription factor in the Toll-like receptor (TLR) pathways, thereby negatively regulating inflammation. However, its role in the TLR signaling pathway in fish is still largely ...

锌指蛋白A20是一种内源性保护蛋白，其可通过A20自身的去K-63泛素酶及K-48泛素酶对同一底物实行去泛素化及泛素化实现负反馈地抑制NF-κB炎症信号通路的传导，在炎症疾病领域受到密切关注 [3 - 4]。 本课题组的前期研究揭示，A20对髓核细胞具有内源性的保护作用，减弱LPS刺激引起的炎症信号NF-κB过度激活、传导及相关亲水基质的分解 [5 -...

2019年4月15日 · Our experimental results showed that, in LPS-treated BV2 cells, zinc supplement induced expression of A20 and augmented its inhibitory effects on NF-κB signaling, leading to decline of phosphorylation levels of p65 and IκB.

Nrf2 转录因子通过上调抗氧化基因表达和 TNFα 诱导的蛋白 3（TNFAIP3，又名 A20）去泛素酶通过控制 NF-kB 信号抑制组织炎症来抑制细胞应激和控制炎症。 在这里，我们报告 Nrf2 是炎症刺激 LPS 在单核细胞/骨髓衍生巨噬细胞 (MDMΦs) 中诱导A20所必需的，但在肺巨噬细胞 (LDMΦs) 中则不需要。 LPS 诱导的 A20 表达在Nrf2 -/- MDMΦs 中显着降低，并且没有通过补充抗氧化剂恢复。 Nrf2 缺乏显着损害 LPS 刺激A20 mRNA 表达Nrf2 -/- MDMΦs 和 ChIP 测定显示 Nrf2 在 …

2014年12月4日 · Here, we demonstrate that upon injection of low-dose LPS, mice with DC-specific A20 deletion (CD11c-Cre A20 fl/fl) died within 6 h, whereas A20 fl/fl controls survived. LPS-induced mortality in CD11c-Cre A20 fl/fl mice was characterized by increased serum levels of IL-2, IL-10, IL-12, IFN-γ, and TNF. Upon LPS stimulation, the activation of NF ...

2009年7月15日 · The state of tolerance, which lasts 20-26 h, temporally coincides with LPS-induced expression of the anti-inflammatory ubiquitin-editing enzyme A20. Small interfering RNA silencing of A20 prevents tolerance, whereas ectopic expression of A20 blocks responses to LPS and CpG DNA, but not to IL-17 or UV.

2011年2月4日 · Silencing of A20 restored TRAF6 expression and NF-κB activation and resulted in increased bone resorption in LPS-treated cultures. A20 appeared important in the control of bone resorption and could represent a therapeutic target to treat patients with bone resorption associated with inflammatory diseases.