Center for Inflammation Research, VIB, Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Center for Inflammation Research, VIB, Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Trends Immunol. 2020 May;41(5):421-435. doi: 10.1016/j.it.2020.03.001. Epub 2020 Mar 30.
A20 is a potent anti-inflammatory molecule, and mutations in TNFAIP3, the gene encoding A20, are associated with a wide panel of inflammatory pathologies, both in human and mouse. The anti-inflammatory properties of A20 are commonly attributed to its ability to suppress inflammatory NF-κB signaling by functioning as a ubiquitin-editing enzyme. However, A20 also protects cells from death, independently of NF-κB regulation, and recent work has demonstrated that cell death may drive some of the inflammatory conditions caused by A20 deficiency. Adding to the fact that the protective role of A20 does not primarily rely on its catalytic activities, these findings shed new light on A20 biology.
A20 是一种强效的抗炎分子，编码 A20 的基因 TNFAIP3 的突变与人类和小鼠的多种炎症性病理有关。A20 的抗炎特性通常归因于其作为一种泛素修饰酶抑制炎症 NF-κB 信号的能力。然而，A20 还能独立于 NF-κB 调节保护细胞免于死亡，最近的研究表明，细胞死亡可能导致由 A20 缺乏引起的一些炎症情况。此外，A20 的保护作用并不主要依赖于其催化活性，这些发现为 A20 的生物学提供了新的视角。
