炎症酶活性是由ZBTB16依赖ASC的SUMOylation控制的
Danfeng Dong1,2, Yuzhang Du1,2, Xuefeng Fei1,2
1Department of Laboratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Nature communications
|December 20, 2023
概括
含有指和BTB域的蛋白质16 (ZBTB16) 通过控制含有CARD (ASC) 的亡相关的斑状蛋白质的SUMOylation来调节炎酶组合. 切除ZBTB16可降低Muckle-Wells综合征小鼠模型中的炎症性疾病严重程度.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 炎症体是关键的免疫复合体,参与天生的免疫和炎症性疾病.
- 不调节的炎症酶激活有助于各种临床条件.
- 卡斯帕酶-1和NLR适应蛋白ASC是炎症酶组合的核心.
研究的目的:
- 阐明一种新的炎症酶组合的调节机制.
- 为了确定控制ASC功能的因素.
- 研究ZBTB16在炎症酶介导炎症中的生理作用.
主要方法:
- 研究了ASC的翻译后修改.
- 确定ZBTB16作为ASC SUMOylation的调节剂.
- 利用Muckle-Wells综合征的小鼠模型来评估体内功能.
主要成果:
- 证明ASC功能在炎酶组合中是通过SUMOylation调节的.
- 确定了核ZBTB16作为ASC SUMOylation的促进剂.
- 表明ZBTB16的切除减少了在Muckle-Wells综合征小鼠模型中的炎症病原体.
结论:
- ZBTB16通过ASC SUMOylation控制着炎症细胞组合.
- 这种依赖于ZBTB16的途径代表了调节促炎反应的新机制.
- 准ZBTB16可能为炎症酶驱动疾病提供治疗潜力.
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