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在Asp³³³之后,RIPK3的卡斯帕斯分裂对于小鼠胚胎发生是不可或缺的

Kim Newton¹, Katherine E Wickliffe², Allie Maltzman²

¹Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA, 94080, USA. knewton@gene.com.

Cell death and differentiation

|January 8, 2024

概括

在小鼠发育过程中,RIPK3 (受体相互作用蛋白激酶3) 的卡斯帕斯-8裂变对于预防老鼠亡并不是必不可少的. 在Caspase-8中使用.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
发育生物学是发展生物学.

背景情况:

众所周知,Caspase-8可以抑制亡,一种编程细胞死亡的形式.
目前尚不清楚酶-8对RIPK3的分裂是否对这种抑制至关重要.

研究的目的:

为了研究RIPK3通过caspase-8的裂变在亡抑制中的作用.
为了确定RIPK3裂变是否对小鼠正常发育至关重要.

主要方法:

产生的Ripk3D333A/D333A模拟小鼠缺乏Asp333裂部位.
分析小鼠的生存能力,发育和死细胞灭绝的敏感性.
在各种诱导死亡的条件下对巨细胞死亡进行分析.

主要成果:

Ripk3D333A/D333A小鼠是可活的,正常发育,这表明RIPK3裂变对于发育并不重要.
与野生类型相比,这些小鼠对TNF诱导的亡不表现出增加的敏感性.
RIPK3的裂变依赖于下游的caspase-3,并且发生在亡开始后.

结论:

通过Caspase-8介导的RIPK3裂变对于小鼠发育和亡抑制是不可或缺的.
其他卡斯巴-8基质的裂变,如RIPK1,足以防止亡.
RIPK3裂变是亡的结果,而不是预防亡的主要机制.

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Caspases

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...