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在Crassostrea hongkongensis中,ChRIPK1导致了亡信号通路的缺陷

Yucheng Yang¹, Liang Zeng¹, Tianxiang Lin¹

¹Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Key Laboratory of Tropical Marine Bioresources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, China; University of Chinese Academy of Sciences, Beijing, 100049, China.

Fish & shellfish immunology

|July 1, 2024

概括

这项研究克隆了基因ChRIPK1和ChTAK1,揭示了ChRIPK1调节了血细胞的编程细胞死亡,特别诱导了亡,而不是亡,并在免疫反应中发挥作用.

科学领域:

* 分子生物学 * 分子生物学
* 免疫学免疫学
* 无脊椎动物动物学

背景情况:

*受体相互作用蛋白激酶1 (RIPK1) 和转化生长因子β激活激酶1 (TAK1) 在编程细胞死亡途径,如亡和亡中至关重要.
*对无脊椎动物,特别是双动物的RIPK1/TAK1功能进行的研究有限.

研究的目的:

*为了克隆和描述 (C. hongkongensis) RIPK1 (ChRIPK1) 和 TAK1 (ChTAK1) 的特征.
* 为了研究ChRIPK1和ChTAK1在编程细胞死亡和中的免疫调节中的作用.

主要方法:

*用于基因克隆的cDNA末端的快速放大 (RACE).
*用于基因表达分析的定量逆转录PCR (qRT-PCR).
*光测定,双化酶记者测定和敲击实验.

主要成果:

* ChRIPK1与人类的RIPK1具有有限的同质性,缺乏N端激酶域,但具有DD和RHIM域.
*ChRIPK1和ChTAK1在的地幔和中高度表达;ChRIPK1在细菌感染时在血细胞和中升高调节.
*ChRIPK1激活NF-κB信号通路,并诱导血细胞的亡,但不是亡.

结论:

*ChRIPK1参与了的免疫调节和编程细胞死亡.
* ChRIPK1诱导血细胞的亡,独立于亡途径.
*这些发现为了解无脊椎动物编程细胞死亡机制提供了基础.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.C. hongkongensisensis 这种植物是这就是ChRIPK1的原因.在 ChTAK1 中,细胞因子 (cytokines) 是一种细胞因子.尸体灭 (Necroptosis) 是一种死亡的过程.炎症前驱性炎症前驱性

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