在Crassostrea gigas中,CgIκB2通过Rel/NF-κB信号负面调节干扰素样蛋白的表达
Jixiang Niu1, Sicong Wang1, Xue Qiao1
1Liaoning Key Laboratory of Marine Animal Immunology and Disease Control, Dalian Ocean University, Dalian, 116023, China; Functional Laboratory of Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266235, China; Liaoning Key Laboratory of Marine Animal Immunology, Dalian Ocean University, Dalian, 116023, China; Dalian Key Laboratory of Aquatic Animal Disease Prevention and Control, Dalian Ocean University, Dalian, 116023, China.
Fish & shellfish immunology
|August 22, 2024
概括
太平洋鱼的海.
科学领域:
- 海洋生物学 海洋生物学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- NF-κB 抑制剂 (IκBs) 是 Rel/NF-κB 信号通路中的关键调节剂.
- 这一途径对宿主抗病毒免疫非常重要,包括脊椎动物的干扰素 (IFN) 激活.
研究的目的:
- 研究IκB (CgIκB2) 对太平洋 (Crassostrea gigas) 中的干扰素样蛋白 (CgIFNLP) 表达的免疫调节作用.
- 阐明Rel/NF-κB和IRF信号通路在本规则中的参与.
主要方法:
- 在多 (I:C) 刺激后,对血细胞中CgIκB2,CgIFNLP,CgIRF8和CgRelmRNA表达的定量分析.
- 使用RNA干扰 (RNAi) 来抑制CgIκB2和CgRel的表达.
- 蛋白质丰富度和核转位使用免疫光分析进行评估.
主要成果:
- 多 (I:C) 刺激改变了CgIκB2mRNA的表达,最初是下调,然后是上调.
- 抑制CgIκB2导致CgIFNLP,CgIRF8和CgRel的表达增加,并增强了CgIRF8和CgRel的核转移.
- 在聚 (I:C) 刺激后,对CgRel的抑制导致CgIFNLP表达的降低.
结论:
- CgIκB2对太平洋的CgIFNLP表达进行负面调节.
- 这种调节通过调节Rel/NF-κB和IRF信号通路来实现.
- CgIκB2在的抗病毒免疫反应中起着重要作用.
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