Akirin interacts with Bap60 and 14-3-3 proteins to regulate the expression of antimicrobial peptides in the kuruma shrimp (Marsupenaeus japonicus)

Akirin interacts with Bap60 and 14-3-3 proteins to regulate the expression of antimicrobial peptides in the kuruma shrimp (Marsupenaeus japonicus)
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Akirin 与 Bap60 和 14-3-3 蛋白相互作用,调节库鲁玛虾 (Marsupenaeus japonicus) 中抗菌肽的表达。

DOI:
10.1016/j.dci.2015.10.015
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发表时间:
2016-02-01
影响因子:
2.9
通讯作者:
Wang, Jin-Xing
Wang, Jin-Xing
中科院分区:
生物学3区
文献类型:
--
作者:
Liu, Ning;Wang, Xian-Wei;Wang, Jin-Xing

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Akirin是最近发现的一种在先天免疫应答中起重要作用的核因子。Akirin是果蝇免疫缺陷(IMD)途径的NF-κ B因子的正调节剂;其与哺乳动物肿瘤坏死因子受体(TNFR)信号传导途径具有广泛的相似性。然而,一些研究发现,在TLR、IL-1 β和TNF α治疗后,Akirin 2敲除小鼠中NF-κ B转录靶点也被强烈抑制。因此,Akirin在免疫应答中的功能需要进一步阐明。在这项研究中,Akirin同源物中的库鲁马虾(Marsupenaeus kuruma)的。主要表达于血细胞、心脏和肠道。革兰氏阴性菌鳗弧菌的攻击上调Akirin的表达,但没有显着影响革兰氏阳性菌金黄色葡萄球菌的挑战。Akirin的敲低抑制了几种IMD-Relish靶效应物(抗菌肽,AMP)的表达。Akirin有限的调节谱可能与Brahma(SWI/SNF)ATP依赖的染色质重塑复合物的组分Bap 60相关。此外,Akirin还与14-3-3相互作用,其抑制Akirin靶AMP的表达。结果表明,Akirin通过与Relish相互作用参与了IMD-Relish途径。Akirin与Bap 60的相互作用正向调节Akirin Relish功能,其与14-3-3的相互作用负向调节Akirin Relish功能。(C)2015爱思唯尔有限公司版权所有。
Akirin is a recently discovered nuclear factor that plays important roles in innate immune responses. Akirin is a positive regulator of the NF-kappa B factor of the Drosophila immune deficiency (IMD) pathway; Which shares extensive similarities with the mammalian tumor necrosis factor receptor (TNFR) signaling pathway. However, some studies found that the NF-kappa B transcriptional targets were also strongly repressed in akirin2 knockout mice following TLR, IL-1 beta and TNF alpha treatment. Therefore, the function of Akirin in the immune response requires further clarification. In this study, an Akirin homolog in the kuruma shrimp (Marsupenaeus japonicus) was identified. It was mainly expressed in hemocytes, heart and intestines. The expression of Akirin was upregulated by challenge with the Gram-negative bacterium Vibrio anguillarum, but was not significantly influenced by challenge with the Gram-positive bacterium Staphylococcus aureus. Knockdown of Akirin suppressed the expression of several IMD-Relish target effectors (antimicrobial peptides, AMPs). The limited regulating spectrum of Akirin might be associated with Bap60, a component of the Brahma (SWI/SNF) ATP-dependent chromatin-remodeling complex. In addition, Akirin also interacts with 14-3-3, which inhibited the expression of Akirin-target AMPs. The results suggested that Akirin is involved in the IMD-Relish pathway by interacting with Relish. The interaction of Akirin with Bap60 positively regulated the Akirin Relish function, and its interaction with 14-3-3 negatively regulated the Akirin Relish function. (C) 2015 Elsevier Ltd. All rights reserved.