Grouper TRAF4, a Novel, CP-Interacting Protein That Promotes Red-Spotted Grouper Nervous Necrosis Virus Replication.
Grouper TRAF4, a Novel, CP-Interacting Protein That Promotes Red-Spotted Grouper Nervous Necrosis Virus Replication.
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石斑鱼 TRAF4，一种新型 CP 相互作用蛋白，可促进红斑石斑鱼神经坏死病毒复制。
DOI：
10.3390/ijms22116136
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发表时间：
2021-06-07
影响因子：
5.6
通讯作者：
Wei J
中科院分区：
文献类型：
--
作者：
Wu S;Sun M;Zhang X;Liao J;Liu M;Qin Q;Wei J
肿瘤坏死因子受体相关因子（TRAFs）在免疫调节、炎症反应和细胞凋亡等生物学过程中发挥重要作用。TRAF 4属于TRAF家族，在许多生物过程中起着重要作用。与其他TRAF蛋白相比，TRAF 4在硬骨鱼中的功能还很不清楚。在本研究中，橙色斑点石斑鱼的TRAF 4同源物（EcTRAF 4）的特点。该基因全长1413 bp，编码471个氨基酸，预测分子量为54.27 kDa。EcTRAF 4与石斑鱼TRAF 4的同源性为99.79%。lanceolatus）。EcTRAF 4转录本在所有检查的组织中普遍且差异表达。用红斑石斑鱼神经坏死病毒（RGNNV）刺激后，GS细胞中的EcTRAF 4表达显著上调。EcTRAF 4蛋白分布于GS细胞的胞质中。过表达的EcTRAF 4在体外病毒感染期间促进RGNNV复制。酵母双杂交和免疫共沉淀试验表明，EcTRAF 4与RGNNV的外壳蛋白（CP）相互作用。EcTRAF 4可抑制IFN 3、IFN刺激反应元件（ISRE）和核因子-κB（NF-κB）的活化。过表达的EcTRAF 4也降低了干扰素（IFN）相关分子和促炎因子的表达。总之，这些结果表明，EcTRAF 4在RGNNV感染中起着至关重要的作用。
Tumor necrosis factor receptor-associated factors (TRAFs) play important roles in the biological processes of immune regulation, the inflammatory response, and apoptosis. TRAF4 belongs to the TRAF family and plays a major role in many biological processes. Compared with other TRAF proteins, the functions of TRAF4 in teleosts have been largely unknown. In the present study, the TRAF4 homologue (EcTRAF4) of the orange-spotted grouper was characterized. EcTRAF4 consisted of 1413 bp encoding a 471-amino-acid protein, and the predicted molecular mass was 54.27 kDa. EcTRAF4 shares 99.79% of its identity with TRAF4 of the giant grouper (E. lanceolatus). EcTRAF4 transcripts were ubiquitously and differentially expressed in all the examined tissues. EcTRAF4 expression in GS cells was significantly upregulated after stimulation with red-spotted grouper nervous necrosis virus (RGNNV). EcTRAF4 protein was distributed in the cytoplasm of GS cells. Overexpressed EcTRAF4 promoted RGNNV replication during viral infection in vitro. Yeast two-hybrid and coimmunoprecipitation assays showed that EcTRAF4 interacted with the coat protein (CP) of RGNNV. EcTRAF4 inhibited the activation of IFN3, IFN-stimulated response element (ISRE), and nuclear factor-κB (NF-κB). Overexpressed EcTRAF4 also reduced the expression of interferon (IFN)-related molecules and pro-inflammatory factors. Together, these results demonstrate that EcTRAF4 plays crucial roles in RGNNV infection.
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影响因子：
2.7
作者：
Wei, Jingguang;Huang, Youhua;Qin, Qiwei
通讯作者：
Qin, Qiwei
影响因子：
7.3
作者：
Park HH
通讯作者：
Park HH
影响因子：
4.8
作者：
REGNIER, CH;TOMASETTO, C;RIO, MC
通讯作者：
RIO, MC
DOI：
10.1073/pnas.052124799
发表时间：
2002-04-16
影响因子：
11.1
作者：
Régnier, CH;Masson, R;Rio, MC
通讯作者：
Rio, MC
影响因子：
4.5
作者：
Huang, Xiaohong;Huang, Youhua;Qin, Qiwei
通讯作者：
Qin, Qiwei