GSK3β Plays a Negative Role During White Spot Syndrome Virus (WSSV) Infection by Regulating NF-κB Activity in Shrimp Litopenaeus vannamei.
GSK3β Plays a Negative Role During White Spot Syndrome Virus (WSSV) Infection by Regulating NF-κB Activity in Shrimp Litopenaeus vannamei.
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DOI：
10.3389/fimmu.2020.607543
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发表时间：
2020
影响因子：
7.3
通讯作者：
Shi L
中科院分区：
文献类型：
--
作者：
Zhang S;Zhu L;Hou C;Yuan H;Yang S;Dehwah MAS;Shi L
Glycogen synthase kinase-3 (GSK3), a cytoplasmic serine/threonine-protein kinase involved in a large number of key cellular processes, is a little-known signaling molecule in virus study. In this study, a GSK3 protein which was highly similar to GSK3β homologs from other species in Litopenaeus vannamei (designated as LvGSK3β) was obtained. LvGSK3β was expressed constitutively in the healthy L. vannamei, at the highest level in the intestine and the lowest level in the eyestalk. White spot syndrome virus (WSSV) reduced LvGSK3β expression was in immune tissues including the hemocyte, intestine, gill and hepatopancreas. The inhibition of LvGSK3β resulted in significantly higher survival rates of L. vannamei during WSSV infection than the control group, and significantly lower WSSV viral loads in LvGSK3β-inhibited L. vannamei were observed. Knockdown of LvGSK3β by RNAi resulted in increases in the expression of LvDorsal and several NF-κB driven antimicrobial peptide (AMP) genes (including ALF, PEN and crustin), but a decrease in LvCactus expression. Accordingly, overexpression of LvGSK3β could reduce the promoter activity of LvDorsal and several AMPs, while the promoter activity of LvCactus was increased. Electrophoretic mobility shift assays (EMSA) showed that LvDorsal could bind to the promoter of LvGSK3β. The interaction between LvGSK3β and LvDorsal or LvCactus was confirmed using co-immunoprecipitation (Co-IP) assays. In addition, the expression of LvGSK3β was dramatically reduced by knockdown of LvDorsal. In summary, the results presented in this study indicated that LvGSK3β had a negative effect on L. vannamei by mediating a feedback regulation of the NF-κB pathway when it is infected by WSSV.
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DOI：
10.3390/v10080409
发表时间：
2018-08-04
期刊：
Viruses
影响因子：
--
作者：
Deng L;Zeng Q;Wang M;Cheng A;Jia R;Chen S;Zhu D;Liu M;Yang Q;Wu Y;Zhao X;Zhang S;Liu Y;Yu Y;Zhang L;Chen X
通讯作者：
Chen X
影响因子：
7.3
作者：
Liao, Xuzheng;Wang, Chenggui;Zhang, Shuang
通讯作者：
Zhang, Shuang
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DOI：
10.1007/s12275-015-4661-z
发表时间：
2015-01
期刊：
Journal of microbiology (Seoul, Korea)
影响因子：
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作者：
Kim JY;Park SY;Lyoo HR;Koo ES;Kim MS;Jeong YS
通讯作者：
Jeong YS
通过 PI3K/Akt/GSK-3α/β 途径抑制猪流行性腹泻病毒的增殖
影响因子：
3.7
作者：
Kong N;Wu Y;Meng Q;Wang Z;Zuo Y;Pan X;Tong W;Zheng H;Li G;Yang S;Yu H;Zhou EM;Shan T;Tong G
通讯作者：
Tong G
影响因子：
5.4
作者：
Guendel, Irene;Iordanskiy, Sergey;Kashanchi, Fatah
通讯作者：
Kashanchi, Fatah