A tumour necrosis factor receptor-like protein encoded by Singapore grouper iridovirus modulates cell proliferation, apoptosis and viral replication
Yu, Yepin; Huang, Youhua; Wei, Shina; Li, Pengfei; Zhou, Lingli; Ni, Songwei; Huang, Xiaohong; Qin, Qiwei; Huang, XH; Qin, QW (reprint author), Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, 164 West Xingang Rd, Guangzhou 510301, Guangdong, Peoples R China.
2016
发表期刊JOURNAL OF GENERAL VIROLOGY
卷号97页码:756-766
摘要It has been demonstrated that tumour necrosis factor receptor (TNFR) homologues encoded by viruses are usually involved in virus immune evasion by regulating the host immune response or mediating apoptotic cell death. Here, a novel TNFR-like protein encoded by Singapore grouper iridovirus (SGIV VP51) was cloned and characterized. Amino acid analysis showed that VP51 contained three cysteine-rich domains (CRDs) and a transmembrane domain at its C terminus. The expression of VP51 in vitro enhanced cell proliferation, and affected cell cycle progression via altering the G1/S transition. Furthermore, VP51 overexpression improved cell viability during SGIV infection via inhibiting virus-induced apoptosis, evidenced by the reduction of apoptotic bodies and the decrease of caspase-3 activation. In addition, overexpression of VP51 increased viral titre and the expression of viral structural protein gene MCP and cell proliferation promoting gene ICP-18. In contrast, the expression of the viral apoptosis inducing gene, LITAF, was significantly decreased. Although all three CRDs were essential for the action of VP51, CRD2 and CRD3 exerted more crucial roles on virus-induced apoptosis, viral gene transcription and virus production, while CRD1 was more crucial for cell proliferation. Together, SGIV TNFR-like products not only affected cell cycle progression and enhanced cell growth by increasing the expression of the virus encoded cell proliferation gene, but also inhibited virus-induced apoptotic cell death by decreasing the expression of the viral apoptosis inducing gene. Our results provided new insights into understanding the underlying mechanism by which iridovirus regulated the apoptotic pathway to complete its life cycle.
部门归属[Yu, Yepin; Huang, Youhua; Wei, Shina; Li, Pengfei; Zhou, Lingli; Ni, Songwei; Huang, Xiaohong; Qin, Qiwei] Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, 164 West Xingang Rd, Guangzhou 510301, Guangdong, Peoples R China; [Yu, Yepin; Li, Pengfei; Zhou, Lingli; Ni, Songwei] Univ Chinese Acad Sci, 19 Yuquan Rd, Beijing 100049, Peoples R China ; LMB
学科领域Biotechnology & Applied Microbiology ; Virology
文献类型期刊论文
条目标识符http://ir.scsio.ac.cn/handle/344004/15487
专题中科院海洋生物资源可持续利用重点实验室
通讯作者Huang, XH; Qin, QW (reprint author), Chinese Acad Sci, South China Sea Inst Oceanol, Key Lab Trop Marine Bioresources & Ecol, 164 West Xingang Rd, Guangzhou 510301, Guangdong, Peoples R China.
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Yu, Yepin,Huang, Youhua,Wei, Shina,et al. A tumour necrosis factor receptor-like protein encoded by Singapore grouper iridovirus modulates cell proliferation, apoptosis and viral replication[J]. JOURNAL OF GENERAL VIROLOGY,2016,97:756-766.
APA Yu, Yepin.,Huang, Youhua.,Wei, Shina.,Li, Pengfei.,Zhou, Lingli.,...&Qin, QW .(2016).A tumour necrosis factor receptor-like protein encoded by Singapore grouper iridovirus modulates cell proliferation, apoptosis and viral replication.JOURNAL OF GENERAL VIROLOGY,97,756-766.
MLA Yu, Yepin,et al."A tumour necrosis factor receptor-like protein encoded by Singapore grouper iridovirus modulates cell proliferation, apoptosis and viral replication".JOURNAL OF GENERAL VIROLOGY 97(2016):756-766.
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