The Effect of Exon 7 Deletion during the Evolution of TRIMCyp Fusion Proteins on Viral Restriction, Cytoplasmic Body Formation and Multimerization
文献类型：期刊论文
| 作者 | Liu FL1; Kuang YQ1,2; Mu D1,2; Zheng HY1,3; Zhu JW1,2; Zheng YT[*]1 |
| 刊名 | PLOS ONE
 |
| 出版日期 | 2015 |
| 卷号 | 10期号:3页码:e0121666 |
| 通讯作者 | zhengyt@mail.kiz.ac.cn |
| 合作状况 | 其它 |
| 英文摘要 | TRIMCyp is a fusion protein consisting of the TRIM5 gene product and retrotransposed Cyclophilin A (CypA). Two primate TRIMCyp fusion proteins with varying anti-HIV-1 activities independently evolved in owl monkeys and Old World monkeys. In addition, Old World monkey TRIMCyps lack exon7, which encodes amino acids in the Linker2 region. Previous studies on TRIM5 alpha indicated that this region affects anti-retroviral activity, cytoplasmic body formation, and multimerization. The effects of exon7 deletion on the functions of the TRIMCyp are unclear. In this study, we found that the cytoplasmic bodies and multimers of owl monkey TRIMCyp (omTRIMCyp) are different from those of northern pig-tailed macaque TRIMCyp (npmTRIMCyp). In addition, we demonstrated that exon7 deletion affected cytoplasmic body formation and multimerization. Moreover, we unexpectedly found two chimeric proteins of omTRIMCyp and npmTRIMCyp that failed to block HIV-1 replication, despite the presence of CypA in omTRIMCyp. Further studies indicated that the cytoplasmic bodies and spontaneous multimerization were not responsible for TRIMCyp anti-HIV-1 activity. Moreover, potent viral restriction is associated with higher amounts of monomeric TRIMCyp when the CypA domain is able to recognize and bind to the HIV-1 capsid. Our results suggested that the deletion of exon7 during the evolution of TRIMCyp affected its function. |
| 收录类别 | SCI |
| 资助信息 | This work was supported in part by grants from the National Natural Science Foundation of China (81172876, 81202366, U0832601, 31271322), the National Basic Research Program of China (2012CBA01305), the Knowledge Innovation Program of CAS (KSCX2-EW-R-13), the Twelfth Five-Year Key Scientific and Technological Program of China (2012ZX10001-006, 2012ZX10001-007, 2013ZX10001-002) and Yunnan province (2013FB073), and “The Dawn of West China” Talent Training Program of CAS. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. |
| 语种 | 英语 |
| WOS记录号 | WOS:000352134700117 |
| 公开日期 | 2015-05-11 |
| 源URL | [http://159.226.149.42:8088/handle/152453/8326]  |
| 专题 | 昆明动物研究所_分子免疫药理学 昆明动物研究所_动物模型与人类重大疾病机理重点实验室 |
| 作者单位 | 1.Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China 2.Kunming College of Life Science, University of the Chinese Academy of Sciences, Kunming, Yunnan, China 3.University of Science and Technology of China, Hefei, Anhui, China |
| 推荐引用方式 GB/T 7714 | Liu FL,Kuang YQ,Mu D,et al. The Effect of Exon 7 Deletion during the Evolution of TRIMCyp Fusion Proteins on Viral Restriction, Cytoplasmic Body Formation and Multimerization[J]. PLOS ONE,2015,10(3):e0121666. |
| APA | Liu FL,Kuang YQ,Mu D,Zheng HY,Zhu JW,&Zheng YT[*].(2015).The Effect of Exon 7 Deletion during the Evolution of TRIMCyp Fusion Proteins on Viral Restriction, Cytoplasmic Body Formation and Multimerization.PLOS ONE,10(3),e0121666. |
| MLA | Liu FL,et al."The Effect of Exon 7 Deletion during the Evolution of TRIMCyp Fusion Proteins on Viral Restriction, Cytoplasmic Body Formation and Multimerization".PLOS ONE 10.3(2015):e0121666. |
入库方式： OAI收割
来源：昆明动物研究所
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