Truncation of cytoplasmic tail of eiav env increases the pathogenic necrosis
文献类型：期刊论文
| 作者 | Meng, Qinglai1,2,4; Li, Shenwei1; Liu, Lianxing1,2,4; Xu, Jianqing1; Liu, Yong1; Zhang, Yaozhou3; Zhang, Xiaoyan1; Shao, Yiming1,2 |
| 刊名 | Virus research
 |
| 出版日期 | 2008-05-01 |
| 卷号 | 133期号:2页码:201-210 |
| 关键词 | Eiav Envelope Truncation Necrosis Apoptosis Mitochondrial depolarization |
| ISSN号 | 0168-1702 |
| DOI | 10.1016/j.virusres.2008.01.004 |
| 通讯作者 | Zhang, xiaoyan(zhangxy@chinaaids.en) |
| 英文摘要 | Equine infectious anemia virus (eiav), like other lentiviruses, has a transmembrane glycoprotein with an unusually long cytoplasmic tail (ct). viral envelope (env) proteins having ct truncations just downstream the putative membrane-spanning domain (pmsd) are assumed to exist among all wild-type budded virions, and also in some cell-adapted strains. to determine whether ct-truncated env proteins can cause particularly deleterious effects on the env expressing cells and/or their neighboring cells, plasmids encoding codon-optimized env, gene including full-length (pe863) or ct-truncated (pe686* and pe676*) were transiently transfected into 293t cells, respectively. data from intracellular protein expression and cell death assays revealed that ct-truncated env, compared to full-length env, not only induced comparable apoptosis, but also caused much more intensive mitochondria-mediated necrosis that could simultaneously induce significant decrease of intracellular protein expression in the env expressing cells. moreover, results from flow cytometric analysis showed that mitochondrial depolarization preceded the caspase activation in cells no matter which env, construct was delivered, and indicated that both full-length and ct-truncated env proteins share a common intrinsic mitochondrial pathway to induce apoptosis. our results partially elucidate the mechanisms underlying cell death resulting from eiav pathogenesis. (c) 2008 elsevier b.v. all rights reserved. |
| WOS关键词 | INFECTIOUS-ANEMIA VIRUS ; HUMAN-IMMUNODEFICIENCY-VIRUS ; TRANSMEMBRANE GLYCOPROTEIN ; GENOMIC ORGANIZATION ; CELL-DEATH ; ENVELOPE ; APOPTOSIS ; PROTEIN ; LENTIVIRUS ; RECEPTOR |
| WOS研究方向 | Virology |
| WOS类目 | Virology |
| 语种 | 英语 |
| WOS记录号 | WOS:000255467700009 |
| 出版者 | ELSEVIER SCIENCE BV |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2375508 |
| 专题 | 武汉病毒研究所 |
| 通讯作者 | Zhang, Xiaoyan |
| 作者单位 | 1.Chinese Ctr Dis Control & Prevent, State Key Lab Infect Dis Prevent & Control, Natl Ctr AIDS STD Control & Prevent, Beijing 100050, Peoples R China 2.Chinese Acad Sci, Wuhan Inst Virol, State Key Lab Virol, Wuhan 430071, Peoples R China 3.Zhejiang Sci Tech Univ, Inst Biochem, Coll Life Sci, Hangzhou 310018, Peoples R China 4.Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China |
| 推荐引用方式 GB/T 7714 | Meng, Qinglai,Li, Shenwei,Liu, Lianxing,et al. Truncation of cytoplasmic tail of eiav env increases the pathogenic necrosis[J]. Virus research,2008,133(2):201-210. |
| APA | Meng, Qinglai.,Li, Shenwei.,Liu, Lianxing.,Xu, Jianqing.,Liu, Yong.,...&Shao, Yiming.(2008).Truncation of cytoplasmic tail of eiav env increases the pathogenic necrosis.Virus research,133(2),201-210. |
| MLA | Meng, Qinglai,et al."Truncation of cytoplasmic tail of eiav env increases the pathogenic necrosis".Virus research 133.2(2008):201-210. |
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来源：武汉病毒研究所
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