期刊文献+

日本脑炎病毒引起细胞凋亡的信号转导通路研究进展 被引量:2

Progress on JEV Induced Apoptosis Signaling Pathway
下载PDF
导出
摘要 日本脑炎病毒(JEV)是虫媒传染性病毒,感染动物后会产生严重的脑炎症状,严重威胁着公共卫生安全。病毒粒子主要通过胞吞作用进入宿主细胞,在细胞浆复制,在细胞内部膜结构上成熟。JEV侵入神经细胞引起脑炎症状,其机理可能与JEV诱导细胞凋亡有关。目前,研究人员就有关JEV诱导细胞凋亡信号转导途径方面做了大量研究工作。在被JEV感染的细胞内会发生一系列蛋白酶激活与抑制反应,继而发生线粒体外膜通透性改变、氧化应激以及内质网应激等诱导细胞发生凋亡。凋亡机制和信号转导通路的研究对JEV的致病机理以及它与宿主之间的相互作用有重要意义。论文对JEV诱导细胞发生细胞周期抑制和凋亡的现象、信号转导通路进行了综述,并对研究方向进行了展望。 Japanese encephalitis virus,a mosquito-born flavivirus,causes acute encephalitis in infected animals.And now it is threatening public health.After transporting across the cell membrane by endocytosis,the JEV particles replicate in cytoplasma,and mature on the inner membrane.Interestingly,the replication of JEV causes apoptosis on infected cells.Till now,scientists have done lots of research on this apoptotic progress.The progress of JEV induced apoptosis involves a series of activation and inactivation of protease.Virus replication causes mitochondrial permeability transition,oxidative stress,endoplasmic reticulum stress in cells,and finally triggers apoptosis.Since apoptosis partially contributes to the cytopathic effect on cells and the symptoms on animals,apoptotic research is a significant part of uncovering the pathological mechanism.Growth arresting and apoptotic pathways were described in this paper.
出处 《动物医学进展》 CSCD 北大核心 2011年第5期108-112,共5页 Progress In Veterinary Medicine
基金 西北农林科技大学青年学术骨干项目(E111020901) 教育部新世纪优秀人才支持计划(NCET-07-0701)
关键词 日本脑炎病毒 细胞凋亡 信号转导 JEV apoptosis signal transduction
  • 相关文献

参考文献4

二级参考文献78

共引文献22

同被引文献37

  • 1路凯.纳米氧化铈暴露可导致巨噬细胞凋亡[D].广东广州:华南理工大学轻工与食品学院,2010. 被引量:1
  • 2Malhotra D, Thimmulappa R, Vij N, et al. Heightened endo- plasmic reticulum stress in the lungs of patients with chronic obstructive pulmonary disease: the role of Nrf2-regulated proteasomal activity[J]. Am J Respir Crit Care Med, 2009, 180(12) :1196-1207. 被引量:1
  • 3Carroll T P,Greene C M,O'Connor C A, et al. Evidence for unfolded protein response activation in monocytes from indi- viduals with alpha-1 antitrypsin deficiency[J]. J Immunol, 2010,184 (8): 4538-4546. 被引量:1
  • 4Promlek T, Ishiwata-Kimata Y,Shido M,et al.Membrane ab- errancy and unfolded proteins activate the endoplasmic reticu- lure stress sensor Irel in different ways[J]. Mol Biol Cell, 2011,22(18) :3520-3532,. 被引量:1
  • 5Nakamura D, Tsuru A, Ikegami K, et al.Mammalian ER stress sensor IRElbeta specifically down-regulates the synthesis of secretory pathway proteins[J]. FEBS Lett, 2011,585 (1) :133- 138. 被引量:1
  • 6Fang N, Zhang W,Xu S, et at.TRIB3 alters endoplasmic retic- ulum stress-induced [3-cell apoptosis via the NF-gB pathway FJ].Metabolism, 2014,63(6) :822-830. 被引量:1
  • 7Yamazaki H, Hiramatsu N, Hayakawa K, et al. Activation of the Akt-NF-kappaB pathway by subtilase cytotoxin through theATF6 branch of the unfolded protein response[J].J Im- munol, 2009,183 (2) : 1480-1487. 被引量:1
  • 8Liu C M, Zheng G H, Ming Q L, et al. Protective efect of quercetin on lead-induced oxidative stress and endoplasmic re- ticulum stress in rat liver via the IRE1/JNK and PI3K/Akt pathway[J].Free Radical Res,2013,47(3):192-201. 被引量:1
  • 9Cao S S,Kaufman R J.Endoplasmic reticulum stress and oxi- dative stress in cell fate decision and human disease[J].An- tioxidants & Redox Signaling, 2014,21 (3) : 396-413. 被引量:1
  • 10Overley-Adamson B, Artlett C M, Stephens C, et al.Targeting the unfolded protein response,XBP1 ,and the NLRP3 inflam- masome in fibrosis and caneer[J].Cancer Biol Ther, 2014,15 (4) :452-462. 被引量:1

引证文献2

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部