期刊文献+

BclGs对肿瘤细胞促凋亡功能的初步研究

Characteristics of apoptosis induced by BclGs in tumor cell
在线阅读 下载PDF
导出
摘要 为了探讨仅含有BH3结构域的促凋亡蛋白BclGs的促凋亡机理,从人睾丸cDNA文库中克隆BclGs基因编码区,将其与pEGFP-C1载体连接,构建载体pEGFP-BclGs,转染COS7细胞和多种肿瘤细胞(如Hela、HepG2和MCF7等),研究BclGs对肿瘤细胞的促凋亡功能。结果表明,pEGFP-BclGs可以诱导不同的肿瘤细胞凋亡,但凋亡率存在差别;BclGs在不同细胞的线粒体中均呈点状分布。线粒体是诱导肿瘤细胞凋亡的有效细胞器,BclGs在线粒体中呈点状分布。 In order to investigate the molecular mechanism of BH3-only proapoptotic BclGs inducing apoptosis,BclGs gene was cloned from human testis cDNA library and constructed into the expressing vector pEGFP-C1. The fusion protein pGFP-BclGs was successfully detected by fluorescent microscope analysis and Western blotting. The result demonstrated that BclGs could induce several tumor cells apoptosis, but showed difference in apoptosis rate. Therefore ,the conclusion can be drawn that the plastochondria was an effective cell organ which can induce the tumor cell to apoptosis,and BclGs assumes the punctual distribution in plastochondria.
出处 《西北农林科技大学学报(自然科学版)》 CSCD 北大核心 2007年第3期29-32,37,共5页 Journal of Northwest A&F University(Natural Science Edition)
基金 国家自然科学基金项目(30200043)
关键词 BclGs BH3结构域 肿瘤细胞 亚细胞定位 BclGs BH3 domain tumor cell subcellular localization
  • 相关文献

参考文献13

  • 1Guo B,Godzik A,Reed J C.Bcl-G,a novel pro-apoptotic member of the Bcl-2 family[J].J Biol Chem,2001,276(4):2780-2786.
  • 2Reed J C,Haldar S,Croce C M,et al.Complementation by BCL-2 and C-HA-RAS on co genes in malignant transformation of rat embryo fibroblasts[J].Mol Cell Boil,1990,10(8):4370-4374.
  • 3Adachi M,Zhang Y B,Imai K,et al.Mutation of BAD within the BH3 domain impairs its phosphorylation-mediated regulation[J].FEBS Letters,2003,551:147-152.
  • 4Verma S,Zhao L J,Chinnadurai G,et al.Phosphorylation of the pro-apoptotic protein BIK:mapping of phosphorylation sites and effect on apoptosis[J].J Biol Chem,2001,276:4671-4676.
  • 5Li H,Zhu H,Xu C,et al.Cleavage of BID by caspase-8 mediates the mitochondrial damage in the Fas pathway to apoptosis[J].Cell,1998,94:491-501.
  • 6柳向军,张令强,刘小林,贺福初.细胞凋亡中的Bcl-2家族蛋白及其BH3结构域的功能研究[J].生物化学与生物物理进展,2006,33(3):221-225. 被引量:21
  • 7Borner C.The Bcl-2 protein family:sensors and checkpoints for life-or-death decisions[J].Mol Immunol,2003,39:615-647
  • 8Kroemer G,Reed J C.Mitochondrial control of cell death[J].Nat Med,2000,6:513-519.
  • 9Gross A,McDonnell J M,Korsmeyer S J.BCL-2 family members and the mitochondria in apoptosis[J].Genes Dev,1999,13:1899-1911.
  • 10Coultas L,Bouillet P,Loveland K L,et al.Concomitant loss of proapoptotic BH3-only Bcl-2 antagonists Bik and Bim arrests spermatogenesis[J].EMBO J,2005,24(22):3963-3973.

二级参考文献33

  • 1Li H,Zhu H,Xu C,et al.Cleavage of BID by caspase-8 mediates the mitochondrial damage in the Fas pathway to apoptosis.Cell,1998,94 (4):491~501
  • 2Zha J,Weiler S,Oh K J,et al.Post-translational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis.Science,2000,290 (5497):1761 ~ 1765
  • 3Lutter M,Fang M,Luo X,et al.Cardiolipin provides specificity for targeting oftBid to mitochondria.Nat Cell Biol,2000,2 (10):754~761
  • 4Lutter M,Perkins G A,Wang X.The pro-apoptotic Bcl-2 family member tBid localizes to mitochondrial contact sites.BMC Cell Biol,2001,2:22
  • 5Seo S Y,Chen Y B,Ivanovska I,et al.BAD is a pro-survival factor prior to activation of its pro-apoptotic function.J Biol Chem,2004,279 (40):42240~42249
  • 6Chen D,Zhou Q.Caspase cleavage of BimEL triggers a positive feedback amplification of apoptotic signaling.Proc Natl Acad Sci USA,2004,101 (5):1235~ 1240
  • 7Zinkel S S,Hurov K E,Ong C,et al.A role for proapoptotic BID in the DNA-damage response.Cell,2005,122 (4):579~591
  • 8Kamer I,Sarig R,Zaltsman Y,et al.Proapoptotic BID is an ATM effector in the DNA-damage response.Cell,2005,122 (4):593 ~603
  • 9Kroemer G,Reed J C.Mitochondrial control of cell death.Nat Med,2000,6 (5):513~519
  • 10Gross A,McDonnell J M,Korsmeyer S J.BCL-2 family members and the mitochondria in apoptosis.Genes Dev,1999,13 (15):1899~1911

共引文献20

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