期刊文献+

未折叠蛋白应答与白内障

下载PDF
导出
摘要 在真核细胞内质网中各种应激因素导致未折叠蛋白聚集时,发生内质网应激,细胞为生存启动未折叠蛋白应答。当未折叠蛋白应答时间过长,可诱发细胞凋亡等一系列效应。近来发现,未折叠蛋白应答与白内障的发生、发展密切相关。本文主要就未折叠蛋白应答通路与白内障的关系作一简要综述。
作者 生晖 卢奕
出处 《中国眼耳鼻喉科杂志》 2013年第1期60-62,共3页 Chinese Journal of Ophthalmology and Otorhinolaryngology
基金 上海市卫生局新百人计划(XBR2011056) 上海市优秀学科带头人(11XD1401200)
  • 相关文献

参考文献19

  • 1Schrsder M. Endoplasmic reticulum stress responses [ J ]. Cell Mol Life Sci, 2008,65 ( 6 ) : 862-894.
  • 2Cullinan SB, Diehl JA. Coordination of ER and oxidative stress signaling: the PER1E/Nd2 signaling pathway[J]. Int J Biochem Cell Biol, 2006,38(3) :317-332.
  • 3Liu Y, Adachi M, Zhao S, et al. Preventing oxidative stress: a new role for XBP1 [J]. Cell Death Differ, 2009,16(6) :847-857.
  • 4Bommiasamy H, Back SH, Fagone P, et al. ATF6alpha induces XBPl-independent expansion of the endoplasmic reticulum [ J ]. J Cell Sci, 2009,122 : 1626-1636.
  • 5Marciniak SJ, Yun CY, Oyadomari S, et al. CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum [ J ]. Genes Dev, 2004, 18 (24) :3066-3077.
  • 6Puthalakath H, O 'Reilly LA, Gunn P, et al. ER stress triggers apoptosis by activating BH3-only protein Bim[J]. Cell, 2007, 129 (7) :1337-1349.
  • 7Szegezdi E, Logue SE, Gorman AM, et al. Mediators of endoplasmic reticulum stress-induced apoptosis [ J ]. EMBO Rep, 2006, 7 (9) : 880-885.
  • 8Szegezdi E, Macdonald DC, Ni Chonghaile T, et al. Bel-2 family on guard at the ER [ J ]. Am J Physiol Cell Physiol, 2009, 296 (5) : C941-953.
  • 9Klee M, Pallauf K, Aleald S, et al. Mitoehondrial apoptosis induced by BH3-only molecules in the exclusive presence of endoplasmie reticular Bak [ J ]. EMBO J, 2009, 28 ( 12 ) : 1757-1768.
  • 10Shiraishi H, Okamoto H, Yoshimura A, et al. ER stress-induced apoptosis and caspase-12 activation occurs downstream of mitochondrial apoptosis involving Apaf-1 [ J ]. J Cell Sei, 2006, 119 (Pt 19) :3958-3966.

二级参考文献11

  • 1Li W C, Kuszak J R, Dunn K. lens epithelial cell apopotosis appears to be a common cellular basis for non-congenital cataract development in humans and animals [ J ]. J Cell Biol, 1995, 130( 1 ) : 169-181.
  • 2Lai E, Teodoro T, Volchuk A. Endoplasmic reticulum stress: signaling the unfolded protein response[J]. Physiology, 2007, 62( 1 ) : 193-201.
  • 3Shinohara T, Ikesugi K, Mulhem M L. Cataracts: role of the unfolded protein response[J]. Med Hypotheses, 2006, 66(2) : 365-370.
  • 4Szegezdi E, Fitzgerald U, Samali A. Caspase-12 and ER- stress-mediated apoptosis:the story, so far[J]. Ann N Y Acad Sci, 2003, 1010:186-194.
  • 5Qian Y, Tiffany-Castiglioni E. lead-induced endoplasmic reticulum (ER) stress responses in the nervous system [ J]. Neurochem Res, 2003, 28( 1 ) : 153-162.
  • 6DeGracia D J, Montie H L. Cerebral ischemia and the unfolded protein response[J]. J Neurochem, 2004, 91( 1 ) : 1-8.
  • 7Rao R V, Hermel E, Castro-Obregon S, et al. Coupling endoplasmic reticulum stress to the cell death program[ J]. J Biol Chem, 2001, 276(36):33869-33874.
  • 8Ferri K F, Kroemer G. Organelle-specific initiation of cell death pathways[J]. Nat Cell Biol, 2001, 3(11):E255-263.
  • 9Tu B P, Weissman J S. Oxidative protein folding in eukaryotes: mechanisms and consequences [ J ]. J Cell Biol, 2004, 164(3) :341-346.
  • 10Li W C, Spector A. lens epithelial cell apoptosis is an early event in the development of UVB-induced cataract[J]. Free Radical Biology Medicine, 1996, 20(3) :301-311.

共引文献4

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