期刊文献+

自噬与衰老的关系

下载PDF
导出
摘要 在正常细胞生长和发育过程中,生物大分子的生物合成和分解代谢存在一种重要的平衡。环境变化通过多种调节机制,促进机体生长和发育,最终保持生物合成和分解代谢平衡。在真核细胞中,蛋白质降解主要通过泛素-蛋白酶体途径和自噬-溶酶体途径完成:蛋白酶体途径局限于胞浆和细胞核,主要参与短寿命蛋白质的降解;而溶酶体途径由囊泡状细胞器组成,其内含有多种水解酶包括蛋白酶负责物质降解。众所周知,溶酶体途径负责长寿命蛋白质的降解。其中自噬(autophagy)是溶酶体途径的主要成分,它将包括蛋白质和受损细胞器在内的胞浆成分输送入溶酶体,从而将其降解。1自噬的提出自噬一词来源于希腊语,本意是‘‘吞噬自己”。
出处 《成都医学院学报》 CAS 2012年第3期347-351,共5页 Journal of Chengdu Medical College
基金 国家重点基础研究计划(973计划)项目(NO:2011CBA01003) 国家重大科学研究计划项目(NO:2011CB964904) 国家自然科学基金项目(NO:30870920)
关键词 自噬 衰老
  • 相关文献

参考文献63

  • 1Klionsky DJ,Emr SD. Autophagy as a regulated pathway of cellular degradation[J]. Science, 2000,290 ( 5497) : 1717-1721.
  • 2Salminen A, Kaarniranta K. Regulation of the aging process by autophagy[J]. Trends Mol Med,2009,15(5) :217-224.
  • 3Ohsumi Y. Autophagy in yeast, bulk protein degradation in the vacuole[J]. Seikagaku, 1997,69( 1 ) : 39-44.
  • 4Ohsumi Y. Molecular dissection of autophagy: two ubiquitin- like systems[J]. Nat Rev Mol Cell Biol,2001,2(3) :211-216.
  • 5Ohsumi Y, Ohsumi M, Baba M. Autophagy in yeast[J]. Tanpakushitsu Kakusan Koso, 1993,38(1 ): 46-52.
  • 6Klionsky DJ, Cregg JM, Dunn WA Jr, et al. A unified nomenclature for yeast autophagy-related genes[J]. Dev Cell, 2003,5(4) :539-545.
  • 7Chang YY, Neufeld TP. An Atgl/Atg13 complex with multiple roles in TOR-mediated autophagy regulation[J]. Mol Biol Cell, 2009,20 (7) : 2004-2014.
  • 8Kamada Y, Funakoshi T, Shintani T, et al. Tot-mediated induction of autophagy via an Apgl protein kinase complex [J]. J Cell Biol,2000,150(6) :1507-1513.
  • 9Scott RC, Juhdsz G, Neufeld TP. Direct induction of autophagy by Atgl inhibits cell growth and induces apoptotie cell death[J]. Curr Biol, 2007,17 (1): 1-11.
  • 10Cheong H ,Nair U,Geng J,et al. The Atgl kinase complex is involved in the regulation of protein recruitment to initiate sequestering vesicle formation for nonspeeifie autophagy in Saeeharomyees cerevisiae [J]. Mol Biol Cell, 2008, 19 ( 2 ) : 668-681.

二级参考文献17

  • 1王道毅 邹文俊 陈守春 李忌.衰老问题:衰老的自由基理论[J].自由基生命科学进展,2001,8:19-23.
  • 2Nystrom T The free-radical hypothesis of aging goes prokaryotic[J]. Cell Mol Life Sci, 2003,60( 7):1333-1341.
  • 3Droge W. Oxidative stress and aging[J]. Adv Exp Med Biol,2003,543:191-200.
  • 4Stadtman ER, Levine RL. Free radical-mediated oxidation of free amino acids and amino acid residues in proteins[J]. Amino Acids, 2003,25 (3-4): 207-218.
  • 5Herrera B, Alvarez AM, Sanchez A, Fernandez M, et al. Reactive oxygen species (ROS) mediates the mitochondrial- dependent apoptosis introduced by transforming growth, h factor (beta) in fetal hepatocytes [J]. FASEB J, 2001,21 ( 6 ): 62 -70.
  • 6Levine RL. Carbonyl modified proteins in cellular regulation,aging, and disease [J]. Free Radical Bio Med,2002, 32(9):790-796.
  • 7Raha S, Robinson BH. Mitochondria, oxygen free radicals,disease and aging[J]. TIBS, 2000,25: 502-508.
  • 8Fusako Maehira, Yoshio Nakama, Norio Ohmine, et al. Age-related changes in the oxidation-reduction characteristics and the 8-OHdG accumulation in liver, lung, brain of SAM R1 and SAM RI[J]. International congress series, 2004,1260:259-262.
  • 9Berdanier CD, Everts HB. Mitochondrial DNA in aging degenerative disease [J]. Mutation Research, 2001,475 ( 1 - 2 ) :169-184.
  • 10Raha S, Robinson BH. Mitochondria, oxygen free radicals,and apoptosis[J]. Amj Med Genet, 2001,106(1):62-70.

共引文献26

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