期刊文献+

Akt/PKB信号转导通路与脑缺血 被引量:3

Akt/PKB signaling pathway and cerebral ischemia
原文传递
导出
摘要 Akt被生长因子介导的受体酪氨酸激酶磷酸化激活后可激活一系列底物分子,包括Forkhead转录因子等,对细胞生存和死亡进行调控。随着脑缺血后Akt磷酸化水平(Ser473)的改变,其上游、下游蛋白磷酸化水平也发生变化。预处理可能通过改变Akt蛋白磷酸化水平而产生缺血耐受。Akt/PKB信号转导通路功能障碍可能介导了脑缺血后神经元死亡。 After being activated by the growth factor-mediated receptor tyrosine kinase phosphorylation, Akt activates a series of substrate molecules, including Forkhead transcription factors etc, which regulate cell survival and death. With the changes of Akt phosphorylation levels (Ser473) after cerebral ischemia, its upstream and downstream protein phosphorylation levels have also changed. Preconditioning may produce ischemic tolerance by changing the levels of Akt protein phosphorylation. Dysfunction of Akt/PKB signal transduction pathway may mediated neuronal death after cerebral ischemia.
作者 詹丽璇 徐恩
出处 《国际脑血管病杂志》 北大核心 2009年第2期149-152,共4页 International Journal of Cerebrovascular Diseases
基金 基金项目:广东省自然科学基金(8151018201000035)
关键词 蛋白质丝氨酸苏氨酸激酶 蛋白质酪氨酸激酶 脑缺血 缺血预处理 protein-serine-threonine kinases protein-tyrosine kinases cerebral ischemia ischemic preconditioning
  • 相关文献

参考文献22

  • 1Fresno Vara JA, Casado E, de Castro J, et al. PBK/Akt signalling pathway and cancer. Cancer Treat Rev, 2004, 30: 193-204.
  • 2Hanada M, Feng J, Hemmings BA. Structure, regulation and function of PKB/AKT-a major therapeutic target. Biochim Biophys Acta, 2004, 1697: 3-16.
  • 3Kaplan DR, Miller FD. Neurotrophin signal transduction in the nervous system. Curr Olin Neurobiol, 2000, 10: 381-391.
  • 4Fukunaga K,Ishigami T,Kawano T.Transcriptional regulation of neuronal genes and its effect on neural functions:expression and function of forkhead transcription factors in neurons.J Pharmacol Sci,,2005,98: 205- 211.
  • 5Shioda N,han F,Moriguchi S,et al.Constitutively active calcineurin mediates delayed neuronal death through Fas-ligand expression via activation of NFAT and FKHR transcriptional activities in mouse brain ischemia.J Neurochem,2007, 102: 1506-1517.
  • 6Franke TF, Hornik CP, Segev L, et al. PBK/Akt and apoptosis: size matters. Oncogene, 2003, 22: 8983-8998.
  • 7Troussard AA. McDonald PC, Wederell ED, et al. Preferential dependence of breast cancer cells versus normal cells on integrin- linked kinase for protein kinase B/Akt activation and cell survival. Cancer Res, 2006, 66: 393-403.
  • 8Zhao H, Shimohata T, Wang JQ, et al. Akt contributes to neuroprotection by hypothermia against cerebral ischemia in rats. J Neurosci, 2005, 25: 9794-9806.
  • 9Noshita N, Lewen A, Sugawara T, et al. Evidence of phosphorylation of Akt and neuronal stawival after transient focal cerebral isehemia in mice. J Cereb Blood How Metab, 2001,21 : 1442-1450.
  • 10Endo H,Nito C,Kamada H,et al.Activation of the Akt/GSK3β signaling pathway mediates survival of vulnerable hippocarnpal neurons after transient global cerebral ischemia in rats.J Cereb Blood Flow Metab,2006, 26: 1479-1489.

二级参考文献22

  • 1[1]Janoff A.Alterations in lysosomes (intracellular enzymes)during shock; effects of preconditioning (tolerance) and protective drugs[J].Int Anesthesiol Clin,1964,97:251-269.
  • 2[2]Dahl NA,Balfour WM.Prolonged anoxic survival due to anoxia pre-exposure brain ATP,lactate,and pyruvate[J].Am J Physiol,1964,207:452-456.
  • 3[3]Blanco M,Lizasoain I,Sobrino T,et al.Ischemic preconditioning:a novel target for neuroprotective therapy[J].Cerebrovasc Dis,2006,21 Suppl 2:38-47.
  • 4[4]Sharp FR,Bergeron M,Bernaudin M.Hypoxia-inducible factor in brain[J].Adv Exp Med Biol,2001,502:273-291.
  • 5[5]Simon RP.Hypoxia versus ischemia[J].Neurology,1999,52:7-8.
  • 6[6]Ota A,Ikeda T,Abe K,et al.Hypoxic-ischemic tolerance phenomenon observed in neonatal rat brain[J].Am J Obstet Gynecol,1998,179:1075-1078.
  • 7[7]Gidday JM,Fitzgibbons JC,Shah AR,et al.Neuroprotection from ischemic brain injury by hypoxic preconditioning in the neonatal rat[J].Neurosci Lett,1994,168:221-224.
  • 8[8]Miller BA,Perez RS,Shah AR,et al.Cerebral protection by hypoxic preconditioning in a murine model of focal ischemia-reperfusion[J].Neuroreport,2001,12:1663-1669.
  • 9[9]Bernaudin M,Nedelec A,Divoux D,et al.Normobaric hypoxia induces tolerance to focal permanent cerebral ischemia in association with an increased expression of hypoxia-inducible factor-1 and its target genes,erythropoietin and VEGF,in the adult mouse brain[J].J Cereb Blood Flow Metab,2002,22:393-403.
  • 10[10]Huang LE,Bunn HF.Hypoxia-inducible factor and its biomedical relevance[J].J Biol Chem,2003,278:19575 -19578.

共引文献1

同被引文献72

  • 1孙胜,高钰琪,高文详,范明.缺氧预处理保护机制的研究进展[J].国际病理科学与临床杂志,2005,25(4):304-306. 被引量:5
  • 2De Duve C. The lysosome. Sci Am, 1963, 208: 64-72.
  • 3Takeshige K, Baba M, Tsuboi S, et al. Autophagy in yeast dermstrated with proteinase-deticieat mutants and oonditiovs for its induction. J Cell Biol, 1992, 119: 301-311.
  • 4Levine B, Kroemer G. Autophagy in the path0lesis of disease. Cell, 2008, 132: 27-42.
  • 5Klionsky DJ, Emr SD. Autopb_agy as a regulatod pathway of cellular degradation. Science, 2000, 290: 1717q721.
  • 6Nishida K, Kyoi S, Yamaguchi O, et at. The role of autophagy in the heart. Cell Death Differ, 2009, 16: 31-38.
  • 7Lipton P. Ischemic cell death in brain neurons. Physiol Rev, 1999, 79: 1431-1568.
  • 8Ravikumm" B, Sarkar S, Davies JE, et al. Regulation of mammalian autophagy in physiology and pathophysiology. Physiol Rev, 2010, 90: 1383-1435.
  • 9Axe EL, Walker SA, Manifava M, et al. Autophagosome formation from membrane compartments enriched in phosphatidylinositol 3- p hosp hat e and dynamically connect ed t o t he endop lasmic ret iculum. J Cell Biol, 2008, 182: 685-701.
  • 10Halley DW, Rambold AS, Satpute-Krishnan P, et al. Mitochondria supply membranes for autophagosome biogenesis during starvation. Cell, 2010, 141 : 656-667.

引证文献3

二级引证文献6

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