全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

细胞外信号调节激酶在脑缺血损伤中的研究进展

, PP. 243-246

Keywords: 细胞外信号调节激酶,脑缺血,蛋白激酶

Full-Text   Cite this paper   Add to My Lib

Abstract:

References

[1]  Woodburne VL, Hayward NU, Poat JA. The effect of dizocilpine and inadolineon immediate early gene expression in the gerbil global ischemia model [J].Neur opharmacology, 1993, 32(10):1047.
[2]  Mudrick La, Baimbridge KG. Long-term changes in the rat hippocampal form ation following cerebral ischemia [J]. Brain Res, 1989, 493(1):197.
[3]  Wang X, Wang H, Xu L, et al. Significant neuroprotection against ischem ic b rain injury by inhibition of the MEK1 protein kinase in mice: exploration of pot ential mechanism associated with apoptosis [J]. J Pharmacol Exp Ther, 2003, 3 04(1): 172-178.
[4]  Davies SP, Reddy H, Caivano M, et al. Specificity and mechanism of acti on o f some commonly used protein kinase inhibitors [J]. Biochem J, 2000, 351:95-1 05.
[5]  Sweeney MI, Yager JY, Wolzw, et al. Cellular mechanisms involved in brai n ischemia[J]. Can J Physiol Pharmacol, 1995, 73(11):1525-1535.
[6]  Davis RJ. The mitogen-activated protein kinase signal transduction pathw ay [J]. J Biol Chem, 1993, 268:14553.
[7]  彭黎明,王曾礼.细胞凋亡的信号传导机制. 细胞凋亡的基础与临床[M].北京 :人民卫生出版社,2000.40-46.
[8]  徐 勇. MAPK家族与糖尿病并发症[J]. 国外医学内分泌学分册, 2001,(1):8- 10.
[9]  牟金叶,陈晓光. 促分裂原激活的蛋白激酶(MAPK)信号传导通路的研究进展[J ]. 生命科学,2002,208-221.
[10]  Foorce T, Bonventre J. Growth factors and mitogen-activated protein kina se [J]. Hypertension, 1998, 31:152-161.
[11]  Glogowshi EA, Tsiani E, Zhou X, et al. High glucose alters the response of m esangial cell protein kinase C isoforms to endothelin-1 [J]. Kidney Int, 1999 , 55:486-499.
[12]  陈良恩.JNK信号转导通路及其在应激中的作用[J].国外医学生理病理 学与临床分册, 2001, 21(3):169-171.
[13]  Brewster JL, De Valoir T, Dwyer NG, et al. An osmosensing signal transd uction pathway in yeast [J]. Science, 1993, 259:1760-1763.
[14]  许川山,刘志君,唐建民,等.低强度激光促细胞增殖效应与丝裂原激活蛋白激酶 信号传导途径[J]. 中国激光医学杂志,2000,(2):47-48.
[15]  Ailawa R, Komuro I, Yamazaki T, et al. Oxidation stress activates extra cell ular signal-regulated kinases throngh Src and Ras in cultured cardiac monocytes of neonatal rats[J]. J Clin Invest, 1997, 100:1813-1821.
[16]  Ma XL, Kumar S, Gao F, et al. Inhibition of p38 mitogen activated prote in k inase decreases cardiomyocyte apoptosis and improves cardiac function after myoc ardial ischemia and reperfusion [J]. Circulation,1999, 99(13):1685-1691.
[17]  Elaine A, Irving EA, Mark Bamford. Role of mitogen- and stress-activate d kinases in ischemic injury [J]. J Cereb Blood Flow Metab, 2002, 22:631-647 .
[18]  Lipto SA, Roserberg PA. Excitatory amino acids as a final common pathwa y for neurologic disorders [J]. N Engl T Med, 1994, 330: 613-622.
[19]  Vanhoutte P, Barnier JV, Guibert B, et al. Glutamate induces phosphoryl atio n of Elk-1 and CREB, along with c-fos activation, via an extracellular signal-re gulated kinase-dependent pathway in brain slices[J].Mol Cell Biol,1997,19(1): 136-146.
[20]  Singer CA, Figueroa Masot XA, Batchelor RH, et al. The mitogen-activate d pr otein kinase pathway mediates estrogen neuroprotection after glutamate toxicity in primary cortical neurons [J]. J Neurosci, 1999, 19(7): 2455-2463.
[21]  Schwarzschild MA, Cole RL, Meyers MA, et al. Contrasting calcium depend enci es of SAPK and ERK activations by glutamate in cultured striatal neurons[J]. J Neurochem,1999, 72(6): 2248-2255.
[22]  Walton KM, DiRocco R, Bartlett BA, et al. Activation of p38MAPK in micr oglia after ischemia [J]. J Neurochem,1998,70(4):1764-1767.
[23]  Herdegen T, Claret FX, Kallunki T, et al. Lasting N-terminal phosphoryl atio n of c-Jun and activation of c-Jun N-terminal kinases after neuronal injury[J] . neurosci, 1998, 18(14): 5124-5135.
[24]  Ozawa H, Shioda S, Dohi K, et al. Delayed neuronal cell death in the ra t hi ppocampus is mediated by the mitogen-activated protein kinase signal transductio n pathway [J]. Neurosci Letters, 1999, 262:57-60.
[25]  Oh SW, Ahn YM, Kang UG, et al.Differential activation of c-Jun N- terminal protein kinase and p38 in rat hippocampus and cerebellum after electroconvulsive shock[J]. Neurosci Letters, 1999, 271: 101-104.
[26]  蔡 琪,李晓玫,王海燕.缺血/再灌注损伤时丝裂原活化蛋白激酶信号转导通路 的变化[J]. 中国病理生理杂志,2000,16(12): 1335-1337.
[27]  Namura S, Iihara K, Takama S, et al. Intravenous administration of MEK inhi bitor U0126 affords brain protection against forebrain ischemia and focal cerebr al ischemia[J]. Proc Natl Acad Sci USA,2001, 98:11569-11574.
[28]  Hu BR, Liu CL, Park DJ. Alteration of MAP kinase pathways after transie nt forebrain ischemia [J]. J Cereb Blood Flow Metab,2000, 20:1089-1095.
[29]  Stanciu M, Wang Y, Kentor R, et al. Persistent activation of ERK contri butes to glutamate-induced oxidative in a neuronal cell line and primary cortica l neuronal cultures[J]. J Biol Chem, 2000, 275:12200-12206.
[30]  Irving EA, Ray AM, Staton PC, et al. Neuroprotection with the MEK in hibitor U0126 following ischemic injury [J]. J Cereb Blood Flow Metab, 2001, 21(Suppl 1):S379.
[31]  Rving EA, Barone FC, Reith AD, et al. Differential activation of MAPK/E RK a nd p38/SAPK in neurons and glia following focal cerebral ischemia in the rat[J ]. Mol Brain Res, 2000, 77:65-75.
[32]  Wu DC, Ye W, Che XM, et al. Activation of mitogen- activated protein ki nase after permanent cerebral artery occlusion in mouse brain [J]. J Cereb Bl ood Flow Metab,2000, 20:1320-1330.
[33]  Alessandrini A, Namura S, Moskowitz MA, et al. MEK1 protein kinase inhi bition protects against damage resulting from focal cerebral ischemia[J]. Pro c Natl Acad Sci USA, 1999, 96(22):12866-12869.
[34]  Pereira DB, Carvalho AP, Duarte CB. Non-specific effects of the MEK inh ibit ors PD98059 and U0126 on glutamate release from hippocampal synaptosomes[J]. Neuropharmacology, 2002, 42:9-19.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133