bip介导内质网应激诱导的tau蛋白过度磷酸化及伴侣蛋白sil1的保护作用

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1、分类号学号D200978057学校代码10487密级博士学位论文Bip介导内质网应激诱导的tau蛋白过度磷酸化及伴侣蛋白Sil1的保护作用学位申请人：刘赞朝学科专业：病理学与病理生理学指导教师：王建枝田青教授答辩日期：2012年5月ADissertationSubmittedinPartialFulfillmentoftheRequirementsfortheDegreeofDoctorofPhilosophyinMedicineBipmediatesERstress-inducedtauhyperphosphoryl

2、ationandtheprotectionofSil1Postgraduate:LiuZan-ChaoMajor:PathologyandPathophysiologySupervisor：Prof.WangJian-Zhi,Prof.TianQingHuazhongUniversityofScience&TechnologyWuhan430030,ChinaMay,2012独创性声明本人声明所呈交的学位论文是我个人在导师的指导下进行的研究工作及取得的研究成果。据我所知，除文中已标明引用的内容外，本论文不包含任何其他人

3、或集体已经发表或撰写过的研究成果。对本文的研究做出贡献的个人和集体，均已在文中以明确方式标明。本人完全意识到本声明的法律结果由本人承担。学位论文作者签名：刘赞朝日期：年月日学位论文版权使用授权书本学位论文作者完全了解学校有关保留、使用学位论文的规定，即：学校有权保留并向国家有关部门或机构送交论文的复印件和电子版，允许论文被查阅和借阅。本人授权华中科技大学可以将本学位论文的全部或部分内容编入有关数据库进行检索，可以采用影印、缩印或扫描等复制手段保存和汇编本学位论文。保密□，在______年解密后适用本授权数。本论文属于不

4、保密□√。（请在以上方框内打“√”）学位论文作者签名：刘赞朝指导教师签名：王建枝田青日期：年月日日期：年月日目录中文摘要····························································································(1)英文摘要····························································································(3)前言······

5、······················································································(5)材料和方法·························································································(7)结果··········································································

6、··················(23)1Bip在内质网应激诱导剂诱导tau过度磷酸化中的关键作用······················(23)2过表达Bip通过激活GSK-3β诱导tau过度磷酸化··································(25)3过表达Bip促进GSK-3β与tau结合····················································(32)4ER应激时、过表达Bip后及Tg2576小鼠脑中Sil1水平下调··········

7、·············(34)5过表达Sil1改善TG和Bip过表达诱导的GSK-3β激活及tau过度磷酸化······················································································(37)6Bip上调及Sil1下调对原代神经元轴突生长的影响··································(43)讨论··················································

8、··········································(45)小结····························································································(50)创新点···················