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dc.contributor.advisor王光辉
dc.contributor.author周梦璐
dc.date.accessioned2018-12-05T01:48:58Z
dc.date.available2018-12-05T01:48:58Z
dc.date.issued2018-04-12
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/170774
dc.description.abstract凋亡抑制蛋白IAPs调控细胞的多种生物学进程,其过表达与肿瘤生长、不良预后及疗效相关,在大多数人类恶性肿瘤中表达异常升高。cIAPs参与细胞命运的调控过程。TNFα结合TNFR1引起TRADD、TRAF2、TRAF5、cIAP1、cIAP2以及蛋白激酶RIP1的募集形成复合物I。cIAPs介导复合物I组分的泛素化,如RIP1,进而诱导IKK复合物的募集。IKKβ磷酸化NF-κB抑制子IκB,使其靶向泛素化依赖的蛋白酶体降解,从而使NF-κB转移至细胞核启动靶基因的表达。在缺乏cIAPs的情况下,RIP1从膜结合的复合物I上解离,与FADD、caspase8形成复合物II,导致caspase8的...
dc.description.abstractApoptosis inhibitory protein IAPs regulate a variety of biological processes. cIAPs are abnormally elevated in most human malignancies, and their overexpression is associated with tumor growth, poor prognosis and efficacy. cIAPs are involved in the regulation of cell fate. TNFα binds TNFR1 to induce TRADD, TRAF2, TRAF5, cIAP1, cIAP2 and protein kinase RIP1 to form complex I. cIAPs mediate the ubiq...
dc.language.isozh_CN
dc.relation.urihttps://catalog.xmu.edu.cn/opac/openlink.php?strText=60368&doctype=ALL&strSearchType=callno
dc.source.urihttps://etd.xmu.edu.cn/detail.asp?serial=59625
dc.subject蓝花楹酮
dc.subjectcIAP2
dc.subject细胞凋亡
dc.subjectRIP1
dc.subjectJacaranone
dc.subjectcIAP2
dc.subjectapoptosis
dc.subjectRIP1
dc.title蓝花楹酮调控cIAP2介导的TNFα生死转换的作用机制研究
dc.title.alternativeThe Mechanism on the Regulation of Jacaranone in cIAP2-mediated TNFα Survival and Death Conversion
dc.typethesis
dc.date.replied2017-05-11
dc.description.note学位:医学硕士
dc.description.note院系专业:药学院_药理学
dc.description.note学号:32320141153439


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