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dc.contributor.advisor林圣彩
dc.contributor.author孙玉
dc.date.accessioned2018-12-05T01:37:35Z
dc.date.available2018-12-05T01:37:35Z
dc.date.issued2018-04-09
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/169901
dc.description.abstract蛋白激酶ULK1和ULK2可以在多种外界刺激下启动自噬的发生。然而,对于ULK1和ULK2这两个激酶的生理功能的研究,目前仍然十分有限。在本论文中,我们构建了肝脏组织特异性敲除Ulk1和Ulk2基因的小鼠,并发现该小鼠虽然可以正常存活,但表现出显著肝肿大的表型。出人意料的是,在过夜饥饿的肝脏特异性敲除Ulk1和Ulk2的小鼠肝脏组织中,自噬可以正常发生。有意思的是,我们发现,与对照小鼠相比,肝脏特异性缺失Ulk1和Ulk2的小鼠对于APAP诱导的肝损伤有着很强的抵抗能力。更进一步的研究发现,尽管Ulk1和Ulk2的缺失并不影响APAP所诱导的细胞自噬过程,但是它们对于此时JNK信号通路的激活是...
dc.description.abstractThe Ser/Thr kinases ULK1 and ULK2 regulate autophagy initiation under various stress conditions. However, the physiological functions of these kinases are not well-characterized. In this thesis, we show that mice with liver-specific double knockout of Ulk1 and Ulk2 (Ulk1/2 LDKO) are viable but exhibit overt hepatomegaly phenotype. Surprisingly, Ulk1/2 LDKO mice display normal autophagic activity i...
dc.language.isozh_CN
dc.relation.urihttps://catalog.xmu.edu.cn/opac/openlink.php?strText=59963&doctype=ALL&strSearchType=callno
dc.source.urihttps://etd.xmu.edu.cn/detail.asp?serial=60125
dc.subjectULK1
dc.subjectAPAP
dc.subjectJNK
dc.subjectULK1
dc.subjectAPAP
dc.subjectJNK
dc.titleULK1/2调控对乙酰氨基酚诱导的肝损伤的机制研究
dc.title.alternativeThe Mechanism of the Regulation of APAP-induced Liver Injury by ULK1/2
dc.typethesis
dc.date.replied2017-05-12
dc.description.note学位:理学硕士
dc.description.note院系专业:生命科学学院_生物化学与分子生物学
dc.description.note学号:21620141152562


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