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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 陳瑞華 | zh_TW |
dc.contributor.author | 廖峻傑 | zh_TW |
dc.contributor.author | Chun-Chieh Liao | en |
dc.date.accessioned | 2021-07-11T15:46:39Z | - |
dc.date.available | 2024-02-28 | - |
dc.date.copyright | 2018-10-11 | - |
dc.date.issued | 2018 | - |
dc.date.submitted | 2002-01-01 | - |
dc.identifier.citation | An, H., and Harper, J.W. (2018). Systematic analysis of ribophagy in human cells reveals bystander flux during selective autophagy. Nat Cell Biol 20, 135-143.
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Oncotarget 8, 1429-1437. | - |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/79133 | - |
dc.description.abstract | 細胞自噬是一種細胞中維持養分恆定的機制,通過溶酶體來降解、回收受損蛋白質和細胞器以及有害物質。然而,細胞自噬機制仍未完全解開。迄今為止,關於長鏈非編碼RNA在各種細胞過程中的作用,包括細胞自噬,已經獲得了越來越多的了解。在這裡,我們發現了一種新的長鏈非編碼RNA,BCRP3,可以正向調控細胞自噬的進程。我們發現過度表現BCRP3可以在基礎上增加了細胞自噬小體的形成,而這樣的現象也發生在多種細胞自噬誘導的條件下。通過剖析細胞自噬小體形成的不同步驟,我們發現BCRP3增強了ATG16L1匯集在細胞自噬小體發生處的現象。機制上,BCRP3不影響ATG5-ATG12-ATG16L1複合物的形成,但可以促進ATG16L1和WIPI2之間的結合。RNA pull-down分析顯示BCRP3會結合ATG5-12綴合物和ATG16L1,但不與WIPI2相互作用。 RNA免疫沉澱進一步證實內源性BCRP3結合ATG16L1而不結合WIPI2。綜觀而言,我們的研究將BCRP3鑑定為細胞自噬的正調節因子,並闡述其透過增強ATG5-12-16L1複合物與WIPI2結合以促進自噬小體形成中的作用。 | zh_TW |
dc.description.abstract | Autophagy is a cellular homeostatic mechanism to recycle damaged proteins and organelles and harmful substances through lysosomal degradation. However, the detail mechanism still has not been completely unraveled. To date, increasing knowledge has gained on the roles of long non-coding RNAs in various cellular processes, including autophagy. Here, we identify a novel long non-coding RNA, breakpoint cluster region pseudogene 3 (BCRP3), as a positive regulator of autophagy. We showed that overexpression of BCRP3 increases the formation of autophagosomes in basal, starved and rapamycin-treated conditions. Through dissecting the different steps in autophagosome formation, we found that BCRP3 enhances the recruitment of ATG16L1 to nascent autophagosome. Mechanistically, BCRP3 does not affect the formation of ATG5-ATG12-ATG16L1 complex but promotes the interaction between ATG16L1 and WIPI2 in vivo. RNA pull down analysis revealed that BCRP3 interacts with ATG5-12 conjugate and ATG16L1 but not WIPI2. RNA immunoprecipitation further confirmed that endogenous BCRP3 binds ATG16L1 but not WIPI2. Together, our study identifies BCRP3 as a positive regulator of autophagy and suggests its role in enhancing the binding of ATG5-12-16L1 complex with WIPI2 to promote autophagosome formation. | en |
dc.description.provenance | Made available in DSpace on 2021-07-11T15:46:39Z (GMT). No. of bitstreams: 1 ntu-107-R05448003-1.pdf: 2033891 bytes, checksum: 4855fa1fae23d3a46b6ec44ef711d712 (MD5) Previous issue date: 2018 | en |
dc.description.tableofcontents | 論文口試委員審定書 i
謝辭 ii 中文摘要 iii Abstract iv I. Introduction 1 1. Autophagy 1 1-1. Autophagy 1 1-2. Mechanism of Autophagy 2 1-3. Physiological role of autophagy 6 2. ATG5-12-16L1 complex 7 2-1. ATG5-12 conjugate 7 2-2. ATG16L1 9 3. WIPIs in autophagy 11 4. Long non-coding RNA 13 4-1. Characteristics of long non-coding RNA 13 4-2. Molecular mechanisms for lncRNAs in executing their cellular functions 14 4-3. LncRNA in autophagy 16 II. Material and Methods 19 Plasmid 19 Antibody and Reagent 19 Lentivirus production and infection 20 Cell Culture and Transient Transfection 20 Western Blot 21 Immunoprecipitation 21 Immunofluorescence 22 RT/real-time PCR. 23 Subcellular fractionation assay 24 RNA immunoprecipitation 24 RNA pull-down assay 25 III. Result 26 Characterization of lncRNA BCRP3 26 BCRP3 promotes basal and starvation-induced autophagy 27 BCRP3 does not affect the initiation and nucleation processes of autophagy formation 28 BCRP3 promotes the interaction between ATG16L1 and WIPI2 29 BCRP3 is localized to cytoplasm and interacts with ATG5-12-16L1 but not WIPI2 30 IV. Discussion 31 V. Reference 36 VI. Figure 48 | - |
dc.language.iso | en | - |
dc.title | 一個新穎長鏈非編碼RNA在自噬小體形成所扮演的角色 | zh_TW |
dc.title | Regulation of autophagosome formation by a novel long non-coding RNA | en |
dc.type | Thesis | - |
dc.date.schoolyear | 106-2 | - |
dc.description.degree | 碩士 | - |
dc.contributor.oralexamcommittee | 陳光超;蔡欣祐 | zh_TW |
dc.contributor.oralexamcommittee | ;; | en |
dc.subject.keyword | 細胞自噬,長鏈非編碼RNA,ATG12-5-16L1,WIPI2, | zh_TW |
dc.subject.keyword | autophagy,lncRNA,ATG12-5-16L1,WIPI2, | en |
dc.relation.page | 62 | - |
dc.identifier.doi | 10.6342/NTU201802549 | - |
dc.rights.note | 未授權 | - |
dc.date.accepted | 2018-08-06 | - |
dc.contributor.author-college | 醫學院 | - |
dc.contributor.author-dept | 分子醫學研究所 | - |
dc.date.embargo-lift | 2023-10-11 | - |
顯示於系所單位: | 分子醫學研究所 |
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