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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/82105完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 李芳仁 (Fang-Jen Lee) | |
| dc.contributor.author | Shin-Jin Lin | en |
| dc.contributor.author | 林新晉 | zh_TW |
| dc.date.accessioned | 2022-11-25T05:35:57Z | - |
| dc.date.available | 2026-10-23 | |
| dc.date.copyright | 2021-11-09 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-10-26 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/82105 | - |
| dc.description.abstract | 章節一 胞內體上的Arl4A透過與VPS36的結合進而抑制EGFR的降解 Arl4Ａ (ADP-ribosylation factor-like 4A; Arl4Ａ)是屬於腺嘌呤核苷二磷酸核醣化因子相似蛋白 (Arf-like) 之一。這個蛋白質家族廣為人知的功能主要參與在囊泡傳遞運輸、細胞骨架重組、和胞器的形成等等。其中Arl4A又特別被報導了參與在細胞膜皺褶的形成、細胞骨架的調控、高基氏體的形成等等功能之中；然而Arl4A在囊泡傳遞運輸中扮演何種角色，目前還不明白。配體 (EGF) 誘導的EGFR(受器)內吞作用，並且驅動下游訊息路徑的傳遞，這一連串的過程控制了細胞許多功能。我們發現Arl4A可以透過與VPS36結合，降低了EGFR受器的降解。我們也觀察到Arl4A的敲除，會加速EGFR快速的運輸至溶酶體內進行降解。我們更進一步分析，Arl4A與VPS36蛋白質上氨基酸序列351-356進行結合。我們將此序列突變後導致Arl4A無法與VPS36結合，透過這個突變的VPS36，我們發現EGFR的降解速度會比起野生型來得快。我們的結果顯示著，Arl4A會負調控VPS36的功能，並且減慢EGFR去泛素化的速度，進而減緩EGFR降解的速度。 章節二 Arl4D與EB1的結合有助於EB1招引至中心粒以及幫助微管生成 Arl4D (ADP-ribosylation factor-like 4D; Arl4D)是屬於腺嘌呤核苷二磷酸核醣化因子相似蛋白 (Arf-like) 之一。目前所知，Arl4D可以調控細胞型態、細胞遷移與細胞骨架的重組。EB1是一種位於微管（microtubule）正端（plus end tip）以及中心粒(centrosome)上的蛋白，EB1在中心粒上的成核作用（microtubule nucleation）扮演很重要的角色。在本研究中，我們發現活化態的Arl4D（GTP bound form）會藉由SxLP motif與EB1直接的結合。我們也發現Arl4D會與中心粒有共同定位外，當我們調降（knockdown）Arl4D表達後，微管自中心粒的成核作用會受到抑制，也會影響EB1定位到中心粒的能力。進一步，降低Arl4D與EB1的結能力，也會降低EB1定位於中心粒上與抑制中心粒上的微管成核作用。此外，我們也發現了Arl4D會促進EB1與p150之間的交互作用，此交互作用對於微管的成核與穩定有很大的幫助。總而言之‚我們的結果顯示Arl4D影響EB1與p150在中心粒上的結合，進而調控中心粒上的微管成核作用的新機制。 | zh_TW |
| dc.description.provenance | Made available in DSpace on 2022-11-25T05:35:57Z (GMT). No. of bitstreams: 1 U0001-2210202115060200.pdf: 80130949 bytes, checksum: d48f193eb3e17066600a99994f1440c0 (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | 口試委員審定書....................... i 致謝............................... ii 中文摘要............................ iii Abstract........................... v Abbreviations ..................... vii Table of Contents.................. 1 Introduction ...................... 2 Materials and Methods ............. 14 Results ........................... 24 Ⅰ. Arl4A downregulates EGFR degradation via interacting with ESCRT-II component VPS36 ...... 24 Ⅱ. Arl4D-EB1 interaction promotes centrosomal recruitment of EB1 and microtubule growth…..... 37 Discussion........................... 49 Figures ............................. 60 Reference............................ 132 Appendix..............................144 Publish paper “Arl4D-EB1 interaction promotes centrosomal recruitment of EB1 and microtubule growth publish paper” Molecular Biology of the Cell. 2020 October | |
| dc.language.iso | en | |
| dc.subject | 微管 | zh_TW |
| dc.subject | 腺嘌呤核苷二磷酸核醣化相似因子4 | zh_TW |
| dc.subject | 表皮生長因子受體 | zh_TW |
| dc.subject | 微管尖端蛋白 | zh_TW |
| dc.subject | Arl4 | en |
| dc.subject | End-binding protein 1 | en |
| dc.subject | Microtubule | en |
| dc.subject | Epidermal growth factor receptor | en |
| dc.title | 探討腺嘌呤核苷二磷酸核糖化因子相似蛋白四(Arl4s)之功能 | zh_TW |
| dc.title | Functional Characterization of ADP-Ribosylation Factor-Like Protein 4s (Arl4s) | en |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 張智芬(Hsin-Tsai Liu),劉雅雯(Chih-Yang Tseng),嚴仲陽,陳瑞華,周祖述 | |
| dc.subject.keyword | 腺嘌呤核苷二磷酸核醣化相似因子4,表皮生長因子受體,微管,微管尖端蛋白, | zh_TW |
| dc.subject.keyword | Arl4,Epidermal growth factor receptor,Microtubule,End-binding protein 1, | en |
| dc.relation.page | 143 | |
| dc.identifier.doi | 10.6342/NTU202104031 | |
| dc.rights.note | 同意授權(限校園內公開) | |
| dc.date.accepted | 2021-10-26 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 分子醫學研究所 | zh_TW |
| dc.date.embargo-lift | 2026-10-23 | - |
| 顯示於系所單位： | 分子醫學研究所 | |
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