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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 林琬琬(Wan-Wan Lin) | |
dc.contributor.author | Kai-Chun Lin | en |
dc.contributor.author | 林凱君 | zh_TW |
dc.date.accessioned | 2021-06-08T01:06:17Z | - |
dc.date.copyright | 2014-10-15 | |
dc.date.issued | 2014 | |
dc.date.submitted | 2014-08-19 | |
dc.identifier.citation | Akdis, M., and Akdis, C.A. (2009). Therapeutic manipulation of immune tolerance in allergic disease. Nat Rev Drug Discov 8, 645-660.
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/18459 | - |
dc.description.abstract | 5’-Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a sensor of cellular and whole body energy homeostasis that coordinates metabolism pathway in order to balance energy supply with demand. Recently, many studies have revealed that AMPK activation exerts anti-inflammatory and anti-immunosuppressive effects through blunting the release of inflammatory mediators in a variety of cell types and models of inflammatory diseases. In allergic conditions, antigen-induced aggregation of high affinity IgE receptor, FcεRI, on mast cells has been demonstrated to use Lyn and/or Fyn kinase-dependent pathways to initiate a serious of activating signaling events. Although it is well known that AMPK exerts a negative effect on FcεRI-dependent mast cells signals and anaphylaxis through regulating downstream signal of Fyn, the precise regulation between Lyn, the major expressed Src family kinase (SFK) in mast cells and basophils, and AMPK in the context of FcεRI signaling has not been fully elucidated. In this study, we are interested to investigate whether AMPK plays a regulatory role in FcεRI-activated Lyn signaling in rat RBL-2H3 basophilic leukemia cells. As a result, we found that inhibitory AMPK phosphorylation at site Ser485/491 is increased upon FcεRI activation. Signaling cascade of Lyn-Syk-Akt mediates AMPK phosphorylation at Ser485/491, demonstrating that AMPK inhibition is downstream of FcεRI-activated Lyn signaling. Moreover, we showed that AMPK negatively regulates basophils activation and cytokine TNFα release through regulating protein interaction among FcεRI β and γ subunits and receptor proximal molecules, Lyn and Syk. Notably, RBL-2H3 cells predominantly express AMPKα2 isoform, whereas both AMPKα1 and α2 isoforms all participate in FcεRI β and/or γ subunits phosphorylation in vitro. The exact detailed molecular mechanism in this aspect needs further investigation in the future. | en |
dc.description.provenance | Made available in DSpace on 2021-06-08T01:06:17Z (GMT). No. of bitstreams: 1 ntu-103-R01443001-1.pdf: 4071382 bytes, checksum: 81321378edfc6681ec46198fe9b9d732 (MD5) Previous issue date: 2014 | en |
dc.description.tableofcontents | 口試委員會審訂書 I
誌謝 II Abstract IV 中文摘要 VI Abbreviations 1 Introduction 4 Materials and Methods 22 Results 30 Discussion 38 Figures 45 References 59 | |
dc.language.iso | en | |
dc.title | 探討AMPK在大鼠嗜鹼性白血病細胞株RBL-2H3調控FcεRI所誘導的訊息傳遞 | zh_TW |
dc.title | AMPK regulation of FcεRI-mediated signal transduction in RBL-2H3 rat basophilic leukemia cells | en |
dc.type | Thesis | |
dc.date.schoolyear | 102-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 符文美(Wen-Mei Fu),江伯倫,曾賢忠(Shiang-Jong Tzeng) | |
dc.subject.keyword | 腺?磷酸活化激?,嗜鹼性白血球,高親和力免疫球蛋白E受體, | zh_TW |
dc.subject.keyword | AMPK,RBL-2H3,FcεRI,Lyn,Syk,Akt, | en |
dc.relation.page | 70 | |
dc.rights.note | 未授權 | |
dc.date.accepted | 2014-08-19 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 藥理學研究所 | zh_TW |
顯示於系所單位: | 藥理學科所 |
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ntu-103-1.pdf 目前未授權公開取用 | 3.98 MB | Adobe PDF |
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