| 書(shū)目名稱 | Ubiquitin Chains: Degradation and Beyond |
| 編輯 | Arnab De |
| 視頻video | http://file.papertrans.cn/941/940213/940213.mp4 |
| 概述 | Nominated as an outstanding Ph.D. thesis by Columbia University, New York, USA.Insightful and in-depth evaluation of the evidence for K63-linked regulatory ubiquitination in regulating cell-signalling |
| 叢書(shū)名稱 | Springer Theses |
| 圖書(shū)封面 |  |
| 描述 | This thesis examines the evidence for regulatory ubiquitination by focusing on A20. It provides an insightful and in-depth evaluation of the current literature by critically examining the evidence of K63-linked regulatory ubiquitination in regulating cell-signalling. It is also the first thesis to directly test the role of regulatory ubiquitination in NF-kB signaling .in vivo.. The case for regulatory ubiquitination has been to a large extent predicated upon the presumed deubiquitinase activity of A20, long considered a key regulator of inflammatory responses as mice lacking A20 die from multi-organ inflammation and cachexia. The theses reports the creation and characterization of a knock-in mouse that expresses a mutated form of A20 which selectively lacks the deubiquitinase activity. The knock-in mice surprisingly display completely normal NF-κB activation with no accompanying inflammatory phenotype. Given that the presumed role of A20 as a deubiquitinase has been used to support the importance of regulatory K63-linked ubiquitination in NF-kB signaling, this study will help focus future research efforts into alternative target pathways that do not depend on K63 ubiquitination. In |
| 出版日期 | Book 2015 |
| 關(guān)鍵詞 | NF-κB signaling; adaptive response; innate immunity; pattern-recognition receptors; regulatory ubiquitin |
| 版次 | 1 |
| doi | https://doi.org/10.1007/978-3-319-14965-3 |
| isbn_softcover | 978-3-319-38534-1 |
| isbn_ebook | 978-3-319-14965-3Series ISSN 2190-5053 Series E-ISSN 2190-5061 |
| issn_series | 2190-5053 |
| copyright | Springer International Publishing Switzerland 2015 |
|Archiver|手機(jī)版|小黑屋|
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