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020 ▼a 9780438078444
035 ▼a (MiAaPQ)AAI10684963
035 ▼a (MiAaPQ)berkeley:17493
040 ▼a MiAaPQ ▼c MiAaPQ ▼d 247004
0820 ▼a 576
1001 ▼a De Leon, Justin A.
24510 ▼a Mixed Signals: Regulation of Host Metabolism by an Intracellular Bacterial Pathogen.
260 ▼a [S.l.]: ▼b University of California, Berkeley., ▼c 2017.
260 1 ▼a Ann Arbor: ▼b ProQuest Dissertations & Theses, ▼c 2017.
300 ▼a 59 p.
500 ▼a Source: Dissertation Abstracts International, Volume: 79-10(E), Section: B.
500 ▼a Adviser: Russell E. Vance.
5021 ▼a Thesis (Ph.D.)--University of California, Berkeley, 2017.
520 ▼a A hallmark of all pathogens is an ability to acquire nutrients from hosts. In order to do this, pathogens must overcome both the tight regulation of host nutrients and the host defense mechanisms deployed to protect these nutrients.
520 ▼a In the introductory chapter of this dissertation, I begin with a discussion of innate immunity. I discuss the now appreciated view of the innate immune system as a sensor of patterns of pathogenesis. I then argue, based on our studies in Legione
520 ▼a In chapter two, I provide experimental evidence that nutrient acquisition is a pattern of pathogenesis. I discuss my work describing how L. pneumophila alters a key metabolic signaling pathway, the mechanistic target of rapamycin complex 1 (mTOR
520 ▼a I then close with a perspective chapter that describes the additional questions my work has given rise to and the state of the bacterial molecular pathogenicity field as a whole.
590 ▼a School code: 0028.
650 4 ▼a Microbiology.
690 ▼a 0410
71020 ▼a University of California, Berkeley. ▼b Molecular & Cell Biology.
7730 ▼t Dissertation Abstracts International ▼g 79-10B(E).
773 ▼t Dissertation Abstract International
790 ▼a 0028
791 ▼a Ph.D.
792 ▼a 2017
793 ▼a English
85640 ▼u http://www.riss.kr/pdu/ddodLink.do?id=T14996742 ▼n KERIS ▼z 이 자료의 원문은 한국교육학술정보원에서 제공합니다.
980 ▼a 201812 ▼f 2019
990 ▼a ***1012033