LDR | | 02084nam u200397 4500 |
001 | | 000000419173 |
005 | | 20190215163450 |
008 | | 181129s2018 |||||||||||||||||c||eng d |
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▼a 9780438115552 |
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▼a (MiAaPQ)AAI10830418 |
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▼a (MiAaPQ)wisc:15448 |
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▼a MiAaPQ
▼c MiAaPQ
▼d 247004 |
082 | 0 |
▼a 574 |
100 | 1 |
▼a Jones, Elaina K. |
245 | 14 |
▼a The Role of D52 in Acinar Homeostasis. |
260 | |
▼a [S.l.]:
▼b The University of Wisconsin - Madison.,
▼c 2018. |
260 | 1 |
▼a Ann Arbor:
▼b ProQuest Dissertations & Theses,
▼c 2018. |
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▼a 123 p. |
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▼a Source: Dissertation Abstracts International, Volume: 79-11(E), Section: B. |
500 | |
▼a Adviser: Guy E. Groblewski. |
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▼a Thesis (Ph.D.)--The University of Wisconsin - Madison, 2018. |
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▼a D52 is a cytosolic, peripheral membrane associated protein that binds a number of membrane trafficking associated proteins and is highly expressed in pancreatic acinar cells. Work by the Groblewski lab has identified a role for D52 in regulating |
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▼a Pancreatitis induces acinar cell dedifferentiation to a duct-like exocrine progenitor state as a mechanism of recovery. The dedifferentiated progenitors proliferate to repopulate the gland before differentiating back into acinar cells under the |
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▼a In Chapter four, we utilized an inducible model of acinar specific D52 deletion (D52--/--) to investigate the impact of losing D52 expression, an early event in the onset of pancreatitis. Loss of D52 alone caused significant acinar cell damage, |
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▼a School code: 0262. |
650 | 4 |
▼a Cellular biology. |
690 | |
▼a 0379 |
710 | 20 |
▼a The University of Wisconsin - Madison.
▼b Nutritional Sciences. |
773 | 0 |
▼t Dissertation Abstracts International
▼g 79-11B(E). |
773 | |
▼t Dissertation Abstract International |
790 | |
▼a 0262 |
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▼a Ph.D. |
792 | |
▼a 2018 |
793 | |
▼a English |
856 | 40 |
▼u http://www.riss.kr/pdu/ddodLink.do?id=T14999431
▼n KERIS
▼z 이 자료의 원문은 한국교육학술정보원에서 제공합니다. |
980 | |
▼a 201812
▼f 2019 |
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▼a ***1012033 |