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Mechanisms of TRAF3 Mediated Regulation of B Cell Survival

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서명/저자사항Mechanisms of TRAF3 Mediated Regulation of B Cell Survival.
개인저자Mambetsariev, Nurbek.
단체저자명The University of Iowa. Immunology.
발행사항[S.l.]: The University of Iowa., 2018.
발행사항Ann Arbor: ProQuest Dissertations & Theses, 2018.
형태사항145 p.
기본자료 저록Dissertation Abstracts International 79-12B(E).
Dissertation Abstract International
ISBN9780438151161
학위논문주기Thesis (Ph.D.)--The University of Iowa, 2018.
일반주기 Source: Dissertation Abstracts International, Volume: 79-12(E), Section: B.
Adviser: Gail A. Bishop.
요약The adaptor protein TNF receptor-associated factor 3 (TRAF3) regulates signaling through B lymphocyte receptors, including CD40, BAFF receptor and Toll-like receptors, and also plays a critical role inhibiting B cell homoeostatic survival. Consi
요약We show here that TRAF3 is a resident nuclear protein that associated with the transcriptional regulator cyclic AMP response element binding protein (CREB) in both mouse and human B cells. The TRAF-C domain of TRAF3 was necessary and sufficient
요약We also show that TRAF3 deficiency led to induction of two proteins important for glucose metabolism, Glut1 and Hexokinase 2 (HXK2). This was associated with increased glucose uptake. In the absence of TRAF3, anaerobic glycolysis and oxidative p
요약Finally, loss of TRAF3 resulted in the induction of the pro-survival kinase proviral insertion in murine lymphoma 2 (Pim2) in B cells independently of non --canonical NF-kappaB activation. TRAF3-deficient B cells and multiple myeloma cells displ
요약Collectively, these findings provide insight into how TRAF3 regulates B cell survival. Our improved understanding of how loss of TRAF3 promotes development of B cell malignancies allows for the development of novel therapeutic strategies that ta
일반주제명Immunology.
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