Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-4332
Authors: Srokowski, Cathy Cecilia
Title: The role of CYLD in dendritic cell function
Online publication date: 28-Apr-2009
Year of first publication: 2009
Language: english
Abstract: Deubiquitination of NF-κB members by CYLD is crucial in controlling the magnitude and nature of cell activation. The naturally occurring CYLD splice variant, devoid of exons 7 and 8, lacks TRAF2 and NEMO binding sites. The role of this splice variant in dendritic cell (DC) function was analyzed using CYLDex7/8 mice, which lack the full-length CYLD (FL-CYLD) transcript and over-express the short splice variant (sCYLD). Bone marrow derived DCs (BMDC) from CYLDex7/8 mice display a hyper-reactive phenotype in vitro and in vivo and have a defect in establishing tolerance using DEC205-mediated antigen targeting to resting DCs. This phenotype was accompanied by an increased nuclear translocation of the IκB molecule Bcl-3, and increased degradation of cytoplasmic p105 in CYLDex7/8 BMDCs after stimulation. This suggests that in contrast to FL-CYLD, sCYLD is a positive regulator of NF-κB activity and its over-expression induces a hyper-reactive phenotype in DCs.
DDC: 570 Biowissenschaften
570 Life sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 10 Biologie
Place: Mainz
ROR: https://ror.org/023b0x485
DOI: http://doi.org/10.25358/openscience-4332
URN: urn:nbn:de:hebis:77-19847
Version: Original work
Publication type: Dissertation
License: In Copyright
Information on rights of use: https://rightsstatements.org/vocab/InC/1.0/
Appears in collections:JGU-Publikationen

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