APA
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Hövelmeyer N., Wunderlich, F., Massoumi, R., Jakobsen, C., Song, J., Song, J., … Waisman, A. (2007). Regulation of B cell homeostasis and activation by the tumor suppressor gene CYLD. Journal of Experimental Medicine.
Chicago/Turabian
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Hövelmeyer N., F. Wunderlich, R. Massoumi, C. Jakobsen, Jian Song, Jian Song, M. Wörns, et al. “Regulation of B Cell Homeostasis and Activation by the Tumor Suppressor Gene CYLD.” Journal of Experimental Medicine (2007).
MLA
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Hövelmeyer N., et al. “Regulation of B Cell Homeostasis and Activation by the Tumor Suppressor Gene CYLD.” Journal of Experimental Medicine, 2007.
BibTeX Click to copy
@article{n2007a,
title = {Regulation of B cell homeostasis and activation by the tumor suppressor gene CYLD},
year = {2007},
journal = {Journal of Experimental Medicine},
author = {Hövelmeyer, N. and Wunderlich, F. and Massoumi, R. and Jakobsen, C. and Song, Jian and Song, Jian and Wörns, M. and Merkwirth, Carsten and Kovalenko, A. and Aumailley, M. and Strand, D. and Brüning, J. and Galle, P. and Wallach, D. and Fässler, R. and Waisman, A.}
}
B cell homeostasis is regulated by multiple signaling processes, including nuclear factor-κB (NF-κB), BAFF-, and B cell receptor signaling. Conditional disruption of genes involved in these pathways has shed light on the mechanisms governing signaling from the cell surface to the nucleus. We describe a novel mouse strain that expresses solely and excessively a naturally occurring splice variant of CYLD (CYLDex7/8 mice), which is a deubiquitinating enzyme that is integral to NF-κB signaling. This shorter CYLD protein lacks the TRAF2 and NEMO binding sites present in full-length CYLD. A dramatic expansion of mature B lymphocyte populations in all peripheral lymphoid organs occurs in this strain. The B lymphocytes themselves exhibit prolonged survival and manifest a variety of signaling disarrangements that do not occur in mice with a complete deletion of CYLD. Although both the full-length and the mutant CYLD are able to interact with Bcl-3, a predominant nuclear accumulation of Bcl-3 occurs in the CYLD mutant B cells. More dramatic, however, is the accumulation of the NF-κB proteins p100 and RelB in CYLDex7/8 B cells, which, presumably in combination with nuclear Bcl-3, results in increased levels of Bcl-2 expression. These findings suggest that CYLD can both positively and negatively regulate signal transduction and homeostasis of B cells in vivo, depending on the expression of CYLD splice variants.