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Regulation of B cel...
Regulation of B cell homeostasis and activation by the tumor suppressor gene CYLD
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Hovelmeyer, Nadine (författare)
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Wunderlich, F Thomas (författare)
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- Massoumi, Ramin (författare)
- Lund University,Lunds universitet,Cellpatologi, Malmö,Forskargrupper vid Lunds universitet,Cell Pathology, Malmö,Lund University Research Groups
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Jakobsen, Charlotte G (författare)
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Song, Jian (författare)
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Worns, Marcus A (författare)
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Merkwirth, Carsten (författare)
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Kovalenko, Andrew (författare)
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Aumailley, Monique (författare)
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Strand, Dennis (författare)
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Bruning, Jens C (författare)
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Galle, Peter R (författare)
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Wallach, David (författare)
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- Fässler, Reinhard (författare)
- Lund University,Lunds universitet,Tumörmikromiljö,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Tumor microenvironment,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine
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(creator_code:org_t)
- 2007-10-08
- 2007
- Engelska.
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Ingår i: Journal of Experimental Medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 204:11, s. 2615-2627
- Relaterad länk:
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http://dx.doi.org/10...
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http://jem.rupress.o...
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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Abstract
Ämnesord
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- B cell homeostasis is regulated by multiple signaling processes, including nuclear factor-kappaB (NF-kappaB), 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 (CYLD(ex7/8) mice), which is a deubiquitinating enzyme that is integral to NF-kappaB 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-kappaB proteins p100 and RelB in CYLD(ex7/8) 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.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
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Hovelmeyer, Nadi ...
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Wunderlich, F Th ...
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Massoumi, Ramin
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Jakobsen, Charlo ...
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Song, Jian
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Worns, Marcus A
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visa fler...
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Merkwirth, Carst ...
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Kovalenko, Andre ...
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Aumailley, Moniq ...
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Strand, Dennis
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Bruning, Jens C
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Galle, Peter R
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Wallach, David
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Fässler, Reinhar ...
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visa färre...
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