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Cyld inhibits tumor...
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Massoumi, RaminLund University,Lunds universitet,Cellpatologi, Malmö,Forskargrupper vid Lunds universitet,Cell Pathology, Malmö,Lund University Research Groups
(författare)
Cyld inhibits tumor cell proliferation by blocking Bcl-3-dependent NF-kappaB signaling
- Artikel/kapitelEngelska2006
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LIBRIS-ID:oai:lup.lub.lu.se:07a4ce8e-e1d4-48c8-886c-23b9a0b66216
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https://lup.lub.lu.se/record/1136403URI
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https://doi.org/10.1016/j.cell.2006.03.041DOI
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Språk:engelska
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Sammanfattning på:engelska
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Mutations in the CYLD gene cause tumors of hair-follicle keratinocytes. The CYLD gene encodes a deubiquitinase that removes lysine 63-linked ubiquitin chains from TRAF2 and inhibits p65/p50 NF-kappaB activation. Here we show that mice lacking Cyld are highly susceptible to chemically induced skin tumors. Cyld-/- tumors and keratinocytes treated with 12-O-tetradecanoylphorbol-13 acetate (TPA) or UV light are hyperproliferative and have elevated cyclin D1 levels. The cyclin D1 elevation is caused not by increased p65/p50 action but rather by increased nuclear activity of Bcl-3-associated NF-kappaB p50 and p52. In Cyld+/+ keratinocytes, TPA or UV light triggers the translocation of Cyld from the cytoplasm to the perinuclear region, where Cyld binds and deubiquitinates Bcl-3, thereby preventing nuclear accumulation of Bcl-3 and p50/Bcl-3- or p52/Bcl-3-dependent proliferation. These data indicate that, depending on the external signals, Cyld can negatively regulate different NF-kappaB pathways; inactivation of TRAF2 controls survival and inflammation, while inhibition of Bcl-3 controls proliferation and tumor growth.
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Chmielarska, Katarzyna
(författare)
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Hennecke, Katharina
(författare)
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Pfeifer, Alexander
(författare)
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Fassler, Reinhard
(författare)
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Cellpatologi, MalmöForskargrupper vid Lunds universitet
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Cell: Elsevier BV125:4, s. 665-6771097-41720092-8674
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Cell
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