SIRT2 regulates NF-κB-dependent gene expression through deacetylation of p65 Lys310
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- Karin M. Rothgiesser
- Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Winterthurerstraße 190, 8057 Zurich, Switzerland
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- Süheda Erener
- Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Winterthurerstraße 190, 8057 Zurich, Switzerland
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- Susanne Waibel
- Institut für Biochemie und Molekularbiologie, Medical School, RWTH Aachen University, Pauwelsstraße 30, 52074 Aachen, Germany
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- Bernhard Lüscher
- Institut für Biochemie und Molekularbiologie, Medical School, RWTH Aachen University, Pauwelsstraße 30, 52074 Aachen, Germany
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- Michael O. Hottiger
- Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Winterthurerstraße 190, 8057 Zurich, Switzerland
説明
<jats:p>NF-κB regulates the expression of a large number of target genes involved in the immune and inflammatory response, apoptosis, cell proliferation, differentiation and survival. In this study, we identified SIRT2 as a deacetylase of the transcription factor p65. SIRT2 is a member of the family of sirtuins, which are NAD+-dependent deacetylases involved in several cellular processes. SIRT2 interacts with p65 in the cytoplasm and deacetylates p65 in vitro and in vivo at Lys310. Moreover, p65 is hyperacetylated at Lys310 in Sirt2−/− cells after TNFα stimulation, which results in the increase in expression of a subset of p65 acetylation-dependent target genes. Our work provides evidence that p65 is deacetylated by SIRT2 in the cytoplasm to regulate the expression of specific NF-κB-dependent genes.</jats:p>
収録刊行物
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- Journal of Cell Science
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Journal of Cell Science 123 (24), 4251-4258, 2010-12-15
The Company of Biologists
