Loss of Sirt2 increases and prolongs a caerulein-induced pancreatitis permissive phenotype and induces spontaneous oncogenic Kras mutations in mice
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-018-34792-y.pdf
Reference50 articles.
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2. Guerra, C. et al. Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. Cancer Cell 11, 291–302, https://doi.org/10.1016/j.ccr.2007.01.012 (2007).
3. Dryden, S. C., Nahhas, F. A., Nowak, J. E., Goustin, A. S. & Tainsky, M. A. Role for human SIRT2 NAD-dependent deacetylase activity in control of mitotic exit in the cell cycle. Mol Cell Biol 23, 3173–3185 (2003).
4. Serrano, L. et al. The tumor suppressor SirT2 regulates cell cycle progression and genome stability by modulating the mitotic deposition of H4K20 methylation. Genes Dev 27, 639–653, https://doi.org/10.1101/gad.211342.112 (2013).
5. Wang, F. & Tong, Q. SIRT2 suppresses adipocyte differentiation by deacetylating FOXO1 and enhancing FOXO1′s repressive interaction with PPARgamma. Mol Biol Cell 20, 801–808, https://doi.org/10.1091/mbc.E08-06-0647 (2009).
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