Cellular senescence stably arrests cell proliferation in response to numerous stress stimuli, many of which can initiate or promote aging and age-related diseases. As such, research on therapeutic strategies exploting senescence targeting for healthspan improvement has gained immense momentum. Within this context, our group investigates the impact of dynamic epigenome and transcriptome changes in senescence to unravel “achilles heels” of senescent cells . We anticipate that our research will lay tangible groundwork to exploit senescence targeting as a means to improve or extend healthy lifespan.
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Publications
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2016Derepression of hTERT gene expression promotes escape from oncogene-induced cellular senescence., Proc Natl Acad Sci U S A. 2016 Aug 23;113(34):E5024-33..
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2016USP1 Regulates Cellular Senescence by Controlling Genomic Integrity, Cell Rep 2016 May;15(7):1401-11.
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2015MicroRNAs and lncRNAs in senescence: A re-view, IUBMB Life 2015 Apr;67(4):255-67.
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2014Long noncoding RNA PANDA and scaffold-attachment-factor SAFA control senescence entry and exit, Nat Commun 2014;5:5323.
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2013Sumoylation at chromatin governs coordinated repression of a transcriptional program essential for cell growth and proliferation, Genome Res. 2013 Oct;23(10):1563-79.
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2012[A new player in PML-mediated cellular senescence: TBX2 gets into the loop], Med Sci (Paris) 2012 Mar;28(3):248-50.
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2012Senescence is an endogenous trigger for microRNA-directed transcriptional gene silencing in human cells, Nat. Cell Biol. 2012 Mar;14(3):266-75.
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2011Physical and functional interaction between PML and TBX2 in the establishment of cellular senescence, EMBO J. 2012 Jan;31(1):95-109.
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2009PARP-1 transcriptional activity is regulated by sumoylation upon heat shock, EMBO J. 2009 Nov;28(22):3534-48.
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2009[A review of cellular senescence: friend or foe of tumorigenesis?], Med Sci (Paris) 2009 Feb;25(2):153-60.
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