We are using in vitro and in vivo reprogramming system to investigate how cellular plasticity is regulated during physiological and pathological processes. Our aim is to understand how aberrant cellular plasticity is induced during tumorigenesis and how to modulate cellular plasticity for regeneration especially in ageing related diseases.
Vieillissement et longévité
D’après l’OMS, entre 2000 et 2050, la proportion de la population mondiale de plus de 60 ans doublera pour passer d’environ 11% à 22%. Actuellement la plupart des personnes âgées décèdent de maladies non […]
Cellular plasticity and Ageing
Ageing is associated with losing normal cellular plasticity (regeneration capacity) while acquiring abnormal cellular dys-plasticity (cancer). Cellular reprogramming is associated with a gain in the potential for differentiation and self-renewal. Could common pathways be […]
Cellular plasticity and Cancer
Aberrant cellular plasticity (“dys-plasticity”) could occur in vivo, which contributes significantly to disease development, especially in cancer. Recently, we showed p27-/- cells are dysplastic due to the derepression of Sox2, an essential pluripotency gene. […]
2014 – present G5 Group Leader, Institut Pasteur
2012 – 2014 Staff scientist, Tumor Suppression Group, Spanish National Research Centre
2007 – 2012 Postdoctral Fellow, Tumor Suppression Group, Spanish National Research Centre
2001 – 2007 Ph.D. in Molecular Medicine, University of Texas Health Science Center at San Antonio
San Antonio, Texas, USA
1995 – 1999 Bachelor in Ecology, FuDan University,
2017Δ133p53 represses p53-inducible senescence genes and enhances the generation of human induced pluripotent stem cells, Cell Death Differ. 2017 Jun;24(6):1017-1028.
2016Genomic stability during cellular reprogramming: Mission impossible? Mutat Res. 2016 Jun;788:12-6,, Mutat Res. 2016 Jun;788:12-6.
2015Limiting replication stress during somatic cell reprogramming reduces genomic instability in induced pluripotent stem cells, Nat Commun. 2015 Aug 21;6:8036.
2014Deletion of individual Ku subunits in mice causes an NHEJ-independent phenotype potentially by altering apurinic/apyrimidinic site repair, PLoS ONE 2014;9(1):e86358.
2013Reprogramming activity of NANOGP8, a NANOG family member widely expressed in cancer, Oncogene 2014 May;33(19):2513-9.
2013Ku80-deleted cells are defective at base excision repair, Mutat. Res. 2013 May-Jun;745-746:16-25.
2012p27(Kip1) directly represses Sox2 during embryonic stem cell differentiation, Cell Stem Cell 2012 Dec;11(6):845-52.
2011Increased dosage of tumor suppressors limits the tumorigenicity of iPS cells without affecting their pluripotency, Aging Cell 2012 Feb;11(1):41-50.
2011Trex2 enables spontaneous sister chromatid exchanges without facilitating DNA double-strand break repair, Genetics 2011 Aug;188(4):787-97.
2011Epigenetic regulation of Nanog expression by Ezh2 in pluripotent stem cells, Cell Cycle 2011 May;10(9):1488-98.
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