Zobrazeno 1 - 10
of 21
pro vyhledávání: '"Boris Bardot"'
Autor:
Anne Fajac, Iva Simeonova, Julia Leemput, Marc Gabriel, Aurélie Morin, Vincent Lejour, Annaïg Hamon, Jeanne Rakotopare, Wilhelm Vaysse-Zinkhöfer, Eliana Eldawra, Marina Pinskaya, Antonin Morillon, Jean-Christophe Bourdon, Boris Bardot, Franck Toledo
Publikováno v:
eLife, Vol 13 (2024)
The Trp53 gene encodes several isoforms of elusive biological significance. Here, we show that mice lacking the Trp53 alternatively spliced (AS) exon, thereby expressing the canonical p53 protein but not isoforms with the AS C-terminus, have unexpect
Externí odkaz:
https://doaj.org/article/24d352706ace432cafb1b14b25ca0b61
Publikováno v:
Nature Communications, Vol 7, Iss 1, Pp 1-12 (2016)
P53 is regarded as the guardian of the genome, however it is known that mice with increased p53 activity display characteristics of dyskeratosis congenita. Here the authors show that increased p53 activity leads to the repression of telomere maintena
Externí odkaz:
https://doaj.org/article/980839b6474840f591fdd5fbe70b2a32
Autor:
Iva Simeonova, Sara Jaber, Irena Draskovic, Boris Bardot, Ming Fang, Rachida Bouarich-Bourimi, Vincent Lejour, Laure Charbonnier, Claire Soudais, Jean-Christophe Bourdon, Michel Huerre, Arturo Londono-Vallejo, Franck Toledo
Publikováno v:
Cell Reports, Vol 3, Iss 6, Pp 2046-2058 (2013)
Mutations in p53, although frequent in human cancers, have not been implicated in telomere-related syndromes. Here, we show that homozygous mutant mice expressing p53Δ31, a p53 lacking the C-terminal domain, exhibit increased p53 activity and suffer
Externí odkaz:
https://doaj.org/article/686d4f67f2fc40f1a5ee582240159315
Autor:
Iva Simeonova, Vincent Lejour, Boris Bardot, Rachida Bouarich-Bourimi, Aurélie Morin, Ming Fang, Laure Charbonnier, Franck Toledo
Publikováno v:
PLoS Genetics, Vol 8, Iss 6, p e1002731 (2012)
Evolutionary forces that shape regulatory networks remain poorly understood. In mammals, the Rb pathway is a classic example of species-specific gene regulation, as a germline mutation in one Rb allele promotes retinoblastoma in humans, but not in mi
Externí odkaz:
https://doaj.org/article/1d8fff3c538b4d53a41141e9eb573efc
Autor:
Eléonore, Toufektchan, Vincent, Lejour, Romane, Durand, Neelam, Giri, Irena, Draskovic, Boris, Bardot, Pierre, Laplante, Sara, Jaber, Blanche P, Alter, José-Arturo, Londono-Vallejo, Sharon A, Savage, Franck, Toledo
Publikováno v:
Science Advances
We demonstrate a direct link between germline p53 activation and telomere dysfunction.
Dyskeratosis congenita is a cancer-prone inherited bone marrow failure syndrome caused by telomere dysfunction. A mouse model recently suggested that p53 regu
Dyskeratosis congenita is a cancer-prone inherited bone marrow failure syndrome caused by telomere dysfunction. A mouse model recently suggested that p53 regu
Autor:
Sara Jaber, Ming Fang, Michel Huerre, Boris Bardot, Laure Charbonnier, Claire Soudais, Franck Toledo, Rachida Bouarich-Bourimi, Jean-Christophe Bourdon, Iva Simeonova, Irena Draskovic, Vincent Lejour, Arturo Londoño-Vallejo
Publikováno v:
Cell Reports
Cell Reports, Elsevier Inc, 2013, 3 (6), pp.2046-2058. ⟨10.1016/j.celrep.2013.05.028⟩
Cell Reports, 2013, 3 (6), pp.2046-2058. ⟨10.1016/j.celrep.2013.05.028⟩
Cell Reports, Elsevier Inc, 2013, 3 (6), pp.2046-2058. 〈10.1016/j.celrep.2013.05.028〉
Cell Reports, Vol 3, Iss 6, Pp 2046-2058 (2013)
Cell Reports, Elsevier Inc, 2013, 3 (6), pp.2046-2058. ⟨10.1016/j.celrep.2013.05.028⟩
Cell Reports, 2013, 3 (6), pp.2046-2058. ⟨10.1016/j.celrep.2013.05.028⟩
Cell Reports, Elsevier Inc, 2013, 3 (6), pp.2046-2058. 〈10.1016/j.celrep.2013.05.028〉
Cell Reports, Vol 3, Iss 6, Pp 2046-2058 (2013)
International audience; Mutations in p53, although frequent in human cancers , have not been implicated in telomere-related syndromes. Here, we show that homozygous mutant mice expressing p53 D31 , a p53 lacking the C-terminal domain, exhibit increas
Publikováno v:
Nature Communications
Nature Communications, Vol 7, Iss 1, Pp 1-12 (2016)
Nature Communications, 2016, 7, pp.11091. ⟨10.1038/ncomms11091⟩
Nature Communications, Nature Publishing Group, 2016, 7, pp.11091. ⟨10.1038/ncomms11091⟩
Nature Communications, Vol 7, Iss 1, Pp 1-12 (2016)
Nature Communications, 2016, 7, pp.11091. ⟨10.1038/ncomms11091⟩
Nature Communications, Nature Publishing Group, 2016, 7, pp.11091. ⟨10.1038/ncomms11091⟩
Germline mutations affecting telomere maintenance or DNA repair may, respectively, cause dyskeratosis congenita or Fanconi anaemia, two clinically related bone marrow failure syndromes. Mice expressing p53Δ31, a mutant p53 lacking the C terminus, mo
Autor:
Iva Simeonova, Rachida Bouarich-Bourimi, Franck Toledo, Aart G. Jochemsen, A Hamon, Boris Bardot, Vincent Lejour, J Leemput, Ming Fang, L Plancke
Publikováno v:
Oncogene
Oncogene, Nature Publishing Group, 2015, 34, pp.2943-2948. ⟨10.1038/onc.2014.230⟩
Oncogene, 34(22), 2943-2948
Oncogene, 2015, 34, pp.2943-2948. ⟨10.1038/onc.2014.230⟩
Oncogene, Nature Publishing Group, 2015, 34, pp.2943-2948. ⟨10.1038/onc.2014.230⟩
Oncogene, 34(22), 2943-2948
Oncogene, 2015, 34, pp.2943-2948. ⟨10.1038/onc.2014.230⟩
Mdm4, a protein related to the ubiquitin-ligase Mdm2, is an essential inhibitor of tumor suppressor protein p53. In both human and mouse cells, the Mdm4 gene encodes two major transcripts: one encodes the full-length oncoprotein (designated below as
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a7ad5da391afd624dc8127225a40eb48
https://hal-centralesupelec.archives-ouvertes.fr/hal-02457193
https://hal-centralesupelec.archives-ouvertes.fr/hal-02457193
Publikováno v:
Experimental Cell Research. 304:202-223
Notch signaling is required for the development of almost all animal tissues. It is a cell surface receptor that generates intracellular signals in response to Delta binding its extracellular domain. Notch response to Delta is affected by mutations i
Publikováno v:
The Journal of Cell Biology
Notch signaling is repeatedly used during animal development to specify cell fates. Using atomic force microscopy on live cells, chemical inhibitors, and conventional analyses, we show that the rate of Notch signaling is linked to the adhesion force