Julie Caramel
Centre national de la recherche scientifique
4 Papers
Julie Caramel is an academic researcher from Centre national de la recherche scientifique. The author has contributed to research in topics: BMI1 & Stem cell. The author has an hindex of 4, co-authored 4 publications. Previous affiliations of Julie Caramel include University of Montpellier.
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Papers
E4F1 deficiency results in oxidative stress-mediated cell death of leukemic cells.
Elodie Hatchi,Geneviève Rodier,Matthieu Lacroix,Julie Caramel,Olivier Kirsh,Chantal Jacquet,Emilie Schrepfer,Sylviane Lagarrigue,Laetitia K. Linares,Gwendaline Lledo,Sylvie Tondeur,Pierre Dubus,Claude Sardet,Laurent Le Cam,Laurent Le Cam +14 more
TL;DR: Deletion of E4F1 inflicts mitochondrial damage and oxidative stress on murine and human myeloid leukemia cells but not healthy macrophages.
E4F1 connects the Bmi1-ARF-p53 pathway to epidermal stem cell-dependent skin homeostasis.
TL;DR: Comment on: Lacroix M, et al.
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The Transcription Factor E4F1 Coordinates CHK1-Dependent Checkpoint and Mitochondrial Functions
Geneviève Rodier,Olivier Kirsh,Olivier Kirsh,Martin A. Baraibar,Thibault Houlès,Matthieu Lacroix,Hélène Delpech,Elodie Hatchi,Elodie Hatchi,Stéphanie Arnould,Dany Severac,Emeric Dubois,Julie Caramel,Julie Caramel,Eric Julien,Bertrand Friguet,Bertrand Friguet,Laurent Le Cam,Claude Sardet +18 more
TL;DR: It is shown that another factor, the multifunctional protein E4F1, directly controls genes involved in mitochondria functions and cell-cycle checkpoints, including Chek1, a major component of the DNA damage response.
Transcription factor E4F1 is essential for epidermal stem cell maintenance and skin homeostasis
Matthieu Lacroix,Julie Caramel,Perrine Goguet-Rubio,Laetitia K. Linares,Soline Estrach,Elodie Hatchi,Geneviève Rodier,Gwendaline Lledo,Carine de Bettignies,Amélie Thépot,Céline Deraison,Karim Chebli,Alain Hovnanian,Pierre Hainaut,Pierre Dubus,Claude Sardet,Laurent Le Cam +16 more
TL;DR: A regulatory axis essential for ESC-dependent skin homeostasis implicating E4F1 and the Bmi1–Arf–p53 pathway is identified and identified, indicating that the lesions observed in the E 4F1 mutant skin result, at least in part, from cell-autonomous alterations in ESC maintenance.