LiPiCS Services (Lyon-France)
contact : Eric JULIEN (CNRS/Inserm)
Protein-protein interactions are a key factor to understand a protein function. As we tried to identify molecular mechanisms explaining the pro and anti-tumoral effect of a well known transcription family, we developped a Bimolecular Fluorescence Complementation based asssay to screen in live cell line for whole interactome of a target. Reaching higher robustness than other screening technology, we performed comparative analysis to understand the effect of differents effectors and mutations on target interactome.
LiPiCS Services (Lyon-France)
contact : Eric JULIEN (CNRS/Inserm)
Protein-protein interactions are a key factor to understand a protein function. As we tried to identify molecular mechanisms explaining the pro and anti-tumoral effect of a well known transcription family, we developped a Bimolecular Fluorescence Complementation based asssay to screen in live cell line for whole interactome of a target. Reaching higher robustness than other screening technology, we performed comparative analysis to understand the effect of differents effectors and mutations on target interactome.
INTEGRAGEN, Genopole Campus, Evry (Paris)
contact : Pierre-François ROUX (equipe L. LeCam-INSERM)
INTEGRAGEN, Genopole Campus, Evry (Paris)
contact : Pierre-François ROUX (equipe L. LeCam-INSERM)
Institut Pasteur, Department of Developmental and Stem Cell Biology
contact : Alexandre Djiane (IRCM)
Institut Pasteur, Department of Developmental and Stem Cell Biology
contact : Alexandre Djiane (IRCM)
Institut Pasteur, Department of Developmental and Stem Cell Biology
contact : Alexandre Djiane (IRCM)
Institut Pasteur, Department of Developmental and Stem Cell Biology
contact : Alexandre Djiane (IRCM)
INSERM U1280
Institute for Integrative Biology of the Cell (I2BC)
University Paris-Saclay-CEA-CNRS; Gif/Yvette
contact : Alexandre Djiane (Inserm-IRCM)
INSERM U1280
Institute for Integrative Biology of the Cell (I2BC)
University Paris-Saclay-CEA-CNRS; Gif/Yvette
contact : Alexandre Djiane (Inserm-IRCM)
CNRS UMR 9019 Paris-Saclay
Intégrité du génome et cancer
Gustave Roussy, Villejuif
contact : Eric JULIEN (Inserm/CNRS)
Replication stress resulting from slowing or stalling of DNA replication forks is a major driver of genome instability during cancer initiation and progression. DNA replication can be challenged as a consequence of oncogene activation or by agents that interfere with DNA synthesis, such as the ones used in chemotherapy. To accomplish genome duplication and prevent chromosomal instability, cells have evolved mechanisms that protect, stabilize and/or restart replication forks while delaying cell cycle progression, which avoids entering mitosis with under-replicated DNA. Over the last years, however, work from several laboratories including ours has shown that cells can progress into mitosis with under-replicated DNA. This led to the identification of mechanisms, mediated by the Fanconi anemia (FA) and Homologous Recombination (HR) repair pathways, that promote post-replication repair and rescue of under-replicated DNA in mitosis, allowing cells to divide and continue proliferating. I will discuss how these findings have advanced our understanding of the link between replication stress and genome instability; I will present a molecular pathway that connects mitochondrial stress and functions of FA proteins in genome maintenance; finally, I will show that mechanisms involved in mitotic rescue of under-replicated DNA may represent promising targets to selectively kill cancer cells that sustain intrinsically high levels of replication stress.
CNRS UMR 9019 Paris-Saclay
Intégrité du génome et cancer
Gustave Roussy, Villejuif
contact : Eric JULIEN (Inserm/CNRS)
Replication stress resulting from slowing or stalling of DNA replication forks is a major driver of genome instability during cancer initiation and progression. DNA replication can be challenged as a consequence of oncogene activation or by agents that interfere with DNA synthesis, such as the ones used in chemotherapy. To accomplish genome duplication and prevent chromosomal instability, cells have evolved mechanisms that protect, stabilize and/or restart replication forks while delaying cell cycle progression, which avoids entering mitosis with under-replicated DNA. Over the last years, however, work from several laboratories including ours has shown that cells can progress into mitosis with under-replicated DNA. This led to the identification of mechanisms, mediated by the Fanconi anemia (FA) and Homologous Recombination (HR) repair pathways, that promote post-replication repair and rescue of under-replicated DNA in mitosis, allowing cells to divide and continue proliferating. I will discuss how these findings have advanced our understanding of the link between replication stress and genome instability; I will present a molecular pathway that connects mitochondrial stress and functions of FA proteins in genome maintenance; finally, I will show that mechanisms involved in mitotic rescue of under-replicated DNA may represent promising targets to selectively kill cancer cells that sustain intrinsically high levels of replication stress.
Centre d'Immunologie de Marseille-Luminy (CMIL), CNRS-INSERM, Université Aix-Marseille
contact : Laurent Le Cam (Inserm)
Centre d'Immunologie de Marseille-Luminy (CMIL), CNRS-INSERM, Université Aix-Marseille
contact : Laurent Le Cam (Inserm)
Located in the Parc Euromédecine, the Institut de Recherche en Cancérologie de Montpellier (U1194) is located on the Val d'Aurelle Campus (ICM, Institut régional du Cancer Montpellier/ Val d'Aurelle).
U1194 Research Centre supported by Inserm, the University of Montpellier and the Institut du Cancer de Montpellier (ICM)
Institut de Recherche en Cancérologie de