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- Fig 1
- Augmentation des échanges entre chromatides sœurs dans des cellules de patients atteints du syndrome de Bloom
- Modèle pour le rôle de la protéine BLM dans la recombinaison homologue.
- Modèle pour la fonction de la protéine BLM dans la mitose
- Fig 1
- Fig. 2
- Figure 1
- Figure 2
- Figure 3
- Fig. 1
- Fig. 2 Réponse cellulaire aux dommages de l'ADN chez les eucaryotes
- Figure 1
- Figure 2 Cellule épithéliale interphasique
- Microscope L5D à déconvolution
- Microscope 2D, n positions
- Microscope 3D à déconvolution
- Microscope L5D à déconvolution
- Microscope confocal inversé - Leica SP5 AOBS, tandem scanner
- Fig. 1 Mechanisms can ensure continuity of DNA synthesis and maintain genome stability
- Fig. 2 The DNA replication checkpoint
- Fig. 3 Site-specific replication fork stalling system
- Fig. 1 Increased sister chromatid exchange in Bloom Syndrome cells
- Fig. 2 A model for BLM's role in homologous recombination
- FIG. 3 A model for BLM's function in mitosis
- Fig. 1 Multiply damaged sites
- Fig. 2 Cellular response to DNA damage in mammalian cells
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- Mounira Amor-Guéret
- Figure 2: BRCA2 functional domains
- Figure 4: DNA binding domain of BRCA2
- Figure 5: Scheme showing the action of PARP inhibition and the consequences of becoming resistant to this inhibition
- PHOTO UNITE UMR3348
- Université Paris-Sud 11
- visuel publication
- Aura Carreira's Lab
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- Figure1 : Our current model for the role of BRCA2 in Homologous recombination
- Molecular surface and ribbon representation of RAD51 bound to BRC4 (PDB code 1n0w). RAD51 is shown in yellow and BRC4 in magenta [Aura Carreira]
- Our current model for the role of BRCA2 in Homologous recombination [Aura Carreira]
Partagez
A major role for mitotic cdc2 kinase inactivation in the establishment of the mitotic DNA damage checkpoint
Date : 2004
Sources :
Cancer Research, 64(24):8954-9
Cdc2 kinase is inactivated when DNA damage occurs during the spindle assembly checkpoint. Here, we show that the level of mitotic Bloom syndrome protein phosphorylation reflects the level of cdc2 activity. A complete inactivation of cdc2 by either introduction of DNA double-strand breaks or roscovitine treatment prevents exit from mitosis. Thus, mitotic cdc2 inactivation plays a major role in the establishment of the mitotic DNA damage checkpoint. In response to mitotic cdc2 inactivation, the M/G(1) transition is delayed after releasing the drug block in nonmalignant cells, whereas tumor cells exit mitosis without dividing and rereplicate their DNA, which results in mitotic catastrophe. This opens the way for new chemotherapeutic strategies.