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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
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- Université Paris-Sud 11
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- 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
Bloom syndrome, genomic instability and cancer: the SOS-like hypothesis
Date : 2006
Sources :
Cancer Letters, 236, 1-12
Bloom syndrome (BS) displays one of the strongest known correlations between chromosomal instability and an increased risk of malignancy at an early age. The prevention of genomic instability and cancer depends on a complex network of pathways induced in response to DNA damage and stalled replication forks, including cell-cycle checkpoints, DNA repair, and apoptosis. Several studies have demonstrated that BLM is involved in the cellular response to DNA damage and stalled replication forks. BLM interacts physically and functionally with several proteins involved in the maintenance of genome integrity and BLM is redistributed and/or phosphorylated in response to several genotoxic stresses. The data concerning the relationship between BLM and these cellular pathways are summarized and the role of BLM in the rescue of arrested replication forks is discussed. Moreover, I speculate that BLM deficiency is lethal, and that BLM-deficient cells escaping apoptotic death do so by constitutively inducing a bacterial SOS-like response including the induction of alternative replication pathway(s) dependent on recombination, contributing to the mutator and hyper-Rec phenotypes characteristic of BS cells. This mechanism may be dependent on the RAD51 gene family, and involved in carcinogenesis in the general population.