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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
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- Figure 2
- Figure 3
- Fig. 1
- Fig. 2 Réponse cellulaire aux dommages de l'ADN chez les eucaryotes
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- 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]
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Possible anti-recombinogenic role of Bloom's syndrome helicase in double-strand break processing
Date : 2003
Sources :
Nucleic Acids Res., 31, 6272-82
Bloom's syndrome (BS) which associates genetic instability and predisposition to cancer is caused by mutations in the BLM gene encoding a RecQ family 3'-5' DNA helicase. It has been proposed that the generation of genetic instability in BS cells could result from an aberrant non-homologous DNA end joining (NHEJ), one of the two main DNA double-strand break (DSB) repair pathways in mammalian cells, the second major pathway being homologous recombination (HR). Using cell extracts, we report first that Ku70/80 and the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs), key factors of the end-joining machinery, and BLM are located in close proximity on DNA and that BLM binds to DNA only in the absence of ATP. In the presence of ATP, BLM is phosphorylated and dissociates from DNA in a strictly DNA-PKcs-dependent manner. We also show that BS cells display, in vivo, an accurate joining of DSBs, reflecting thus a functional NHEJ pathway. In sharp contrast, a 5-fold increase of the HR-mediated DNA DSB repair in BS cells was observed. These results support a model in which NHEJ activation mediates BLM dissociation from DNA, whereas, under conditions where HR is favored, e.g. at the replication fork, BLM exhibits an anti-recombinogenic role.