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- 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
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- 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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- 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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Bloom's syndrome protein response to ultraviolet C radiation and hydroxyurea mediated DNA synthesis inhibition
Date : 2002
Sources :
Oncogene, 21, 2079-2088
Bloom's syndrome (BS) arises through mutations in both copies of the BLM gene that encodes a RecQ 3'-5' DNA helicase. BS patients are predisposed to developing all the cancers that affect the general population, and BS cells exhibit marked genetic instability. We showed recently that BLM protein contributes to the cellular response to ionizing radiation by acting as downstream ATM kinase effector. We now show that following UVC treatment, BLM-deficient cells exhibit a reduction in the number of replicative cells, a partial escape from the G2/M cell cycle checkpoint, and have an altered p21 response. Surprisingly, we found that hydroxyurea-treated BLM-deficient cells exhibit an intact S phase arrest, proper recovery from the S phase arrest, and intact p53 and p21 responses. We also show that the level of BLM falls sharply in response to UVC radiation. This UVC-induced reduction in BLM does not require a functional ATM gene and does not result from a subcellular compartment change. Finally, we demonstrate that exposure to UVC and hydroxyurea treatment both induce BLM phosphorylation via an ATM-independent pathway. These results are discussed in the light of their potential physiological significance with regard to the role of BLM in the cellular pathways activated by UVC radiation or HU-mediated inhibition of DNA synthesis.