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Association of BRCA1 with Rad51 in Mitotic and Meiotic Cells
RNF8 Transduces the DNA-Damage Signal via Histone Ubiquitylation and Checkpoint Protein Assembly
Histone H2AX Is Phosphorylated in an ATR-dependent Manner in Response to Replicational Stress*
It is reported that inhibition of DNA replication by hydroxyurea or ultraviolet irradiation also induces phosphorylation and foci formation of H2AX, and these phospho-H2AX foci colocalize with proliferating cell nuclear antigen, BRCA1, and 53BP1 at the arrested replication fork in S phase cells.
Structural Basis for the Methylation State-Specific Recognition of Histone H4-K20 by 53BP1 and Crb2 in DNA Repair
Dynamic Changes of BRCA1 Subnuclear Location and Phosphorylation State Are Initiated by DNA Damage
PALB2 is an integral component of the BRCA complex required for homologous recombination repair
- Shirley M. H. Sy, M. Huen, Junjie Chen
- BiologyProceedings of the National Academy of Sciences
- 28 April 2009
PALB2 is uncovered as the molecular adaptor between the BRCA proteins, and it is suggested that impaired HR repair is one of the fundamental causes for genomic instability and tumorigenesis observed in patients carrying BRC a1, BRCa2, or PALB2 mutations.
The BRCT Domain Is a Phospho-Protein Binding Domain
It is shown that the BRCA1 BRCT domain directly interacts with phosphorylated BRCa1-Associated Carboxyl-terminal Helicase (BACH1) and this interaction is cell cycle regulated and is required for DNA damage–induced checkpoint control during the transition from G2 to M phase of the cell cycle.
MDC1 maintains genomic stability by participating in the amplification of ATM-dependent DNA damage signals.
Sirtuin 1 modulates cellular responses to hypoxia by deacetylating hypoxia-inducible factor 1alpha.
Ubiquitin-Binding Protein RAP80 Mediates BRCA1-Dependent DNA Damage Response
The identification of receptor-associated protein 80 (RAP80) as a BRCA1-interacting protein in humans suggests the existence of a ubiquitination-dependent signaling pathway involved in the DNA damage response.