Peer-Reviewed Journal Details
Mandatory Fields
Lowndes, NF
2010
October
Dna Repair
The interplay between BRCA1 and 53BP1 influences death, aging, senescence and cancer
Published
()
Optional Fields
BRCA1 53BP1 DNA damage response Homologous recombination Non-homologous end joining Breast cancer STRAND-BREAK REPAIR DNA-DAMAGE RESPONSE CELL-CYCLE DEFICIENCY ATM PROTEINS COMPLEX RECOMBINATION TUMORIGENESIS ACTIVATION
9
1112
1116
In proliferating cells DNA double strand breaks (DSBs) are a common occurrence during DNA replication DSB repair using homologous recombination is essential for the error-free repair of such breaks and proliferating cells require some level of HR activity for their viability The BRCA1 tumour suppressor has an important role in this process and is believed to channel the DSBs into the HR pathway The related 53BP1 gene is known to positively regulate repair of DSBs outside of S phase but via the NHEJ pathway Two new studies suggest a new role for 53BP1 as an inhibitor of HR [1,2] These genetic studies establish that 53BP1, but not other components of the NHEJ machinery, can inhibit the early resection step of HR In cells defective for BRCA1, which is required for efficient HR, the balance between promoting and inhibiting HR is thrown towards inhibition Simultaneous loss of 53BP1 can rescue the HR defect of BRCA1-defective cells and restore cellular viability Here I provide an overview of these studies and discuss their implications for tumourigenesis (C) 2010 Elsevier B V All rights reserved
DOI 10.1016/j.dnarep.2010.07.012
Grant Details
Publication Themes