ArticleCell cycle (Georgetown, Tex.)2008
NFBD1/MDC1, 53BP1 and BRCA1 have both redundant and unique roles in the ATM pathway.
Article in Cell cycle (Georgetown, Tex.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 43 citations in OpenAlex.
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- ALDH1A1 Deficiency in Gorlin Syndrome Suggests a Central Role for Retinoic Acid and ATM Deficits in Radiation Carcinogenesis.Proteomes · 2014Article
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- A novel MCPH1 isoform complements the defective chromosome condensation of human MCPH1-deficient cells.PloS one · 2012Article
- NFBD1/MDC1 regulates Cav1 and Cav2 independently of DNA damage and p53.Molecular cancer research : MCR · 2011Article
- Image-based quantitative determination of DNA damage signal reveals a threshold for G2 checkpoint activation in response to ionizing radiation.Genome integrity · 2010Article
- {Delta}Np73{beta} puts the brakes on DNA repair.Genes & development · 2010Article
- Rad17 plays a central role in establishment of the interaction between TopBP1 and the Rad9-Hus1-Rad1 complex at stalled replication forks.Molecular biology of the cell · 2010Article
- 53BP1-dependent robust localized KAP-1 phosphorylation is essential for heterochromatic DNA double-strand break repair.Nature cell biology · 2010Article
- A mitotic phosphorylation feedback network connects Cdk1, Plk1, 53BP1, and Chk2 to inactivate the G(2)/M DNA damage checkpoint.PLoS biology · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
NFBD1/MDC1, 53BP1 and BRCA1 are DNA damage checkpoint proteins with twin BRCT domains. In order to determine if they have redundant roles in responses to ionizing radiation, we used siRNA and shRNA to deplete NFBD1, 53BP1 and BRCA1 in single, double and triple combinations. These analyses were performed in early passage human foreskin fibroblasts so that checkpoint responses could be assessed in a normal genetic background. We report that NFBD1, 53BP1 and BRCA1 have both unique and redundant functions in radiation-induced phosphorylation and localization events in the ATM-Chk2 pathway. 53BP1, but not NFBD1 and BRCA1, mediates ionizing radiation-induced ATM S1981 autophosphorylation. In contrast, all three mediators collaborate to promote IR-induced Chk2 T68 phosphorylation. NFBD1 and 53BP1, but not BRCA1, work together to mediate pATMS1981, pChk2T68 and NBS1 ionizing radiation induced foci (IRIF). However, the relative importance of NFBD1 and 53BP1 in IRIF formation differ. We also determined the interdependence among mediators in IRIF recruitment. We extend previous findings in cancer cells and mouse cells that NFBD1 is upstream of 53BP1 and BRCA1 to primary human cells. Furthermore, NFBD1 promotes BRCA1 IRIF through both 53BP1-dependent and 53BP1-independent mechanisms.
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