ArticleMolecular and cellular biology1997
Nijmegen breakage syndrome cells fail to induce the p53-mediated DNA damage response following exposure to ionizing radiation.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 118 citations in OpenAlex.
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- Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network.Cells · 2022Review
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- Modeling the interplay between DNA-PK, Artemis, and ATM in non-homologous end-joining repair in G1 phase of the cell cycle.Journal of biological physics · 2019Article
- Meiotic localization of Mre11 and Rad50 in wild type, spo11-1, and MRN complex mutants of Coprinus cinereus.Chromosoma · 2009Article
- Structure of a second BRCT domain identified in the nijmegen breakage syndrome protein Nbs1 and its function in an MDC1-dependent localization of Nbs1 to DNA damage sites.Journal of molecular biology · 2008Article
- Article
- E2F1 induces MRN foci formation and a cell cycle checkpoint response in human fibroblasts.Oncogene · 2006Article
- Genetic and epigenetic features in radiation sensitivity Part I: cell signalling in radiation response.European journal of nuclear medicine and molecular imaging · 2005Review
- Review
- Cellular responses to ionising radiation of AT heterozygotes: differences between missense and truncating mutation carriers.British journal of cancer · 2004Article
- The fission yeast Rad32 (Mre11)-Rad50-Nbs1 complex is required for the S-phase DNA damage checkpoint.Molecular and cellular biology · 2003Article
- P53 and radiation responses.Oncogene · 2003Review
- Article
- AtATM is essential for meiosis and the somatic response to DNA damage in plants.The Plant cell · 2003Article
- Nijmegen breakage syndrome gene, NBS1, and molecular links to factors for genome stability.Oncogene · 2002Review
- Nbs1 promotes ATM dependent phosphorylation events including those required for G1/S arrest.Oncogene · 2002Article
- G2-phase radiation response in lymphoblastoid cell lines from Nijmegen breakage syndrome.Cell proliferation · 2002Article
- Chk2 activation dependence on Nbs1 after DNA damage.Molecular and cellular biology · 2001Article
- Role of Nijmegen breakage syndrome protein in specific T-lymphocyte activation pathways.Clinical and diagnostic laboratory immunology · 2001Article
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Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functionality of the p53-mediated pathway, activated in response to DNA damage, has been assessed in primary fibroblast cell cultures and Epstein-Barr virus-transformed lymphoblastoid cell lines derived from Nijmegen breakage syndrome (NBS) patients. This autosomal recessive disease is characterized by microcephaly, growth and mental retardation, chromosomal instability, radiosensitivity, and high cancer incidence. The recent mapping of the NBS gene to chromosome 8q21 demonstrates that NBS is genetically distinct from ataxia telangiectasia (AT). Changes in p53 protein levels were significantly reduced and delayed in all the NBS fibroblast cell cultures and lymphoblastoid cell lines examined compared to normal cultures over a 4-h period postirradiation (5 Gy). The transcriptional activation of p21(WAF1/CIP1) mRNA was also lower in 12 NBS fibroblast cultures examined. In agreement with an abrogated p53 function, NBS cells exposed to ionizing radiation show an abnormal cell cycle arrest at G1-S and a prolonged accumulation of cells in the G2 phase. In contrast, exposure to the alkylating agent methyl methanesulfonate results in similar increases of p53 and p21(WAF1/CIP1) mRNA in both cell types. The ATM gene transcript was found to be expressed at similar levels in NBS and normal cells, whereas it was strongly reduced in the AT homozygote cells examined. These results suggest that the ATM gene product cannot substitute for that of the NBS gene in the signaling of cellular damage produced by ionizing radiation and that both are involved in the activation of p53. The suboptimal p53-mediated response could contribute to the high cancer risk and radiosensitivity seen in NBS patients.
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