ArticleOncogene2002
Nbs1 promotes ATM dependent phosphorylation events including those required for G1/S arrest.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
42 citing papers in PubMed, 120 citations in OpenAlex.
- Thyroid cancer and double-strand DNA break repair: The potential role of the MRN complex pathogenic variants.Journal of clinical & translational endocrinology · 2026Review
- ATM inhibition exploits checkpoint defects and ATM-dependent double strand break repair in TP53-mutant glioblastoma.Nature communications · 2024Article
- Development and Evolution of DNA-Dependent Protein Kinase Inhibitors toward Cancer Therapy.International journal of molecular sciences · 2022Review
- Shift in GCells · 2021Article
- Review
- The role of poly ADP-ribosylation in the first wave of DNA damage response.Nucleic acids research · 2017Article
- The cell cycle checkpoint inhibitors in the treatment of leukemias.Journal of hematology & oncology · 2017Review
- Article
- Sp1 facilitates DNA double-strand break repair through a nontranscriptional mechanism.Molecular and cellular biology · 2012Article
- Abnormalities in DNA double-strand break response beyond primary immunodeficiency.International journal of hematology · 2011Article
- UV-induced histone H2AX phosphorylation and DNA damage related proteins accumulate and persist in nucleotide excision repair-deficient XP-B cells.DNA repair · 2011Article
- The ubiquitous role of ubiquitin in the DNA damage response.DNA repair · 2010Review
- The MRN complex in double-strand break repair and telomere maintenance.FEBS letters · 2010Review
- Regulation of the DNA Damage Response to DSBs by Post-Translational Modifications.Current genomics · 2010Article
- p53 prevents entry into mitosis with uncapped telomeres.Current biology : CB · 2010Article
- MUC1-C Oncoprotein Interacts Directly with ATM and Promotes the DNA Damage Response to Ionizing Radiation.Genes & cancer · 2010Article
- Meiotic localization of Mre11 and Rad50 in wild type, spo11-1, and MRN complex mutants of Coprinus cinereus.Chromosoma · 2009Article
- Multiple autophosphorylation sites are dispensable for murine ATM activation in vivo.The Journal of cell biology · 2008Article
- Replication independent ATR signalling leads to G2/M arrest requiring Nbs1, 53BP1 and MDC1.Human molecular genetics · 2008Article
- Activation and regulation of ATM kinase activity in response to DNA double-strand breaks.Oncogene · 2007Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell lines from Nijmegen Breakage Syndrome (NBS) and ataxia telangiectasia (A-T) patients show defective S phase checkpoint arrest. In contrast, only A-T but not NBS cells are significantly defective in radiation-induced G1/S arrest. Phosphorylation of some ATM substrates has been shown to occur in NBS cells. It has, therefore, been concluded that Nbs1 checkpoint function is S phase specific. Here, we have compared NBS with A-T cell lines (AT-5762ins137) that express a low level of normal ATM protein to evaluate the impact of residual Nbs1 function in NBS cells. The radiation-induced cell cycle response of these NBS and 'leaky' A-T cells is almost identical; normal G2/M arrest after 2 Gy, intermediate G1/S arrest depending on the dose and an A-T-like S phase checkpoint defect. Thus, the checkpoint assays differ in their sensitivity to low ATM activity. Radiation-induced phosphorylation of the ATM-dependent substrates Chk2, RPAp34 and p53-Ser15 are similarly impaired in AT-5762ins137 and NBS cells in a dose dependent manner. In contrast, NBS cells show normal ability to activate ATM kinase following irradiation in vitro and in vivo. We propose that Nbs1 facilitates ATM-dependent phosphorylation of multiple downstream substrates, including those required for G1/S arrest.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.