ReviewBiomolecules2015
Functional Role of NBS1 in Radiation Damage Response and Translesion DNA Synthesis.
Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Elevated NDRG1 Expression Drives Oxaliplatin Chemoresistance in Bladder Cancer Cells by Promoting Homologous Recombination Repair and Inhibiting GCell biochemistry and biophysics · 2026Article
- Generation of NBS1 knockout in Chinese hamster cells revealed ATR role for radiation and etoposide induced DNA damage in absence of NBS1 proteins.Frontiers in oncology · 2026Article
- Inhibition of ATM enhances the immunogenicity of triple-negative breast cancer by promoting MHC-I expression.Cell death & disease · 2025Article
- Article
- Review
- Clinical measurement of cellular DNA damage hypersensitivity in patients with DNA repair defects.Orphanet journal of rare diseases · 2022Article
- DNA Damage Tolerance Pathways in Human Cells: A Potential Therapeutic Target.Frontiers in oncology · 2021Review
- Review
- The small GTPase RhoU lays downstream of JAK/STAT signaling and mediates cell migration in multiple myeloma.Blood cancer journal · 2018Article
- NBS1 and multiple regulations of DNA damage response.Journal of radiation research · 2016Review
- The role of the Mre11-Rad50-Nbs1 complex in double-strand break repair-facts and myths.Journal of radiation research · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nijmegen breakage syndrome (NBS) is a recessive genetic disorder characterized by increased sensitivity to ionizing radiation (IR) and a high frequency of malignancies. NBS1, a product of the mutated gene in NBS, contains several protein interaction domains in the N-terminus and C-terminus. The C-terminus of NBS1 is essential for interactions with MRE11, a homologous recombination repair nuclease, and ATM, a key player in signal transduction after the generation of DNA double-strand breaks (DSBs), which is induced by IR. Moreover, NBS1 regulates chromatin remodeling during DSB repair by histone H2B ubiquitination through binding to RNF20 at the C-terminus. Thus, NBS1 is considered as the first protein to be recruited to DSB sites, wherein it acts as a sensor or mediator of DSB damage responses. In addition to DSB response, we showed that NBS1 initiates Polη-dependent translesion DNA synthesis by recruiting RAD18 through its binding at the NBS1 C-terminus after UV exposure, and it also functions after the generation of interstrand crosslink DNA damage. Thus, NBS1 has multifunctional roles in response to DNA damage from a variety of genotoxic agents, including IR.
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Registered trials
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.