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- W2100819919 endingPage "2002" @default.
- W2100819919 startingPage "1990" @default.
- W2100819919 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." @default.
- W2100819919 created "2016-06-24" @default.
- W2100819919 creator A5004307987 @default.
- W2100819919 creator A5066590781 @default.
- W2100819919 date "2015-08-20" @default.
- W2100819919 modified "2023-10-13" @default.
- W2100819919 title "Functional Role of NBS1 in Radiation Damage Response and Translesion DNA Synthesis" @default.
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- W2100819919 doi "https://doi.org/10.3390/biom5031990" @default.
- W2100819919 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4598784" @default.
- W2100819919 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26308066" @default.
- W2100819919 hasPublicationYear "2015" @default.
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