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dc.contributor.authorGago-Fuentes, Raquel
dc.contributor.authorOksenych, Valentyn
dc.date.accessioned2021-03-15T09:38:33Z
dc.date.available2021-03-15T09:38:33Z
dc.date.issued2020-12-28
dc.description.abstractNon-homologous end-joining (NHEJ) is a major DNA repair pathway in mammalian cells that recognizes, processes and fixes DNA damage throughout the cell cycle and is specifically important for homeostasis of post-mitotic neurons and developing lymphocytes. Neuronal apoptosis increases in the mice lacking NHEJ factors Ku70 and Ku80. Inactivation of other NHEJ genes, either <i>Xrcc4</i> or <i>Lig4</i>, leads to massive neuronal apoptosis in the central nervous system (CNS) that correlates with embryonic lethality in mice. Inactivation of either <i>Paxx, Mri</i> or <i>Dna-pkcs</i> NHEJ gene results in normal CNS development due to compensatory effects of <i>Xlf</i>. Combined inactivation of <i>Xlf/Paxx, Xlf/Mri </i>and <i>Xlf/Dna-pkcs</i>, however, results in late embryonic lethality and high levels of apoptosis in CNS. To determine the impact of NHEJ factors on the early stages of neurodevelopment, we isolated neural stem and progenitor cells from mouse embryos and investigated proliferation, self-renewal and differentiation capacity of these cells lacking either <i>Xlf, Paxx, Dna-pkcs, Xlf/Paxx</i> or <i>Xlf/Dna-pkcs</i>. We found that XRCC4-like factor (XLF), DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and paralogue of XRCC4 and XLF (PAXX) maintain the neural stem and progenitor cell populations and neurodevelopment in mammals, which is particularly evident in the double knockout models.en_US
dc.identifier.citationGago-Fuentes, Oksenych. Non-Homologous End Joining Factors XLF, PAXX and DNA-PKcs Maintain the Neural Stem and Progenitor Cell Population. Biomolecules. 2020en_US
dc.identifier.cristinIDFRIDAID 1864348
dc.identifier.doi10.3390/biom11010020
dc.identifier.issn2218-273X
dc.identifier.urihttps://hdl.handle.net/10037/20686
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.relation.journalBiomolecules
dc.relation.projectIDinfo:eu-repo/grantAgreement/RCN/FRIMEDBIO/249774/Norway/Mechanisms underlying the function of XLF in DNA double-strand break repair//en_US
dc.relation.projectIDinfo:eu-repo/grantAgreement/RCN/POS-ERC/270491/Norway/Role of novel DNA double strand break repair factors in immune system development//en_US
dc.relation.projectIDinfo:eu-repo/grantAgreement/RCN/?/291217/Norway/?/?/en_US
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2020 The Author(s)en_US
dc.subjectVDP::Medical disciplines: 700en_US
dc.subjectVDP::Medisinske Fag: 700en_US
dc.titleNon-Homologous End Joining Factors XLF, PAXX and DNA-PKcs Maintain the Neural Stem and Progenitor Cell Populationen_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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