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dc.contributor.authorAlbelazi
dc.contributor.authorMartin
dc.contributor.authorMohammed
dc.contributor.authorMutti
dc.contributor.authorElder
dc.date.accessioned2020-07-03T11:19:30Z
dc.identifier.citationGenes, 10 (4), pp. 315 - 315
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3792
dc.identifier.eissn2073-4425
dc.identifier.doi10.3390/genes10040315
dc.description.abstractEndonuclease VIII-like (NEIL) 1 and 3 proteins eliminate oxidative DNA base damage and psoralen DNA interstrand crosslinks through initiation of base excision repair. Current evidence points to a DNA replication associated repair function of NEIL1 and NEIL3, correlating with induced expression of the proteins in S/G2 phases of the cell cycle. However previous attempts to express and purify recombinant human NEIL3 in an active form have been challenging. In this study, both human NEIL1 and NEIL3 have been expressed and purified from E. coli, and the DNA glycosylase activity of these two proteins confirmed using single- and double-stranded DNA oligonucleotide substrates containing the oxidative bases, 5-hydroxyuracil, 8-oxoguanine and thymine glycol. To determine the biochemical role that NEIL1 and NEIL3 play during DNA replication, model replication fork substrates were designed containing the oxidized bases at one of three specific sites relative to the fork. Results indicate that whilst specificity for 5- hydroxyuracil and thymine glycol was observed, NEIL1 acts preferentially on double-stranded DNA, including the damage upstream to the replication fork, whereas NEIL3 preferentially excises oxidized bases from single stranded DNA and within open fork structures. Thus, NEIL1 and NEIL3 act in concert to remove oxidized bases from the replication fork.
dc.format.extent315 - 315
dc.languageeng
dc.language.isoeng
dc.publisherMDPI AG
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleThe Biochemical Role of the Human NEIL1 and NEIL3 DNA Glycosylases on Model DNA Replication Forks
dc.typeJournal Article
rioxxterms.versionofrecord10.3390/genes10040315
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfGenes
pubs.issue4
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Cancer and Genome Instability
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Cancer and Genome Instability
pubs.publication-statusPublished online
pubs.volume10
pubs.embargo.termsNot known
icr.researchteamCancer and Genome Instabilityen_US
dc.contributor.icrauthorMartin, Peteren


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