Base excision repair synthesis of DNA containing 8-oxoguanine in Escherichia coli

Lee, Yong Kyu; Chung, Myung‐Hee

doi:10.1038/emm.2003.15

Cited by 9 publications

(7 citation statements)

References 27 publications

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“…Most reports have proposed a direct role for p53 in this process via its interaction with BER-associated proteins, including DNA polymerase β and AP endonuclease (30–33). In contrast, p53 controls NER by transcriptionally regulating NER proteins, such as p48XPE and XPC (34).…”

Section: Discussionmentioning

confidence: 99%

A novel chemopreventive mechanism of selenomethionine: Enhancement of APE1 enzyme activity via a Gadd45a, PCNA and APE1 protein complex that regulates p53-mediated base excision repair

Jung

Kim

et al. 2013

Oncology Reports

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Organic selenium compounds have been documented to play a role in cancer prevention. Our previous study showed that selenomethionine (SeMet) induces p53 activation without genotoxic effects including apoptosis and cell cycle arrest. In this study, we investigated the mechanism by which organic selenium compounds promote p53-mediated base excision repair (BER) activity. Our data demonstrated for the first time that the interaction between growth arrest and DNA damage-inducible protein 45A (Gadd45a), which is a p53-activated downstream gene, and two BER-mediated repair proteins, proliferating cell nuclear antigen (PCNA) and apurinic/apyrimidinic endonuclease (APE1/Ref-1), was significantly increased in a p53-dependent manner following treatment with organic selenium compounds. Furthermore, we observed that the activity of APE1 was significantly increased in a p53-dependent manner in response to the organic selenium compounds. These results suggest that BER activity is dependent on wild-type p53 activity and is mediated by the modulation of protein interactions between Gadd45a and repair proteins in response to organic selenium compounds. We propose that p53-dependent BER activity is a distinct chemopreventive mechanism mediated by organic selenium compounds, and that this may provide insight into the development of effective chemopreventive strategies against various oxidative stresses that contribute to a variety of human diseases, particularly cancer.

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Section: Discussionmentioning

confidence: 99%

A novel chemopreventive mechanism of selenomethionine: Enhancement of APE1 enzyme activity via a Gadd45a, PCNA and APE1 protein complex that regulates p53-mediated base excision repair

Jung

Kim

et al. 2013

Oncology Reports

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“…As a mechanism of p53 role for BER, most reports have implicated a direct role of p53 protein via protein-protein interactions with BER proteins including DNA polymerase b and AP endonuclease (Gaiddon et al, 1999;Offer et al, 2001;Zhou et al, 2001;Lee and Chung, 2003). In contrast, p53 controls NER by transcriptional regulation of NER proteins including p48XPE and XPC (Adimoolam and Ford, 2002).…”

Section: Discussionmentioning

confidence: 99%

Base excision DNA repair defect in Gadd45a-deficient cells

et al. 2007

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“…Excision of U by uracil DNA glycosylase (UDG), followed by strand scission at the resulting AP sites by FapyG DNA glycosylase (Fpg) generated 3΄-P and 5΄-P termini (Figure 1A) (27). However, direct ligation of U-containing duplex with oligonucleotide into a pEGFPN1 backbone gave a very low yield of the final product which was not sufficient for performing the repair assays (not shown).…”

Section: Methodsmentioning

confidence: 99%

Microhomology-mediated end joining is activated in irradiated human cells due to phosphorylation-dependent formation of the XRCC1 repair complex

et al. 2016

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Microhomology-mediated end joining (MMEJ), an error-prone pathway for DNA double-strand break (DSB) repair, is implicated in genomic rearrangement and oncogenic transformation; however, its contribution to repair of radiation-induced DSBs has not been characterized. We used recircularization of a linearized plasmid with 3΄-P-blocked termini, mimicking those at X-ray-induced strand breaks, to recapitulate DSB repair via MMEJ or nonhomologous end-joining (NHEJ). Sequence analysis of the circularized plasmids allowed measurement of relative activity of MMEJ versus NHEJ. While we predictably observed NHEJ to be the predominant pathway for DSB repair in our assay, MMEJ was significantly enhanced in preirradiated cells, independent of their radiation-induced arrest in the G2/M phase. MMEJ activation was dependent on XRCC1 phosphorylation by casein kinase 2 (CK2), enhancing XRCC1's interaction with the end resection enzymes MRE11 and CtIP. Both endonuclease and exonuclease activities of MRE11 were required for MMEJ, as has been observed for homology-directed DSB repair (HDR). Furthermore, the XRCC1 co-immunoprecipitate complex (IP) displayed MMEJ activity in vitro, which was significantly elevated after irradiation. Our studies thus suggest that radiation-mediated enhancement of MMEJ in cells surviving radiation therapy may contribute to their radioresistance and could be therapeutically targeted.

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Base excision repair synthesis of DNA containing 8-oxoguanine in Escherichia coli

Cited by 9 publications

References 27 publications

A novel chemopreventive mechanism of selenomethionine: Enhancement of APE1 enzyme activity via a Gadd45a, PCNA and APE1 protein complex that regulates p53-mediated base excision repair

A novel chemopreventive mechanism of selenomethionine: Enhancement of APE1 enzyme activity via a Gadd45a, PCNA and APE1 protein complex that regulates p53-mediated base excision repair

Base excision DNA repair defect in Gadd45a-deficient cells

Microhomology-mediated end joining is activated in irradiated human cells due to phosphorylation-dependent formation of the XRCC1 repair complex

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