Poly(ADP-ribose) Polymerase 1 Modulates Interaction of the Nucleotide Excision Repair Factor XPC-RAD23B with DNA via Poly(ADP-ribosyl)ation

Maltseva, Ekaterina A.; Rechkunova, N. I.; Sukhanova, Maria V.; Lavrik, Olga I.

doi:10.1074/jbc.m115.646638

Cited by 32 publications

(19 citation statements)

References 37 publications

(43 reference statements)

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“…The synthesis of radioactive NAD + was carried out from α−[ 32 P]-ATP according to [ 81 ] with modification described in [ 82 ]. The reaction mixtures containing 1 mM ATP, 10 MBq of α−[ 32 P]-ATP, 20 mM MgCl 2 , 2 mM β-nicotinamide mononucleotide, and 5 mg/ml nicotinamide nucleotide adenylyltransferase in 25 mM Tris-HCl, pH7.5 were incubated at 37ºC for 60 min, then stopped by heating up to 90ºC for 3 min.…”

Section: Methodsmentioning

confidence: 99%

Naked mole rat cells display more efficient excision repair than mouse cells

Evdokimov

Kutuzov

Petruseva

et al. 2018

Aging

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Naked mole rat (NMR) is the long-lived and tumor-resistant rodent. NMRs possess multiple adaptations that may contribute to longevity and cancer-resistance. However, whether NMRs have more efficient DNA repair have not been directly tested. Here we compared base excision repair (BER) and nucleotide excision repair (NER) systems in extracts from NMR and mouse fibroblasts after UVC irradiation. Transcript levels of the key repair enzymes demonstrated in most cases higher inducibility in the mouse vs the NMR cells. Ratios of repair enzymes activities in the extracts somewhat varied depending on post-irradiation time. NMR cell extracts were 2–3-fold more efficient at removing the bulky lesions, 1.5–3-fold more efficient at removing uracil, and about 1.4-fold more efficient at cleaving the AP-site than the mouse cells, while DNA polymerase activities being as a whole higher in the mouse demonstrate different patterns of product distribution. The level of poly(ADP-ribose) synthesis was 1.4–1.8-fold higher in the NMR cells. Furthermore, NMR cell extracts displayed higher binding of PARP1 to DNA probes containing apurinic/apyrimidinic site or photo-reactive DNA lesions. Cumulatively, our results suggest that the NMR has more efficient excision repair systems than the mouse, which may contribute to longevity and cancer resistance of this species.

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Section: Methodsmentioning

confidence: 99%

Naked mole rat cells display more efficient excision repair than mouse cells

Evdokimov

Kutuzov

Petruseva

et al. 2018

Aging

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“…DDB2 PARylation leads to the protein’s stabilization and further recruitment [92]. Furthermore, Maltseva et al demonstrated that XPC-RAD23B, an essential complex of the NER pathway, is regulated by PARP-1 [93]. Induction of the NER pathway by platinum-based agents and simultaneous inhibition of PARP-1 could potentially suppress DNA repair.…”

Section: Combination Therapy Using Platinum-based Agents and Ddr-targmentioning

confidence: 99%

Combination Platinum-based and DNA Damage Response-targeting Cancer Therapy: Evolution and Future Directions

Basourakos

Aparicio

et al. 2017

CMC

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Maintenance of genomic stability is a critical determinant of cell survival and is necessary for growth and progression of malignant cells. Interstrand crosslinking (ICL) agents, including platinum-based agents, are first-line chemotherapy treatment for many solid human cancers. In malignant cells, ICL triggers the DNA damage response (DDR). When the damage burden is high and lesions cannot be repaired, malignant cells are unable to divide and ultimately undergo cell death either through mitotic catastrophe or apoptosis. The activities of ICL agents, in particular platinum-based therapies, establish a “molecular landscape,” i.e., a pattern of DNA damage that can potentially be further exploited therapeutically with DDR-targeting agents. If the molecular landscape created by platinum-based agents could be better defined at the molecular level, a systematic, mechanistic rationale(s) could be developed for the use of DDR-targeting therapies in combination/maintenance protocols for specific, clinically advanced malignancies. New therapeutic drugs such as poly(ADP-ribose) polymerase (PARP) inhibitors are examples of DDR-targeting therapies that could potentially increase the DNA damage and replication stress imposed by platinum-based agents in tumor cells and provide therapeutic benefit for patients with advanced malignancies. Recent studies have shown that the use of PARP inhibitors together with platinum-based agents is a promising therapy strategy for ovarian cancer patients with ”BRCAness”, i.e., a phenotypic characteristic of tumors that not only can involve loss-of-function mutations in either BRCA1 or BRCA2, but also encompasses the molecular features of BRCA-mutant tumors. On the basis of these promising results, additional mechanism-based studies focused on the use of various DDR-targeting therapies in combination with platinum-based agents should be considered. This review discusses, in general, (1) ICL agents, primarily platinum-based agents, that establish a molecular landscape that can be further exploited therapeutically; (2) multiple points of potential intervention after ICL agent–induced crosslinking that further predispose to cell death and can be incorporated into a systematic, therapeutic rationale for combination/maintenance therapy using DDR-targeting agents; and (3) available agents that can be considered for use in combination/maintenance clinical protocols with platinum-based agents for patients with advanced malignancies.

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“…64 It was further demonstrated that both XPC and RAD23B are parylated by PARP1 in response to UV irradiation. 65 Whether parylation of these factors is linked to ubiquitylation events as observed for DDB2 is currently unclear but an attractive speculation. Further, XPA shows high affinity for long PAR chains 66 suggesting that parylation might also play a role during damage verification.…”

Section: Regulation Of Poly-ubiquitylation By Parylation and Deubiquimentioning

confidence: 99%

Timing of DNA lesion recognition: Ubiquitin signaling in the NER pathway

Chitale

Richly

2016

Cell Cycle

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Damaged DNA is repaired by specialized repair factors that are recruited in a well-orchestrated manner to the damage site. The DNA damage response at UV inflicted DNA lesions is accompanied by posttranslational modifications of DNA repair factors and the chromatin environment sourrounding the lesion. In particular, mono- and poly-ubiquitylation events are an integral part of the DNA damage signaling. Whereas ubiquitin signaling at DNA doublestrand breaks has been subject to intensive studies comparatively little is known about the intricacies of ubiquitylation events occurring during nucleotide excision repair (NER), the major pathway to remove bulky helix lesions. Both, the global genomic (GG-NER) and the transcription-coupled (TC-NER) branches of NER are subject to ubiquitylation and deubiquitylation processes.Here we summarize our current knowledge of the ubiquitylation network that drives DNA repair in the NER pathway and we discuss the crosstalk of ubiquitin signaling with other prominent post-translational modfications that might be essential to time the DNA damage recognition step.

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Poly(ADP-ribose) Polymerase 1 Modulates Interaction of the Nucleotide Excision Repair Factor XPC-RAD23B with DNA via Poly(ADP-ribosyl)ation

Cited by 32 publications

References 37 publications

Naked mole rat cells display more efficient excision repair than mouse cells

Naked mole rat cells display more efficient excision repair than mouse cells

Combination Platinum-based and DNA Damage Response-targeting Cancer Therapy: Evolution and Future Directions

Timing of DNA lesion recognition: Ubiquitin signaling in the NER pathway

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