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• W3099681622 abstract "Abstract The ubiquitin–proteasome system (UPS) plays crucial roles in regulation of various biological processes, including DNA repair. In mammalian global genome nucleotide excision repair (GG-NER), activation of the DDB2-associated ubiquitin ligase upon UV-induced DNA damage is necessary for efficient recognition of lesions. To date, however, the precise roles of UPS in GG-NER remain incompletely understood. Here, we show that the proteasome subunit PSMD14 and the UPS shuttle factor RAD23B can be recruited to sites with UV-induced photolesions even in the absence of XPC, suggesting that proteolysis occurs at DNA damage sites. Unexpectedly, sustained inhibition of proteasome activity results in aggregation of PSMD14 (presumably with other proteasome components) at the periphery of nucleoli, by which DDB2 is immobilized and sequestered from its lesion recognition functions. Although depletion of PSMD14 alleviates such DDB2 immobilization induced by proteasome inhibitors, recruitment of DDB2 to DNA damage sites is then severely compromised in the absence of PSMD14. Because all of these proteasome dysfunctions selectively impair removal of cyclobutane pyrimidine dimers, but not (6–4) photoproducts, our results indicate that the functional integrity of the proteasome is essential for the DDB2-mediated lesion recognition sub-pathway, but not for GG-NER initiated through direct lesion recognition by XPC." @default.
• W3099681622 created "2020-11-23" @default.
• W3099681622 creator A5002461656 @default.
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• W3099681622 date "2020-11-12" @default.
• W3099681622 modified "2023-10-15" @default.
• W3099681622 title "Functional impacts of the ubiquitin–proteasome system on DNA damage recognition in global genome nucleotide excision repair" @default.
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• W3099681622 doi "https://doi.org/10.1038/s41598-020-76898-2" @default.
• W3099681622 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7665181" @default.
• W3099681622 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33184426" @default.
• W3099681622 hasPublicationYear "2020" @default.
• W3099681622 type Work @default.
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• W3099681622 hasAuthorship W3099681622A5002461656 @default.
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• W3099681622 hasAuthorship W3099681622A5005878397 @default.

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