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The Fanconi Anemia (FA) repair pathway governs the repair of highly genotoxic DNA interstrand crosslinks (ICLs) with the assistance of translesion synthesis (TLS), that is facilitated by site-specific monoubiquitination of PCNA (PCNA-Ub) at lysine 164 (K164). Mutation at this residue (K164R) renders...
ORGANISM(S): Mus musculus (Mouse) 
2024-08-09 | PXD035337 | Pride
The rates at which lesions are removed by DNA repair can vary widely throughout the genome with important implications for genomic stability. We measured the distribution of nucleotide excision repair (NER) rates for UV induced lesions throughout the yeast genome. By plotting these repair rates in r...
ORGANISM(S): Saccharomyces cerevisiae 
The cullin Rtt101 promotes ubiquitin-dependent DNA-Protein Crosslink repair across the cell cycle
The NEIL3 DNA glycosylase is a base excision repair enzyme that excises bulky base lesions from DNA. Although NEIL3 has been shown to unhook interstrand crosslinks (ICL) in Xenopus extracts, how NEIL3 participants in ICL repair in human cells and its corporation with the canonical Fanconi anemia (FA...
ORGANISM(S): Homo sapiens (Human) 
2020-01-20 | PXD016256 | Pride
DNA-protein crosslinks (DPCs) are toxic lesions that inhibit DNA related processes. Post-translational modifications (PTMs), including SUMOylation and ubiquitylation, play a central role in DPC resolution, but whether other PTMs are also involved remains elusive. Here, we identify a DPC repair pathw...
ORGANISM(S): Xenopus laevis (African clawed frog) 
2024-08-06 | PXD043107 | Pride
By covalently linking Watson and Crick strands, DNA interstrand crosslinks (ICLs) are highly toxic lesions that block DNA replication and threaten genome integrity. The Fanconi anemia (FA) pathway orchestrates ICL repair during DNA replication, with ubiquitylated FANCI-FANCD2 (ID2) marking the activ...
ORGANISM(S): Xenopus laevis (African clawed frog) 
2022-02-18 | PXD024280 | Pride
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