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PPL2 Translesion Polymerase Is Essential for the Completion of Chromosomal DNA Replication in the African Trypanosome

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Cellular epigenetic stability and cancer

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PCNA ubiquitination-independent activation of polymerase η during somatic hypermutation and DNA damage tolerance

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FANCD2 and REV1 cooperate in the protection of nascent DNA strands in response to replication stress

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Cellular Responses to Widespread DNA Replication Stress

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Roles of mutagenic translesion synthesis in mammalian genome stability, health and disease

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Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability

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Single Cell Analysis of Human RAD18-Dependent DNA Post-Replication Repair by Alkaline Bromodeoxyuridine Comet Assay

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Redundancy of mammalian Y family DNA polymerases in cellular responses to genomic DNA lesions induced by ultraviolet light

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Persistently stalled replication forks inhibit nucleotide excision repair in <i>trans</i> by sequestering Replication protein A

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Error-prone translesion replication of damaged DNA suppresses skin carcinogenesis by controlling inflammatory hyperplasia

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Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1α axis

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Different Sets of Translesion Synthesis DNA Polymerases Protect From Genome Instability Induced by Distinct Food-Derived Genotoxins

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Excision of translesion synthesis errors orchestrates responses to helix-distorting DNA lesions

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A UVR-induced G2-phase checkpoint response to ssDNA gaps produced by replication fork bypass of unrepaired lesions is defective in melanoma

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Translesion synthesis polymerases are dispensable for C. elegans reproduction but suppress genome scarring by polymerase theta-mediated end joining

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Replicating Damaged DNA in EukaryotesPreprint

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Analysis of CPD Ultraviolet Lesion Bypass in Chicken DT40 Cells: Polymerase η and PCNA Ubiquitylation Play Identical Roles

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Role of non-classical polymerases and SUMO PCNA dependent mechanisms in the maintenance of genome stability

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Comparative whole-genome analyses of articular chondrocytes and skin fibroblasts reveal distinct genome instability landscapes in mesenchymal cell types

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