Mutational signatures associated with apolipoprotein B mRNA-editing enzyme catalytic
polypeptide-like (APOBEC) 3 cytosine deaminase activity have been found in over half of …

Covalent DNA–protein crosslinks (DPCs) are pervasive DNA lesions that interfere with
essential chromatin processes such as transcription or replication. This review strives to …

CRISPR/Cas9 gene editing can inactivate genes in a precise manner. This process involves
DNA double-strand breaks (DSB), which may incur a loss of cell fitness. We hypothesize that …

The initiation, progression, and relapse of cancers often result from mutations occurring
within somatic cells. Consequently, processes that elevate mutation rates accelerate …

Mutation signatures associated with apolipoprotein B mRNA editing catalytic polypeptide-
like 3A/B (APOBEC3A/B) cytidine deaminases are prevalent across cancers, implying their …

The conserved protein HMCES crosslinks to abasic (AP) sites in ssDNA to prevent strand
scission and the formation of toxic dsDNA breaks during replication. Here, we report a non …

Apolipoprotein B mRNA-editing enzyme, catalytic polypeptides (APOBECs) are cytosine
deaminases involved in innate and adaptive immunity. However, some APOBEC family …

Abasic sites are DNA lesions repaired by base excision repair. Cleavage of unrepaired
abasic sites in single-stranded DNA (ssDNA) can lead to chromosomal breakage during …

Genomic analyses have revealed mutational footprints associated with DNA maintenance
gone awry, or with mutagen exposures. Because cancer therapeutics often target DNA …

The cytidine deaminases APOBEC3A (A3A) and APOBEC3B (A3B) are prominent mutators
of human cancer genomes. However, tumor-specific genetic modulators of APOBEC …