Oxidative stress and the resulting damage to genomic DNA are inevitable consequences of
endogenous physiological processes, and they are amplified by cellular responses to …

Oxidatively damaged DNA results from the attack of sugar and base moieties by reactive
oxygen species (ROS), which are formed as byproducts of normal cell metabolism and …

UV-DDB, consisting of subunits DDB1 and DDB2, recognizes UV-induced photoproducts
during global genome nucleotide excision repair (GG-NER). We recently demonstrated a …

Base excision repair (BER) is initialized by DNA glycosylases, which recognize and flip
damaged bases out of the DNA duplex into the enzymes active site, followed by cleavage of …

DNA glycosylases safeguard the genome by locating and excising a diverse array of
aberrant nucleobases created from oxidation, alkylation, and deamination of DNA. Since the …

Combinational therapies provoking cell death are of major interest in oncology. Combining
TORC2 kinase inhibition with the radiomimetic drug Zeocin results in a rapid accumulation …

Cellular damage produced by conditions generating oxidative stress have far-reaching
implications in human disease that encompass, but are not restricted to aging …

Base excision repair (BER) is one of several DNA repair pathways found in all three
domains of life. BER counters the mutagenic and cytotoxic effects of damage that occurs …

A mutated KRAS protein is frequently observed in human cancers. Traditionally, the
oncogenic properties of KRAS missense mutants at position 12 (G12X) have been …

Endogenous and exogenous reactive species cause oxidatively induced DNA damage in
living organisms by a variety of mechanisms. As a result, a plethora of mutagenic and/or …