Travis K. Worley's research while affiliated with Portland State University and other places
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Publications (3)
DNA interstrand cross-links, such as those formed by psoralen-UVA irradiation, are highly toxic lesions in both humans and bacteria, with a single lesion being lethal in Escherichia coli. Despite the lack of effective repair, human cancers and bacteria can develop resistance to cross-linking treatments, although the mechanisms of resistance remain...
Recombination mediator proteins have come into focus as promising targets for cancer therapy, with synthetic lethal approaches now clinically validated by the efficacy of PARP inhibitors in treating BRCA2 cancers and RECQ inhibitors in treating cancers with microsatellite instabilities. Thus, understanding the cellular role of recombination mediato...
UV irradiation induces pyrimidine dimers that block polymerases and disrupt the replisome. Restoring replication depends on the recF pathway proteins which process and maintain the replication fork DNA to allow the lesion to be repaired before replication resumes. Oxidative DNA lesions, such as those induced by hydrogen peroxide (H2O2), are often t...
Citations
... NfxB belongs to the TFRs (21), which have been widely associated with bacterial physiology aspects (26). In clinical isolates, TFR mutations lead to the de-repression of their targets (27), some of which are efflux transporters, thus contributing to AMR and adjusting to changing environments (28). NfxB mutants are commonly found in ciprofloxacin-resistant P. aeruginosa clinical strains (29,30). ...
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... In both bacteria and eukaryotes, genome instability increases when recombination genes are mutated [13][14][15]. Cancer cells that often display high levels of genome instability are replete with mutations in HR and other DNA damage repair genes [16][17][18][19]. In human cells, HR is facilitated primarily by the BRCA2-BRCA1-PALB2 module, which loads RAD51 onto a resected single-stranded end to initiate a homologous search and strand exchange [20,21]. ...
... Together, these results demonstrate that the induction of the oxidative stress response effectively protects cells against H2O2 present in their environment, reducing the formation of oxidative DNA damage down to the basal level within 30 min of continuous oxidative stress. This explains observations from genetic studies that deletion of BER and NER enzymes does not sensitise cells to killing by H2O2 (Hoff et al., 2021). ...
