New research from a team of genome scientists and DNA damage response experts breaks new ground in understanding the function of a protein currently limited in clinical trials for cancer treatments.
University of North Carolina at CharlotteAug 7 2024
"We demonstrate that APE1 promotes SSB-induced ATM DDR through at least two mechanisms: APE1 exonuclease activity-mediated SSB processing and APE1-mediated direct recruitment of ATM to SSBs," researchers wrote. Lead author of "Distinct regulation of ATM signaling by DNA single-strand breaks and APE1," Haichao Zhao offered that the research may support future clinical trials – both for attacking cancer cells and other life-threatening conditions and for protecting non-malignant cells during treatments.
While DNA damage repair research is far more established for cellular response to double-strand breaks , Zhao and Yan say knowledge gaps surrounding SSBs have persisted. In particular, Yan said, molecular biologists have had little to no direct evidence about the precise function of APE1 at SSB sites.
The research from Zhao, et. al., clearly establishes, for the first time, APE1's function as a direct activator of ATM kinase to promote the repair of single-strand DNA damage. The study also provides direct evidence that the ATM-dependent DDR pathway is activated by a SSB of a defined DNA structure.
In the Yan lab, researchers utilized eggs from female Xenopus laevis to produce high-speed supernatant egg extracts, later introducing purified plasmid DNA structures from E. coli. Researchers then incubated different concentrations of SSB and control plasmid in the HSS. In response, the study showed, APE1 was "recruited to SSB plasmid at an early stage of SSB signaling." And, the research reveals ATM is activated by SSBs.
Cancer Cell Cell Cycle DNA Damage Enzyme Genome Kinase Plasmid Protein Research
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