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Abbotts, R.

Publications and source records attributed to Abbotts, R..

2 recordsLinked to original sources

Orchestrated metal ion repositioning defines the dynamic catalytic strategy of the essential DNA repair nuclease APE1

Human AP-endonuclease 1 (APE1) is a vital enzyme in the base excision repair pathway that protects genome stability by eliminating ubiquitous abasic DNA lesions. Despite its importance and therapeutic potential, how APE1 achieves high specificity and single-metalion catalytic efficiency remains unclear. Here, we present a high-resolution structure of the APE1-DNA Michaelis complex coordinated with physiological cofactor Mg2+. Integrating this snapshot with ab initio molecular dynamics and metadynamics simulations reveals a novel "moving metal ion" mechanism in which Mg2+ undergoes orchestrated repositioning to trigger a concerted catalytic reaction, bypassing the formation of an associative pentavalent intermediate. This distinct catalytic strategy, driven by concerted active-site reorganization, enables APE1 to efficiently process damaged DNA using only one metal ion cofactor. A previously unrecognized hydrogen-bonding network couples catalytic water activation to the metal ion movement - two events that strikingly occur on opposite sides of the active site. These findings provide a blueprint for how enzymes synchronize distal active site rearrangements with transition state formation. Our results further suggest that effective AI-targeted inhibitor design should develop capacities to predict mechanistically critical non-canonical rotamers and transient hydrogen-bonding networks. Our combined findings offer a foundation for the design of inhibitors targeting APE1 overexpression in cancer.

biochemistry↗

ZNFX1 is a Novel Master Regulator in Epigenetically-induced Pathogen Mimicry and Inflammasome Signaling in Cancer

DNA methyltransferase and poly(ADP-ribose) polymerase inhibitors (DNMTis, PARPis) induce a stimulator of interferon (IFN) genes (STING)-dependent pathogen mimicry response (PMR) in ovarian (OC) and other cancers. We now show that combining DNMTis and PARPis upregulates expression of a little-studied nucleic-acid sensor, NFX1-type zinc finger-containing 1 protein (ZNFX1). We demonstrate that ZNFX1 is a novel master regulator for PMR induction in mitochondria, serving as a gateway for STING-dependent PMR. In patient OC databases, high ZNFX1 expression levels correlate with advanced stage disease. ZNFX1 expression alone significantly correlates with an increase in overall survival in a phase 3 trial for therapy-resistant OC patients receiving bevacizumab in combination with chemotherapy. In correlative RNA-seq data, inflammasome signaling through ZNFX1 correlates with abnormal vasculogenesis. ZNFX1 controls PMR signaling through the mitochondria and may serve as a biomarker to facilitate offering personalized therapy in OC patients, highlighting the strong translational significance of our findings. Significance statementDNA methyltransferase and poly(ADP-ribose) polymerase inhibitors upregulate expression of a novel nucleic-acid sensor, ZNFX1 that serves as a mitochondrial gateway to STING-dependent interferon/inflammasome signaling with tumor suppressor properties in ovarian cancer.

cancer biology↗