{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThyroid hormone receptor–interacting protein 13 (TRIP13) is an evolutionarily conserved AAA+ ATPase that plays a pivotal role in maintaining genomic stability. By binding to the checkpoint‐antagonist p31(comet), TRIP13 catalyzes the remodeling of HORMA domain proteins—most notably converting active, closed MAD2 into its inactive, open conformation—thereby promoting disassembly of the mitotic checkpoint complex and facilitating timely anaphase onset. This ATPase‐dependent function is essential not only for checkpoint silencing during mitosis but also for ensuring proper chromosome segregation and supporting DNA repair processes such as nonhomologous end joining."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGermline mutations or loss‐of‐function variants in TRIP13 can disrupt these critical mitotic and DNA repair processes, leading to severe checkpoint impairment. Such defects have been linked to developmental abnormalities and cancer predisposition syndromes—including Wilms tumor, mosaic variegated aneuploidy, and oocyte meiotic arrest associated with infertility—highlighting the dosage‐dependent and context‐specific roles of TRIP13 in human biology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "10"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, TRIP13 is frequently overexpressed across a wide range of human malignancies—including cancers of the head and neck, prostate, colorectal, lung, breast, esophagus, liver, cervix, brain, bladder, and pancreas—and its aberrant activity is closely associated with tumor progression, metastasis, and treatment resistance. In these cancers, excessive TRIP13 not only accelerates cell proliferation and epithelial–mesenchymal transition through activation of signaling pathways such as PI3K–AKT–mTOR, EGFR, and Wnt/β‐catenin but also enhances DNA repair capacity, thereby conferring resistance to chemotherapeutic agents (e.g. EGFR–tyrosine kinase inhibitors, nedaplatin, and gemcitabine). These findings underscore the potential of TRIP13 as a prognostic biomarker and therapeutic target, with strategies aimed at inhibiting its ATPase activity or modulating its upstream regulators—such as microRNAs and histone deacetylases—holding promise for overcoming drug resistance and improving clinical outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "43"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kexi Wang, Brianne Sturt-Gillespie, James C Hittle, et al. 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