{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMCM10 serves as a pivotal factor in the initiation of DNA replication by acting as a molecular bridge between the MCM2‐7 helicase and the DNA polymerase α–primase complex. It is recruited to chromatin following pre‐replicative complex assembly, where it enables the proper loading of essential factors (such as And-1/Ctf4 and Cdc45) to facilitate origin unwinding and the assembly of the pre-initiation complex. In addition, high-resolution structural analyses have revealed that MCM10 adopts a ring-shaped architecture that provides a docking surface for replication proteins, thereby ensuring the accurate firing of replication origins."}, {"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": "\nBeyond its initiation role, MCM10 is indispensable for replication elongation and fork stability. It directly interacts with the catalytic subunit of DNA polymerase α—thereby safeguarding its stability—and binds single-stranded DNA via its oligonucleotide/oligosaccharide-binding (OB) fold. MCM10’s activities are finely tuned by post-translational modifications: for instance, SIRT1-mediated deacetylation modulates its DNA-binding properties, while stress signals (such as UV exposure or HIV-1 Vpr action) trigger its proteasomal degradation. Its functional interplay with other replication proteins such as RECQL4 and its regulation by cell cycle–dependent kinases and transcription factors (e.g., E2Fs) further underscore its role as an oligomeric scaffold coordinating the activation and progression phases of DNA replication; failure in MCM10 function elicits checkpoint activation and genomic instability."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "17"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAberrant expression or mutation of MCM10 is increasingly recognized as a contributor to human disease, especially in cancer and developmental disorders. Overexpression of MCM10 is correlated with aggressive tumor behavior and poor clinical outcomes in various malignancies—including urothelial carcinoma, lung adenocarcinoma, glioblastoma, breast, and prostate cancers—supporting its potential utility as a prognostic marker and therapeutic target. In addition, bi-allelic variants in MCM10 have been linked to immunodeficiency syndromes and restrictive cardiomyopathy, highlighting the critical balance MCM10 maintains in preserving genome integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "29"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "James A Wohlschlegel, Suman K Dhar, Tatyana A Prokhorova, et al. 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