{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMinichromosome maintenance protein 8 (MCM8) plays a critical role in governing female reproductive health. Multiple genetic studies have linked common variants and rare pathogenic mutations in MCM8 with alterations in ovarian reserve, age at natural menopause, and primary ovarian insufficiency. In affected individuals and model organisms, loss‐of‐function mutations in MCM8 lead to primary amenorrhea, hypergonadotropic hypogonadism, and sterility, highlighting its essential role in maintaining genomic stability within the germline. These findings suggest that MCM8 is a key modulator of follicle number and ovarian aging, thereby influencing female fertility and endocrine function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its reproductive role, MCM8 is integral to DNA replication and repair. Biochemical and cell‐based studies demonstrate that MCM8 localizes to early G1 chromatin, where it interacts with key replication factors such as CDC6 and components of the pre–replication complex. MCM8 also partners with its paralog MCM9 to form a complex that is rapidly recruited to sites of DNA damage; this facilitates homologous recombination repair through the efficient loading of RAD51 and the resumption of stalled replication forks. Structural and functional analyses further indicate that MCM8, as an active ATP‐dependent helicase, contributes to both replication initiation and the maintenance of genomic integrity during S phase."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond reproduction and genome replication, aberrant expression and dysregulation of MCM8 have been implicated in oncogenesis. Elevated MCM8 levels are observed in a variety of malignancies—including lung, gastric, colorectal, glioblastoma, and chronic myelogenous leukemia—where they are associated with aggressive tumor phenotypes, enhanced cell cycle progression, and resistance to DNA–damaging agents. 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