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Abstract Background: Down syndrome (DS, trisomy 21) is the most prevalent human autosomal aneuploidy, driven by non-disjunction of chromosome 21 during maternal gametogenesis. Centromere-kinetochore complexes mediate accurate chromosome segregation, and centromeric protein dysregulation is linked to chromosome instability; nevertheless, how perturbations of centromere-proximal proteins drive cellular pathogenesis in DS remain poorly defined.
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