Homozygous mutations in the abnormal spindle-like, microcephaly-associated ASPM gene are the leading cause of autosomal recessive primary microcephaly. ASPM is the putative human ortholog of the Drosophila melanogaster abnormal spindles gene (asp), which is essential for mitotic spindle function. Here, we report that downregulation of endogenous ASPM by siRNA decreases protein levels of endogenous BRCA1. ASPM localizes to the centrosome in interphase and to the spindle poles from prophase through telophase. These findings indicate that ASPM may be involved in mitotic spindle function, possibly, through regulation of BRCA1.
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