Abstract
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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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BRCA1 Protein / biosynthesis*
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Cell Line
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Cell Line, Tumor
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Centrosome / metabolism
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Centrosome / ultrastructure*
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DNA / chemistry
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Drosophila melanogaster
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Fluorescent Antibody Technique, Indirect
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Humans
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Immunoblotting
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Microscopy, Fluorescence
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Mutation
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Nerve Tissue Proteins / metabolism
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Nerve Tissue Proteins / physiology*
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Prophase
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RNA, Small Interfering / metabolism
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Spindle Apparatus / metabolism
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Telophase
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Transfection
Substances
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ASPM protein, human
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BRCA1 Protein
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Nerve Tissue Proteins
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RNA, Small Interfering
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DNA