期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 104, 期 8, 页码 2691-2696出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0611132104
关键词
aneuploidy; cell cycle; genomic stability
Numerical and/or structural centrosome abnormalities have been correlated with most solid tumors and hematological malignancies. Tumorigenesis also is linked to defects in the mitotic or spindle assembly checkpoint, a key control mechanism that ensures accurate segregation of chromosomes during mitosis. We have reported that targeted disruption of the Dido gene causes a transplantable myeloclysplastic/myeloproliferative disease in mice. Here, we report that Dido3, the largest splice variant of the Dido gene, is a centrosome-associated protein whose disruption leads to supernumerary centrosomes, failure to maintain cellular mitotic arrest, and early degradation of the mitotic checkpoint protein BubR1. These aberrations result in enhanced aneuploidy in the Dido mutant cells. Dido gene malfunction thus is reported to be part of an impaired signaling cascade that results in a defective mitotic checkpoint, leading to chromosome instability.
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