Role of Hec1 in Spindle Checkpoint Signaling and Kinetochore Recruitment of Mad1/Mad2
摘要：
The spindle checkpoint delays sister chromatid separation until all chromosomes have undergone bipolar spindle attachment. Checkpoint failure may result in chromosome mis-segregation and may contribute to tumorigenesis. We showed that the human protein Hec1 was required for the recruitment of Mps1 kinase and Mad1/Mad2 complexes to kinetochores. Depletion of Hec1 impaired chromosome congression and caused persistent activation of the spindle checkpoint, indicating that high steady-state levels of Mad1/Mad2 complexes at kinetochores were not essential for checkpoint signaling. Simultaneous depletion of Hec1 and Mad2 caused catastrophic mitotic exit, making Hec1 an attractive target for the selective elimination of spindle checkpoint-deficient cells.
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关键词：
Humans Microtubules Mitotic Spindle Apparatus Hela Cells Chromosomes, Human Kinetochores Calcium-Binding Proteins Repressor Proteins RNA, Small Interfering Protein Kinases
DOI：
10.1126/science.1075596
被引量：
年份：
2002
掌桥科研
万方医学
NCBI
Europe PMC
Oxford Univ Press
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