期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 290, 期 20, 页码 12585-12594出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M114.625673
关键词
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资金
- Biotechnology and Biological Sciences Research Council New Investigator Award [BB/H012869/1]
- Cancer Research UK
- BBSRC [BB/H012869/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/H012869/1] Funding Source: researchfish
In this work, we identify physical and genetic interactions that implicate E3 identified by differential display (EDD) in promoting spindle assembly checkpoint (SAC) function. During mitosis, the SAC initiates a mitotic checkpoint in response to chromosomes with kinetochores unattached to spindle pole microtubules. Similar to Budding uninhibited by benzimidazoles-related 1 (BUBR1) siRNA, a bona fide SAC component, EDD siRNA abrogated G(2)/M accumulation in response to the mitotic destabilizing agent nocodazole. Furthermore, EDD siRNA reduced mitotic cell viability and, in nocodazole-treated cells, increased expression of the promitotic progression protein cell division cycle 20 (CDC20). Copurification studies also identified physical interactions with CDC20, BUBR1, and other components of the SAC. Taken together, these observations highlight the potential role of EDD in regulating mitotic progression and the cellular response to perturbed mitosis.
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