期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 489, 期 4, 页码 497-502出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2017.05.180
关键词
MCM7; Cep68; Centrosome splitting; Proteasomal degradation; Ubiquitination
资金
- National Natural Science Foundation of China [31071182, 31271522]
- University of Chinese Academy of Sciences [095102GN00, Y15102GN00]
- Beijing Natural Science Foundation [5152020]
We have recently reported that Rootletin prevents Cep68 from VHL-mediated proteasomal degradation to maintain centrosome cohesion, unveiling the first underlying mechanism of a linker protein required for maintenance of centrosome cohesion. The minichromosome maintenance (MCM) proteins 2-7 have long been noticed to localize to centrosomes, but their functions at the centrosome are presently unknown. Here, we show that MCM7 directly binds to the centrosomal linker protein Cep68 in vitro and complexes with Cep68 and VHL in vivo. Absence of MCM7 weakened the interaction between Cep68 and VHL, whereas MCM7 overexpression facilitated the Cep68-VHL association. As a result of MCM7 over expression, Cep68 was targeted for ubiquitination and proteasomal degradation, thereby rendering centrosome splitting. We propose that Cep68 protein level needs to be fine-tuned in order to ensure that its direct interactors, such as the microcephaly protein Cep215 and PCNT, function properly. (C) 2017 Elsevier Inc. All rights reserved.
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