{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7"],"submitter":["Zhou H"],"pubmed_abstract":["The spindle assembly checkpoint (SAC) arrests cells in mitosis by sensing unattached kinetochores, until all chromosomes are bi-oriented by spindle microtubules. Kinetochore accumulation of the SAC component Mad1-Mad2 is crucial for SAC activation. However, the mechanism by which Mad1-Mad2 accumulation at kinetochores is regulated is not clear. Here we find that Cep57 is localized to kinetochores in human cells, and binds to Mis12, a KMN (KNL1/Mis12 complex/Ndc80 complex) network component. Cep57 also interacts with Mad1, and depletion of Cep57 results in decreased kinetochore localization of Mad1-Mad2, reduced SAC signalling and increased chromosome segregation errors. We also show that the microtubule-binding activity of Cep57 is involved in the timely removal of Mad1 from kinetochores. "],"journal":["Nature communications"],"pagination":["10151"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4729865"],"repository":["biostudies-literature"],"pubmed_title":["Cep57 is a Mis12-interacting kinetochore protein involved in kinetochore targeting of Mad1-Mad2."],"pmcid":["PMC4729865"],"pubmed_authors":["Chen J","Wang T","Zhou H","Teng J","Zheng T"],"additional_accession":[]},"is_claimable":false,"name":"Cep57 is a Mis12-interacting kinetochore protein involved in kinetochore targeting of Mad1-Mad2.","description":"The spindle assembly checkpoint (SAC) arrests cells in mitosis by sensing unattached kinetochores, until all chromosomes are bi-oriented by spindle microtubules. Kinetochore accumulation of the SAC component Mad1-Mad2 is crucial for SAC activation. However, the mechanism by which Mad1-Mad2 accumulation at kinetochores is regulated is not clear. Here we find that Cep57 is localized to kinetochores in human cells, and binds to Mis12, a KMN (KNL1/Mis12 complex/Ndc80 complex) network component. Cep57 also interacts with Mad1, and depletion of Cep57 results in decreased kinetochore localization of Mad1-Mad2, reduced SAC signalling and increased chromosome segregation errors. We also show that the microtubule-binding activity of Cep57 is involved in the timely removal of Mad1 from kinetochores. ","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jan","modification":"2025-04-04T03:42:27.598Z","creation":"2019-03-27T02:07:43Z"},"accession":"S-EPMC4729865","cross_references":{"pubmed":["26743940"],"doi":["10.1038/ncomms10151"]}}