<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Houston J</submitter><funding>National Research Foundation of Korea</funding><funding>National Institutes of Health</funding><funding>National Institute of General Medical Sciences</funding><funding>Ludwig Institute for Cancer Research</funding><funding>NIGMS NIH HHS</funding><funding>National Science Foundation</funding><pagination>2291-2299.e10</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10270731</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>33(11)</volume><pubmed_abstract>During mitosis, chromosomes assemble kinetochores to dynamically couple with spindle microtubules.&lt;sup>1&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>2&lt;/sup> Kinetochores also function as signaling hubs directing mitotic progression by recruiting and controlling the fate of the anaphase promoting complex/cyclosome (APC/C) activator CDC-20.&lt;sup>3&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>4&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>5&lt;/sup> Kinetochores either incorporate CDC-20 into checkpoint complexes that inhibit the APC/C or dephosphorylate CDC-20, which allows it to interact with and activate the APC/C.&lt;sup>4&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>6&lt;/sup> The importance of these two CDC-20 fates likely depends on the biological context. In human somatic cells, the major mechanism controlling mitotic progression is the spindle checkpoint. By contrast, progression th</pubmed_abstract><journal>Current biology : CB</journal><pubmed_title>BUB-1-bound PLK-1 directs CDC-20 kinetochore recruitment to ensure timely embryonic mitoses.</pubmed_title><pmcid>PMC10270731</pmcid><funding_grant_id>1650112</funding_grant_id><funding_grant_id>R01 GM074215</funding_grant_id><funding_grant_id>NRF-2020RC1C1008596</funding_grant_id><funding_grant_id>R35 GM144121</funding_grant_id><funding_grant_id>R01 GM074207</funding_grant_id><pubmed_authors>Kim T</pubmed_authors><pubmed_authors>Oegema K</pubmed_authors><pubmed_authors>Gomez-Cavazos JS</pubmed_authors><pubmed_authors>Deep A</pubmed_authors><pubmed_authors>Houston J</pubmed_authors><pubmed_authors>Desai A</pubmed_authors><pubmed_authors>Lara-Gonzalez P</pubmed_authors><pubmed_authors>Ohta M</pubmed_authors><pubmed_authors>Corbett KD</pubmed_authors></additional><is_claimable>false</is_claimable><name>BUB-1-bound PLK-1 directs CDC-20 kinetochore recruitment to ensure timely embryonic mitoses.</name><description>During mitosis, chromosomes assemble kinetochores to dynamically couple with spindle microtubules.&lt;sup>1&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>2&lt;/sup> Kinetochores also function as signaling hubs directing mitotic progression by recruiting and controlling the fate of the anaphase promoting complex/cyclosome (APC/C) activator CDC-20.&lt;sup>3&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>4&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>5&lt;/sup> Kinetochores either incorporate CDC-20 into checkpoint complexes that inhibit the APC/C or dephosphorylate CDC-20, which allows it to interact with and activate the APC/C.&lt;sup>4&lt;/sup>&lt;sup>,&lt;/sup>&lt;sup>6&lt;/sup> The importance of these two CDC-20 fates likely depends on the biological context. In human somatic cells, the major mechanism controlling mitotic progression is the spindle checkpoint. By contrast, progression th</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jun</publication><modification>2026-04-08T19:48:24.322Z</modification><creation>2026-04-08T14:33:07.942Z</creation></dates><accession>S-EPMC10270731</accession><cross_references><pubmed>37137308</pubmed><doi>10.1016/j.cub.2023.04.021</doi></cross_references></HashMap>