<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Novak B</submitter><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>2780-2785.e2</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9616797</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>32(12)</volume><pubmed_abstract>In 1996, Kim Nasmyth&lt;sup>1&lt;/sup> proposed that the eukaryotic cell cycle is an alternating sequence of transitions from G&lt;sub>1&lt;/sub> to S-G&lt;sub>2&lt;/sub>-M and back again. These two phases correlate to high activity of cyclin-dependent kinases (CDKs) that trigger S-G&lt;sub>2&lt;/sub>-M events and CDK antagonists that stabilize G&lt;sub>1&lt;/sub> phase. We associated these "alternative phases" with the coexistence of two stable steady states of the biochemical reactions among CDKs and their antagonists.&lt;sup>2&lt;/sup>&lt;sup&gt;,&lt;/sup>&lt;sup>3&lt;/sup> Transitions between these steady states (G&lt;sub>1&lt;/sub>-to-S and M-to-G&lt;sub>1&lt;/sub>) are driven by "helper" proteins. The fact that the transitions are irreversible is guaranteed by a "latching" property of the molecular switches, as we have argued in previous publica</pubmed_abstract><journal>Current biology : CB</journal><pubmed_title>Mitotic kinase oscillation governs the latching of cell cycle switches.</pubmed_title><pmcid>PMC9616797</pmcid><funding_grant_id>BB/M00354X/1</funding_grant_id><pubmed_authors>Tyson JJ</pubmed_authors><pubmed_authors>Novak B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mitotic kinase oscillation governs the latching of cell cycle switches.</name><description>In 1996, Kim Nasmyth&lt;sup>1&lt;/sup> proposed that the eukaryotic cell cycle is an alternating sequence of transitions from G&lt;sub>1&lt;/sub> to S-G&lt;sub>2&lt;/sub>-M and back again. These two phases correlate to high activity of cyclin-dependent kinases (CDKs) that trigger S-G&lt;sub>2&lt;/sub>-M events and CDK antagonists that stabilize G&lt;sub>1&lt;/sub> phase. We associated these "alternative phases" with the coexistence of two stable steady states of the biochemical reactions among CDKs and their antagonists.&lt;sup>2&lt;/sup>&lt;sup&gt;,&lt;/sup>&lt;sup>3&lt;/sup> Transitions between these steady states (G&lt;sub>1&lt;/sub>-to-S and M-to-G&lt;sub>1&lt;/sub>) are driven by "helper" proteins. The fact that the transitions are irreversible is guaranteed by a "latching" property of the molecular switches, as we have argued in previous publica</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-19T04:20:19.932Z</modification><creation>2025-04-19T04:20:19.932Z</creation></dates><accession>S-EPMC9616797</accession><cross_references><pubmed>35504285</pubmed><doi>10.1016/j.cub.2022.04.016</doi></cross_references></HashMap>