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The Phosphatase Cdc14 Triggers Mitotic Exit by Reversal of Cdk-Dependent Phosphorylation

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TLDR
This work shows that the Cdc14 phosphatase triggers mitotic exit by three parallel mechanisms, each of which inhibits Cdk activity, and induces degradation of mitotic cyclins.
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This article is published in Molecular Cell.The article was published on 1998-12-01 and is currently open access. It has received 780 citations till now. The article focuses on the topics: Mitotic exit & Polo-like kinase.

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Citations
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Rux is a cyclin-dependent kinase inhibitor (CKI) specific for mitotic cyclin–Cdk complexes

TL;DR: This is the first description in a multicellular organism of a CKI that specifically inhibits mitotic cyclin-Cdk complexes and the stimulating effect of Rux might assist in any S-phase function of CycA-C DK1.
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Bfa1 can regulate Tem1 function independently of Bub2 in the mitotic exit network of Saccharomyces cerevisiae

TL;DR: It is demonstrated that introduction of bfa1Δ suppresses the growth defects associated with the cdc5–1 mutation significantly better than that of bub2Δ, suggesting that Bfa1 may have a previously uncharacterized role in this pathway.
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Assembling the spindle midzone in the right place at the right time.

TL;DR: In budding yeast the conserved phosphatase Cdc14, activated in early anaphase, regulates the formation of the spindle midzone, and the identification of Ase1 as a key CDC14 substrate elucidates how spindleMidzone assembly is coordinated with the metaphase toAnaphase transition.
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Thinking within the D box: initial identification of Cdh1-APC substrates in the nervous system.

TL;DR: These findings may offer a glimpse of the wide spectrum of neural activities that are orchestrated by Cdh1-APC, the anaphase-promoting complex that has a well-established role in cell cycle control.
References
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Cyclin-dependent kinases: engines, clocks, and microprocessors.

TL;DR: This work has shown that Cdk activity is governed by a complex network of regulatory subunits and phosphorylation events whose precise effects on Cdk conformation have been revealed by recent crystallographic studies.
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SKP1 connects cell cycle regulators to the ubiquitin proteolysis machinery through a novel motif, the F-box.

TL;DR: Different skp1 mutants arrest cells in either G1 or G2, suggesting a connection between regulation of proteolysis in different stages of the cycle.
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How proteolysis drives the cell cycle

TL;DR: Proteolysis drives cell cycle progression not only by regulating CDK activity, but by directly influencing chromosome and spindle dynamics, and also how proteolysis may directly trigger the transition from metaphase to anaphase.
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F-Box Proteins Are Receptors that Recruit Phosphorylated Substrates to the SCF Ubiquitin-Ligase Complex

TL;DR: The ubiquitination pathway for the Cdk inhibitor Sic1 is reconstituted using recombinant proteins and the constituents of the SCF complex are members of protein families, likely to serve as the prototype for a large class of E3s formed by combinatorial interactions of related family members.
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The Saccharomyces cerevisiae Cell Cycle

TL;DR: The bibliography is intended more as a guide to the literature than as a historically accurate record of the development of the field; the authors apologize to the earlier workers whose contributions thus get less explicit credit than they deserve.
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