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.About:
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.read more
Citations
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Journal ArticleDOI
The regulation of Net1/Cdc14 by the Hog1 MAPK upon osmostress unravels a new mechanism regulating mitosis
TL;DR: The latest findings related to the SAPK-driven regulation of mitosis upon osmostress in yeast are discussed.
Journal ArticleDOI
What is your assay for sister-chromatid cohesion?
TL;DR: The ability to take advantage of what Tubingen had to offer largely depended on the German university system's commitment to free education, and the course was designed for 6 years, leading to a Diploma in Biochemistry and Physiological Chemistry.
Dissertation
Control of Cardiomyocyte Proliferation by p53/MDM2-Regulated microRNAs
TL;DR: Comparing miRNA expression profiles from cardiac specific p53/MDM2 double knockout mouse hearts and wild type controls revealed 11 miRNAs that were downregulated in the "proliferative" DKO hearts and enriched for mRNA targets involved in cell cycle regulation.
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Mechanism of Regulation of Intrachromatid Recombination and Long-Range Chromosome Interactions in Saccharomyces cerevisiae.
Shamsu Zaman,Malay Choudhury,James C. Jiang,Pankaj Srivastava,Bidyut K. Mohanty,Christopher Danielson,Sean J. Humphrey,S. Michal Jazwinski,Deepak Bastia +8 more
TL;DR: This work provides new mechanistic insights into the regulation of rDNA silencing and intrachromatid recombination by showing that Sir2 recruitment is stringently regulated by Fob1 phosphorylation at specific sites in its C-terminal domain (C-Fob1), which also regulates long-range Ter-Ter interactions.
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Mitotic Expression of Spo13 Alters M-Phase Progression and Nucleolar Localization of Cdc14 in Budding Yeast
Elisa Varela,Ulrich Schlecht,Anca Moina,James D. Fackenthal,Brian K. Washburn,Christa Niederhauser-Wiederkehr,Monika Tsai-Pflugfelder,Michael Primig,Susan M. Gasser,Rochelle Easton Esposito +9 more
TL;DR: Spo13 is a key meiosis-specific regulator required for centromere cohesion and coorientation, and for progression through two nuclear divisions, and it has been shown that it can cause a G2/M arrest and may delay the transition from late anaphase to G1, when overexpressed in mitosis.
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.