ArticleMolecular and cellular biology2008
Pseudosubstrate inhibition of the anaphase-promoting complex by Acm1: regulation by proteolysis and Cdc28 phosphorylation.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 47 citations in OpenAlex.
- The cytochrome P450 enzyme CYP24A1 increases proliferation of mutant KRAS-dependent lung adenocarcinoma independent of its catalytic activity.The Journal of biological chemistry · 2020Article
- The pseudosubstrate inhibitor Acm1 inhibits the anaphase-promoting complex/cyclosome by combining high-affinity activator binding with disruption of Doc1/Apc10 function.The Journal of biological chemistry · 2019Article
- A comprehensive, mechanistically detailed, and executable model of the cell division cycle in Saccharomyces cerevisiae.Nature communications · 2019Article
- APC/C: current understanding and future perspectives.F1000Research · 2019Review
- Building a Regulatory Network with Short Linear Sequence Motifs: Lessons from the Degrons of the Anaphase-Promoting Complex.Molecular cell · 2016Review
- Substrate Recognition by the Cdh1 Destruction Box Receptor Is a General Requirement for APC/CCdh1-mediated Proteolysis.The Journal of biological chemistry · 2016Article
- STUbL-mediated degradation of the transcription factor MATα2 requires degradation elements that coincide with corepressor binding sites.Molecular biology of the cell · 2015Article
- The Ubp15 deubiquitinase promotes timely entry into S phase in Saccharomyces cerevisiae.Molecular biology of the cell · 2015Article
- Degradation of Ndd1 by APC/C(Cdh1) generates a feed forward loop that times mitotic protein accumulation.Nature communications · 2015Article
- Understanding the structural basis for controlling chromosome division.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2015Review
- Spatiotemporal regulation of the anaphase-promoting complex in mitosis.Nature reviews. Molecular cell biology · 2015Review
- Functional characterization of Anaphase Promoting Complex/Cyclosome (APC/C) E3 ubiquitin ligases in tumorigenesis.Biochimica et biophysica acta · 2014Review
- Timely activation of budding yeast APCCdh1 involves degradation of its inhibitor, Acm1, by an unconventional proteolytic mechanism.PloS one · 2014Article
- Modulation of cell cycle control during oocyte-to-embryo transitions.The EMBO journal · 2013Review
- Mutually dependent degradation of Ama1p and Cdc20p terminates APC/C ubiquitin ligase activity at the completion of meiotic development in yeast.Cell division · 2013Article
- Insights into degron recognition by APC/C coactivators from the structure of an Acm1-Cdh1 complex.Molecular cell · 2013Article
- Panta rhei: the APC/C at steady state.The Journal of cell biology · 2013Review
- Structural analysis of human Cdc20 supports multisite degron recognition by APC/C.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- The checkpoint transcriptional response: make sure to turn it off once you are satisfied.Cell cycle (Georgetown, Tex.) · 2012Article
- Structure of the mitotic checkpoint complex.Nature · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The ubiquitin ligase activity of the anaphase-promoting complex (APC)/cyclosome needs to be tightly regulated for proper cell cycle progression. Substrates are recruited to the APC by the Cdc20 and Cdh1 accessory proteins. The Cdh1-APC interaction is inhibited through phosphorylation of Cdh1 by Cdc28, the major cyclin-dependent protein kinase in budding yeast. More recently, Acm1 was reported to be a Cdh1-binding and -inhibitory protein in budding yeast. We found that although Acm1 is an unstable protein and contains the KEN-box and D-box motifs typically found in APC substrates, Acm1 itself is not an APC substrate. Rather, it uses these motifs to compete with substrates for Cdh1 binding, thereby inhibiting their recruitment to the APC. Mutation of these motifs prevented Acm1-Cdh1 binding in vivo and rendered Acm1 inactive both in vitro and in vivo. Acm1 stability was critically dependent on phosphorylation by Cdc28, as Acm1 was destabilized following inhibition of Cdc28, mutation of consensus Cdc28 phosphorylation sites in Acm1, or deletion of the Bmh1 and Bmh2 phosphoprotein-binding proteins. Thus, Cdc28 serves dual roles in inhibiting Cdh1-dependent APC activity during the cell cycle: stabilization of the Cdh1 inhibitor Acm1 and direct phosphorylation of Cdh1 to prevent its association with the APC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.