ArticleThe EMBO journal2021
A new linear cyclin docking motif that mediates exclusively S-phase CDK-specific signaling.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Direct Mapping of CDK2 Substrates in Embryonic Stem Cells Uncovers an AP-Site Repair Mechanism via HMCES Phosphorylation.bioRxiv : the preprint server for biology · 2026Article
- Decoding Cdk1 control: from mitotic thresholds to meiotic specificity.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026Review
- Article
- High-throughput investigation of cyclin docking interactions reveals the complexity of motif binding determinants.Nature communications · 2025Article
- Statistical analysis of sequential motifs at biologically relevant protein-protein interfaces.Computational and structural biotechnology journal · 2024Article
- CDK activity at the centrosome regulates the cell cycle.Cell reports · 2024Article
- CDK signaling via nonconventional CDK phosphorylation sites.Molecular biology of the cell · 2023Review
- Tceal7 Regulates Skeletal Muscle Development through Its Interaction with Cdk1.International journal of molecular sciences · 2023Article
- Emerging approaches to CDK inhibitor development, a structural perspective.RSC chemical biology · 2023Article
- Proteome-wide screening for mitogen-activated protein kinase docking motifs and interactors.Science signaling · 2023Article
- Condensed-phase signaling can expand kinase specificity and respond to macromolecular crowding.Molecular cell · 2022Article
- A synthetic biology approach reveals diverse and dynamic CDK response profiles via multisite phosphorylation of NLS-NES modules.Science advances · 2022Article
- Systematic Discovery of FBXW7-Binding Phosphodegrons Highlights Mitogen-Activated Protein Kinases as Important Regulators of Intracellular Protein Levels.International journal of molecular sciences · 2022Article
- Article
- Orchestrating serine/threonine phosphorylation and elucidating downstream effects by short linear motifs.The Biochemical journal · 2022Review
- The Eukaryotic Linear Motif resource: 2022 release.Nucleic acids research · 2022Article
- Bipartite binding of the N terminus of Skp2 to cyclin A.Structure (London, England : 1993) · 2021Article
- Docking to a Basic Helix Promotes Specific Phosphorylation by G1-Cdk1.International journal of molecular sciences · 2021Article
- Article
- Budding yeast relies on GScience advances · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cyclin-dependent kinases (CDKs), the master regulators of cell division, are activated by different cyclins at different cell cycle stages. In addition to being activators of CDKs, cyclins recognize various linear motifs to target CDK activity to specific proteins. We uncovered a cyclin docking motif, NLxxxL, that contributes to phosphorylation-dependent degradation of the CDK inhibitor Far1 at the G1/S stage in the yeast Saccharomyces cerevisiae. This motif is recognized exclusively by S-phase CDK (S-CDK) Clb5/6-Cdc28 and is considerably more potent than the conventional RxL docking motif. The NLxxxL and RxL motifs were found to overlap in some target proteins, suggesting that cyclin docking motifs can evolve to switch from one to another for fine-tuning of cell cycle events. Using time-lapse fluorescence microscopy, we show how different docking connections temporally control phosphorylation-driven target degradation. This also revealed a differential function of the phosphoadaptor protein Cks1, as Cks1 docking potentiated degron phosphorylation of RxL-containing but not of NLxxxL-containing substrates. The NLxxxL motif was found to govern S-cyclin-specificity in multiple yeast CDK targets including Fin1, Lif1, and Slx4, suggesting its wider importance.
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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.