ArticleeLife2015
STIL binding to Polo-box 3 of PLK4 regulates centriole duplication.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
83 citing papers in PubMed, 132 citations in OpenAlex.
- Ana1/Cep295 regulates centriole elongation via Cep135 and microtubules.The Journal of cell biology · 2026Article
- Design, Synthesis, and Biological Activity Evaluation of Quinazoline-Based PLK4 Inhibitors.Biomedicines · 2026Article
- Discovery of novel dual-targeting inhibitors against PLK1-PBD and PLK4-PB3: structure-guided pharmacophore modelling, virtual screening, molecular docking, molecular dynamics simulation, and biological evaluation.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- PLK4: Master Regulator of Centriole Duplication and Its Therapeutic Potential.Cytoskeleton (Hoboken, N.J.) · 2025Review
- PLK4 Inhibition as a Strategy to Enhance Non-Small Cell Lung Cancer Radiosensitivity.Molecular cancer therapeutics · 2025Article
- The A-C linker controls centriole structural integrity and duplication.Nature communications · 2025Article
- Review
- STIL Overexpression Is Associated with Chromosomal Numerical Abnormalities in Non-Small-Cell Lung Carcinoma Through Centrosome Amplification.Current oncology (Toronto, Ont.) · 2024Article
- Article
- The kinase ZYG-1 phosphorylates the cartwheel protein SAS-5 to drive centriole assembly in C. elegans.EMBO reports · 2024Article
- Generating CRISPR-edited clonal lines of culturedBiology methods & protocols · 2024Article
- Centrosomal organization of Cep152 provides flexibility in Plk4 and procentriole positioning.The Journal of cell biology · 2023Article
- Proteomic profiling of centrosomes across multiple mammalian cell and tissue types by an affinity capture method.Developmental cell · 2023Article
- Towards understanding centriole elimination.Open biology · 2023Review
- A simple Turing reaction-diffusion model explains how PLK4 breaks symmetry during centriole duplication and assembly.PLoS biology · 2023Article
- Molecular Mechanism of STIL Coiled-Coil Domain Oligomerization.International journal of molecular sciences · 2023Article
- Plasmodium falciparum infection of human erythroblasts induces transcriptional changes associated with dyserythropoiesis.Blood advances · 2023Article
- Polo-like kinase 4 homodimerization and condensate formation regulate its own protein levels but are not required for centriole assembly.Molecular biology of the cell · 2023Article
- Disulfide-Bond-Induced Structural Frustration and Dynamic Disorder in a Peroxiredoxin from MAS NMR.Journal of the American Chemical Society · 2023Article
- Appearing and disappearing acts of cilia.Journal of biosciences · 2023Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polo-like kinases (PLK) are eukaryotic regulators of cell cycle progression, mitosis and cytokinesis; PLK4 is a master regulator of centriole duplication. Here, we demonstrate that the SCL/TAL1 interrupting locus (STIL) protein interacts via its coiled-coil region (STIL-CC) with PLK4 in vivo. STIL-CC is the first identified interaction partner of Polo-box 3 (PB3) of PLK4 and also uses a secondary interaction site in the PLK4 L1 region. Structure determination of free PLK4-PB3 and its STIL-CC complex via NMR and crystallography reveals a novel mode of Polo-box-peptide interaction mimicking coiled-coil formation. In vivo analysis of structure-guided STIL mutants reveals distinct binding modes to PLK4-PB3 and L1, as well as interplay of STIL oligomerization with PLK4 binding. We suggest that the STIL-CC/PLK4 interaction mediates PLK4 activation as well as stabilization of centriolar PLK4 and plays a key role in centriole duplication.
Indexed as
Identifiers
What OpenQuestion holds
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.