ArticleThe EMBO journal2010
Phosphorylation of CLIP-170 by Plk1 and CK2 promotes timely formation of kinetochore-microtubule attachments.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 96 citations in OpenAlex.
- Bora, CEP192 and Cenexin regulate distinct Plk1-dependent cell and centrosome cycle transitions.Nature communications · 2026Article
- Switching off CK2-mediated activation of survivin offers new therapeutic opportunities in neuroblastoma.Experimental & molecular medicine · 2026Article
- CDKL5 regulates the initiation of retrograde axonal transport through CLIP170-dynactin complex formation.The FEBS journal · 2026Article
- High-throughput virtual screening, identification andJournal of enzyme inhibition and medicinal chemistry · 2025Article
- Article
- KIF2C condensation concentrates PLK1 and phosphorylated BRCA2 on kinetochore microtubules in mitosis.Nucleic acids research · 2025Article
- Multi-Omic Evaluation of PLK1 Inhibitor-Onvansertib-In Colorectal Cancer Spheroids.Journal of mass spectrometry : JMS · 2025Article
- Elevating PLK1 overcomes BETi resistance in prostate cancer via triggering BRD4 phosphorylation-dependent degradation in mitosis.Cell reports · 2024Article
- PLK1: A Promising Therapeutic Target for Prostate Cancer Treatment.Serican journal of medicine · 2024Article
- Review
- Diptoindonesin G antagonizes AR signaling and enhances the efficacy of antiandrogen therapy in prostate cancer.The Prostate · 2022Article
- Recent Progress on the Localization of PLK1 to the Kinetochore and Its Role in Mitosis.International journal of molecular sciences · 2022Review
- Mitotic protein kinase-driven crosstalk of machineries for mitosis and metastasis.Experimental & molecular medicine · 2022Review
- The Role of Mitotic Kinases and the RZZ Complex in Kinetochore-Microtubule Attachments: Doing the Right Link.Frontiers in cell and developmental biology · 2022Review
- A dimerization-dependent mechanism regulates enzymatic activation and nuclear entry of PLK1.Oncogene · 2022Article
- CK2-mediated phosphorylation of Che-1/AATF is required for its pro-proliferative activity.Journal of experimental & clinical cancer research : CR · 2021Article
- Review
- Cell-cycle phospho-regulation of the kinetochore.Current genetics · 2021Review
- Phospho-regulation of mitotic spindle assembly.Cytoskeleton (Hoboken, N.J.) · 2020Review
- The CINs of Polo-Like Kinase 1 in Cancer.Cancers · 2020Review
5 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
7 authors at 3 institutions in 1 country.
Funding
Abstract
CLIP-170 is implicated in the formation of kinetochore-microtubule attachments through direct interaction with the dynein/dynactin complex. However, whether this important function of CLIP-170 is regulated by phosphorylation is unknown. Herein, we have identified polo-like kinase 1 (Plk1) and casein kinase 2 (CK2) as two kinases of CLIP-170 and mapped S195 and S1318 as their respective phosphorylation sites. We showed that a CK2 unphosphorylatable mutant lost its ability to bind to dynactin and to localize to kinetochores during prometaphase, indicating that the CK2 phosphorylation of CLIP-170 is involved in its dynactin-mediated kinetochore localization. Furthermore, we provide evidence that Plk1 phosphorylation of CLIP-170 at S195 enhances its association with CK2. Finally, we detected defects in the formation of kinetochore fibres in cells expressing the CLIP-S195A and -S1318A, but not the CLIP-S195E and -S1318D, confirming that Plk1- and CK2-associated phosphorylations of CLIP-170 are involved in the timely formation of kinetochore-microtubule attachments in mitosis.
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.