ArticlePloS one2015
Binding of Kif23-iso1/CHO1 to 14-3-3 is regulated by sequential phosphorylations at two LATS kinase consensus sites.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- KIF23 in disease pathogenesis and therapeutics : from molecular mechanisms to clinical translation.Cancer cell international · 2026Review
- KIF23 in disease pathogenesis and its therapeutic and diagnostic potential.Discover oncology · 2026Review
- KIF23 silencing suppresses papillary thyroid carcinoma metastasis by regulating mitophagy via Wnt/β-catenin pathway.Endocrine connections · 2025Article
- The midbody and midbody remnant: from cellular debris to signaling organelle with diagnostic and therapeutic potential.Molecular biology of the cell · 2025Review
- Knockdown of KIF23 alleviates the progression of asthma by inhibiting pyroptosis.BMJ open respiratory research · 2024Article
- SIRT7 promotes the proliferation and migration of anaplastic thyroid cancer cells by regulating the desuccinylation of KIF23.BMC cancer · 2024Article
- Article
- Identification of novel biomarkers involved in pulmonary arterial hypertension based on multiple-microarray analysis.Bioscience reports · 2020Article
- Ser/Thr kinase Trc controls neurite outgrowth ineLife · 2020Article
- Three Cdk1 sites in the kinesin-5 Cin8 catalytic domain coordinate motor localization and activity during anaphase.Cellular and molecular life sciences : CMLS · 2017Article
- Heterogeneity in sarcoma cell lines reveals enhanced motility of tetraploid versus diploid cells.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kif23 kinesin is an essential actor of cytokinesis in animals. It exists as two major isoforms, known as MKLP1 and CHO1, the longest of which, CHO1, contains two HXRXXS/T NDR/LATS kinase consensus sites. We demonstrate that these two sites are readily phosphorylated by NDR and LATS kinases in vitro, and this requires the presence of an upstream -5 histidine residue. We further show that these sites are phosphorylated in vivo and provide evidence revealing that LATS1,2 participate in the phosphorylation of the most C-terminal S814 site, present on both isoforms. This S814 phosphosite was previously reported to constitute a 14-3-3 binding site, which plays a role in Kif23 clustering during cytokinesis. Surprisingly, we found that phosphorylation of the upstream S716 NDR/LATS consensus site, present only in the longest Kif23 isoform, is required for efficient phosphorylation at S814, thus revealing sequential phosphorylation at these two sites, and differential regulation of Kif23-14-3-3 interaction for the two Kif23 isoforms. Finally, we provide evidence that Kif23 is largely unphosphorylated on S814 in post-abscission midbodies, making this Kif23 post-translational modification a potential marker to probe these structures.
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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.