ArticleScientific reports2017
CDKL5 localizes at the centrosome and midbody and is required for faithful cell division.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Variable expression ofProceedings of the National Academy of Sciences of the United States of America · 2024Pooled it
- The CDKL5 kinase undergoes liquid-liquid phase separation driven by a serine-rich C-terminal region.Life science alliance · 2026Article
- Phosphofurin Acidic Cluster Sorting Protein 2 Alleviates Kidney Fibrosis by Inhibiting Tubular Epithelial Cell G2/M Arrest through Cyclin-Dependent Kinase-Like 1.Journal of the American Society of Nephrology : JASN · 2026Article
- The midbody and midbody remnant: from cellular debris to signaling organelle with diagnostic and therapeutic potential.Molecular biology of the cell · 2025Review
- Novel CDKL5 targets identified in human iPSC-derived neurons.Cellular and molecular life sciences : CMLS · 2024Article
- Rett and Rett-related disorders: Common mechanisms for shared symptoms?Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Research progress on the pathogenesis of CDKL5 pathogenic variants and related encephalopathy.European journal of pediatrics · 2023Review
- HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Discovery of a Potent and Selective CDKL5/GSK3 Chemical Probe That Is Neuroprotective.ACS chemical neuroscience · 2023Article
- A Potent and Selective CDKL5/GSK3 Chemical Probe is Neuroprotective.bioRxiv : the preprint server for biology · 2023Article
- Complex CDKL5 translational regulation and its potential role in CDKL5 deficiency disorder.Frontiers in cellular neuroscience · 2023Article
- Primary Cilia Dysfunction in Neurodevelopmental Disorders beyond Ciliopathies.Journal of developmental biology · 2022Review
- CDKL5 deficiency disorder: molecular insights and mechanisms of pathogenicity to fast-track therapeutic development.Biochemical Society transactions · 2022Review
- Phenotypic characterization of Cdkl5-knockdown neurons establishes elongated cilia as a functional assay for CDKL5 Deficiency Disorder.Neuroscience research · 2022Article
- Increased DNA Damage and Apoptosis in CDKL5-Deficient Neurons.Molecular neurobiology · 2020Article
- An Alternative Splice Variant of HIPK2 with Intron Retention Contributes to Cytokinesis.Cells · 2020Article
- CDKL5 promotes proliferation, migration, and chemotherapeutic drug resistance of glioma cells via activation of the PI3K/AKT signaling pathway.FEBS open bio · 2020Article
- Cyclin-Dependent Kinase-Like 5 (CDKL5): Possible Cellular Signalling Targets and Involvement in CDKL5 Deficiency Disorder.Neural plasticity · 2020Review
- Microtubules: A Key to Understand and Correct Neuronal Defects in CDKL5 Deficiency Disorder?International journal of molecular sciences · 2019Review
- ESCRT-III is necessary for the integrity of the nuclear envelope in micronuclei but is aberrant at ruptured micronuclear envelopes generating damage.Oncogenesis · 2019Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cyclin-dependent kinase-like 5 (CDKL5) gene has been associated with rare neurodevelopmental disorders characterized by the early onset of seizures and intellectual disability. The CDKL5 protein is widely expressed in most tissues and cells with both nuclear and cytoplasmic localization. In post-mitotic neurons CDKL5 is mainly involved in dendritic arborization, axon outgrowth, and spine formation while in proliferating cells its function is still largely unknown. Here, we report that CDKL5 localizes at the centrosome and at the midbody in proliferating cells. Acute inactivation of CDKL5 by RNA interference (RNAi) leads to multipolar spindle formation, cytokinesis failure and centrosome accumulation. At the molecular level, we observed that, among the several midbody components we analyzed, midbodies of CDKL5-depleted cells were devoid of HIPK2 and its cytokinesis target, the extrachromosomal histone H2B phosphorylated at S14. Of relevance, expression of the phosphomimetic mutant H2B-S14D, which is capable of overcoming cytokinesis failure in HIPK2-defective cells, was sufficient to rescue spindle multipolarity in CDKL5-depleted cells. Taken together, these results highlight a hitherto unknown role of CDKL5 in regulating faithful cell division by guaranteeing proper HIPK2/H2B functions at the midbody.
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