ArticlePloS one2016
CDKL5 and Shootin1 Interact and Concur in Regulating Neuronal Polarization.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 69 citations in OpenAlex.
- CDKL5 regulates the initiation of retrograde axonal transport through CLIP170-dynactin complex formation.The FEBS journal · 2026Article
- CDKL5 Deficiency Disorder: Revealing the Molecular Mechanism of Pathogenic Variants.International journal of molecular sciences · 2025Article
- Transcriptomic Profiling of Zebrafish Mutant forInternational journal of molecular sciences · 2025Article
- A cross-correction gene therapy approach for CDKL5 deficiency disorder improves the pathological phenotype of CDD patient-derived cortical organoids.Frontiers in bioengineering and biotechnology · 2025Article
- Enhanced hippocampal LTP but normal NMDA receptor and AMPA receptor function in a rat model of CDKL5 deficiency disorder.Molecular autism · 2024Article
- Article
- mGluR5 PAMs rescue cortical and behavioural defects in a mouse model of CDKL5 deficiency disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Epilepsy-Related CDKL5 Deficiency Slows Synaptic Vesicle Endocytosis in Central Nerve Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Active human full-length CDKL5 produced in the Antarctic bacterium Pseudoalteromonas haloplanktis TAC125.Microbial cell factories · 2022Article
- CDKL5 deficiency disorder: molecular insights and mechanisms of pathogenicity to fast-track therapeutic development.Biochemical Society transactions · 2022Review
- Cdkl5 mutant zebrafish shows skeletal and neuronal alterations mimicking human CDKL5 deficiency disorder.Scientific reports · 2022Article
- Neuronal Cytoskeleton in Intellectual Disability: From Systems Biology and Modeling to Therapeutic Opportunities.International journal of molecular sciences · 2021Review
- Treatment with a GSK-3β/HDAC Dual Inhibitor Restores Neuronal Survival and Maturation in an In Vitro and In Vivo Model ofInternational journal of molecular sciences · 2021Article
- Cyclin-dependent-like kinase 5 is required for pain signaling in human sensory neurons and mouse models.Science translational medicine · 2020Article
- The green tea polyphenol epigallocatechin-3-gallate (EGCG) restores CDKL5-dependent synaptic defects in vitro and in vivo.Neurobiology of disease · 2020Article
- CDKL5 deficiency predisposes neurons to cell death through the deregulation of SMAD3 signaling.Brain pathology (Zurich, Switzerland) · 2019Article
- Splicing Mutations Impairing CDKL5 Expression and Activity Can be Efficiently Rescued by U1snRNA-Based Therapy.International journal of molecular sciences · 2019Article
- Microtubules: A Key to Understand and Correct Neuronal Defects in CDKL5 Deficiency Disorder?International journal of molecular sciences · 2019Review
- Neuron-Type Specific Loss of CDKL5 Leads to Alterations in mTOR Signaling and Synaptic Markers.Molecular neurobiology · 2019Article
- Heterozygous CDKL5 Knockout Female Mice Are a Valuable Animal Model for CDKL5 Disorder.Neural plasticity · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the last years, the X-linked cyclin-dependent kinase-like 5 (CDKL5) gene has been associated with epileptic encephalopathies characterized by the early onset of intractable epilepsy, severe developmental delay, autistic features, and often the development of Rett syndrome-like features. Still, the role of CDKL5 in neuronal functions is not fully understood. By way of a yeast two hybrid screening we identified the interaction of CDKL5 with shootin1, a brain specific protein acting as a determinant of axon formation during neuronal polarization. We found evidence that CDKL5 is involved, at least in part, in regulating neuronal polarization through its interaction with shootin1. Indeed, the two proteins interact in vivo and both are localized in the distal tip of outgrowing axons. By using primary hippocampal neurons as model system we find that adequate CDKL5 levels are required for axon specification. In fact, a significant number of neurons overexpressing CDKL5 is characterized by supernumerary axons, while the silencing of CDKL5 disrupts neuronal polarization. Interestingly, shootin1 phosphorylation is reduced in neurons silenced for CDKL5 suggesting that the kinase affects, directly or indirectly, the post-translational modification of shootin1. Finally, we find that the capacity of CDKL5 to generate surplus axons is attenuated in neurons with reduced shootin1 levels, in agreement with the notion that two proteins act in a common pathway. Altogether, these results point to a role of CDKL5 in the early steps of neuronal differentiation that can be explained, at least in part, by its association with shootin1.
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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.