ArticleThe Journal of biological chemistry2015
Synaptic synthesis, dephosphorylation, and degradation: a novel paradigm for an activity-dependent neuronal control of CDKL5.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- The CDKL5 kinase undergoes liquid-liquid phase separation driven by a serine-rich C-terminal region.Life science alliance · 2026Article
- Engineered tRNAs efficiently suppress CDKL5 premature termination codons.Scientific reports · 2024Article
- Cannabinoids and Genetic Epilepsy Models: A Review with Focus on CDKL5 Deficiency Disorder.International journal of molecular sciences · 2024Review
- Novel CDKL5 targets identified in human iPSC-derived neurons.Cellular and molecular life sciences : CMLS · 2024Article
- CDKL5 sculpts functional callosal connectivity to promote cognitive flexibility.Molecular psychiatry · 2024Article
- Cell type-specific expression, regulation and compensation of CDKL5 activity in mouse brain.Molecular psychiatry · 2024Article
- Rett and Rett-related disorders: Common mechanisms for shared symptoms?Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Activity-Dependent Phosphorylation of CDKL5 at Serine 407 Regulates Synaptogenesis and Plasticity.Neuroscience bulletin · 2023Article
- Complex CDKL5 translational regulation and its potential role in CDKL5 deficiency disorder.Frontiers in cellular neuroscience · 2023Article
- Cyclin-dependent-like kinase 5 is required for pain signaling in human sensory neurons and mouse models.Science translational medicine · 2020Article
- Cyclin-Dependent Kinase-Like 5 (CDKL5): Possible Cellular Signalling Targets and Involvement in CDKL5 Deficiency Disorder.Neural plasticity · 2020Review
- Aminoglycoside drugs induce efficient read-through ofRNA biology · 2019Article
- Microtubules: A Key to Understand and Correct Neuronal Defects in CDKL5 Deficiency Disorder?International journal of molecular sciences · 2019Review
- Altered NMDAR signaling underlies autistic-like features in mouse models of CDKL5 deficiency disorder.Nature communications · 2019Article
- Neuron-Type Specific Loss of CDKL5 Leads to Alterations in mTOR Signaling and Synaptic Markers.Molecular neurobiology · 2019Article
- Chemical genetic identification of CDKL5 substrates reveals its role in neuronal microtubule dynamics.The EMBO journal · 2018Article
- Loss of CDKL5 in Glutamatergic Neurons Disrupts Hippocampal Microcircuitry and Leads to Memory Impairment in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- CDKL5 localizes at the centrosome and midbody and is required for faithful cell division.Scientific reports · 2017Article
- Brain phosphorylation of MeCP2 at serine 164 is developmentally regulated and globally alters its chromatin association.Scientific reports · 2016Article
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the X-linked CDKL5 (cyclin-dependent kinase-like 5) gene have been associated with several forms of neurodevelopmental disorders, including atypical Rett syndrome, autism spectrum disorders, and early infantile epileptic encephalopathy. Accordingly, loss of CDKL5 in mice results in autistic-like features and impaired neuronal communication. Although the biological functions of CDKL5 remain largely unknown, recent pieces of evidence suggest that CDKL5 is involved in neuronal plasticity. Herein, we show that, at all stages of development, neuronal depolarization induces a rapid increase in CDKL5 levels, mostly mediated by extrasomatic synthesis. In young neurons, this induction is prolonged, whereas in more mature neurons, NMDA receptor stimulation induces a protein phosphatase 1-dependent dephosphorylation of CDKL5 that is mandatory for its proteasome-dependent degradation. As a corollary, neuronal activity leads to a prolonged induction of CDKL5 levels in immature neurons but to a short lasting increase of the kinase in mature neurons. Recent results demonstrate that many genes associated with autism spectrum disorders are crucial components of the activity-dependent signaling networks regulating the composition, shape, and strength of the synapse. Thus, we speculate that CDKL5 deficiency disrupts activity-dependent signaling and the consequent synapse development, maturation, and refinement.
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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.