ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Aberrant calcium/calmodulin-dependent protein kinase II (CaMKII) activity is associated with abnormal dendritic spine morphology in the ATRX mutant mouse brain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 70 citations in OpenAlex.
- ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025Review
- Aberrant extracellular dopamine clearance in the prefrontal cortex exhibits ADHD-like behavior in NCX3 heterozygous mice.The FEBS journal · 2025Article
- A new mouse model of ATR-X syndrome carrying a common patient mutation exhibits neurological and morphological defects.Human molecular genetics · 2023Article
- Epigenetic genes and epilepsy - emerging mechanisms and clinical applications.Nature reviews. Neurology · 2022Review
- Comparison of Golgi-Cox and Intracellular Loading of Lucifer Yellow for Dendritic Spine Density and Morphology Analysis in the Mouse Brain.Neuroscience · 2022Article
- The regulatory role of endoplasmic reticulum chaperone proteins in neurodevelopment.Frontiers in neuroscience · 2022Review
- Modulation of dendritic spines by protein phosphatase-1.Advances in pharmacology (San Diego, Calif.) · 2021Review
- Atrx Deletion in Neurons Leads to Sexually Dimorphic Dysregulation of miR-137 and Spatial Learning and Memory Deficits.Cell reports · 2020Article
- SAK3 Administration Improves Spine Abnormalities and Cognitive Deficits in AppInternational journal of molecular sciences · 2020Article
- TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020Review
- Neurodevelopmental Disorders Caused by Defective Chromatin Remodeling: Phenotypic Complexity Is Highlighted by a Review of ATRX Function.Frontiers in genetics · 2020Review
- Perspectives for Applying G-Quadruplex Structures in Neurobiology and Neuropharmacology.International journal of molecular sciences · 2019Review
- Glial ensheathment of the somatodendritic compartment regulates sensory neuron structure and activity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- SA4503, A Potent Sigma-1 Receptor Ligand, Ameliorates Synaptic Abnormalities and Cognitive Dysfunction in a Mouse Model of ATR-X Syndrome.International journal of molecular sciences · 2018Article
- Ketamine Self-Administration Elevates αCaMKII Autophosphorylation in Mood and Reward-Related Brain Regions in Rats.Molecular neurobiology · 2018Article
- Targeting G-quadruplex DNA as cognitive function therapy for ATR-X syndrome.Nature medicine · 2018Article
- Physiological and Pathological Roles of CaMKII-PP1 Signaling in the Brain.International journal of molecular sciences · 2017Review
- Endocytosis following dopamine DMolecular psychiatry · 2017Article
- Kalirin is required for BDNF-TrkB stimulated neurite outgrowth and branching.Neuropharmacology · 2016Article
- Caloric restriction improves diabetes-induced cognitive deficits by attenuating neurogranin-associated calcium signaling in high-fat diet-fed mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In humans, mutations in the gene encoding ATRX, a chromatin remodeling protein of the sucrose-nonfermenting 2 family, cause several mental retardation disorders, including α-thalassemia X-linked mental retardation syndrome. We generated ATRX mutant mice lacking exon 2 (ATRX(ΔE2) mice), a mutation that mimics exon 2 mutations seen in human patients and associated with milder forms of retardation. ATRX(ΔE2) mice exhibited abnormal dendritic spine formation in the medial prefrontal cortex (mPFC). Consistent with other mouse models of mental retardation, ATRX(ΔE2) mice exhibited longer and thinner dendritic spines compared with wild-type mice without changes in spine number. Interestingly, aberrant increased calcium/calmodulin-dependent protein kinase II (CaMKII) activity was observed in the mPFC of ATRX(ΔE2) mice. Increased CaMKII autophosphorylation and activity were associated with increased phosphorylation of the Rac1-guanine nucleotide exchange factors (GEFs) T-cell lymphoma invasion and metastasis 1 (Tiam1) and kalirin-7, known substrates of CaMKII. We confirmed increased phosphorylation of p21-activated kinases (PAKs) in mPFC extracts. Furthermore, reduced protein expression and activity of protein phosphatase 1 (PP1) was evident in the mPFC of ATRX(ΔE2) mice. In cultured cortical neurons, PP1 inhibition by okadaic acid increased CaMKII-dependent Tiam1 and kalirin-7 phosphorylation. Together, our data strongly suggest that aberrant CaMKII activation likely mediates abnormal spine formation in the mPFC. Such morphological changes plus elevated Rac1-GEF/PAK signaling seen in ATRX(ΔE2) mice may contribute to mental retardation syndromes seen in human patients.
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