ArticleMolecular psychiatry2012
Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency.
Article in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 108 citations in OpenAlex.
- 14-3-3 proteins: Regulators of cardiac excitation-contraction coupling and stress responses.The Journal of physiology · 2026Review
- 14-3-3ε inhibits premature centriole disengagement by inhibiting the activity of Plk1 and separase.Journal of cell science · 2025Article
- Modular-Based Synergetic Mechanisms of Jasminoidin and Ursodeoxycholic Acid in Cerebral Ischemia Therapy.Biomedicines · 2025Article
- Characterization of multiple binding sites on microtubule associated protein 2c recognized by dimeric and monomeric 14-3-3ζ.The FEBS journal · 2025Article
- Extracellular vesicle signatures from eye lavage as novel non-invasive biomarkers for hypoxic ischaemic insult-findings from a neonatal mouse model.Frontiers in medical technology · 2025Article
- Redundant and Distinct Roles of Two 14-3-3 Proteins inJournal of fungi (Basel, Switzerland) · 2024Article
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- Differential Expression of Proteins Associated with Bipolar Disorder as Identified Using the PeptideShaker Software.International journal of molecular sciences · 2023Article
- YWHAZ variation causes intellectual disability and global developmental delay with brain malformation.Human molecular genetics · 2023Article
- Deficiency of the ywhaz gene, involved in neurodevelopmental disorders, alters brain activity and behaviour in zebrafish.Molecular psychiatry · 2022Article
- Rho-Rho-Kinase Regulates Ras-ERK Signaling Through SynGAP1 for Dendritic Spine Morphology.Neurochemical research · 2022Article
- Hydrophobic cavity-directed azide-acetyllysine photochemistry for profiling non-histone interacting partners of bromodomain protein 1.RSC chemical biology · 2022Article
- 14-3-3 protein regulation of excitation-contraction coupling.Pflugers Archiv : European journal of physiology · 2022Review
- The 14-3-3 Protein Family and Schizophrenia.Frontiers in molecular neuroscience · 2022Review
- 14-3-3 Dysfunction in Dorsal Hippocampus CA1 (dCA1) Induces Psychomotor BehaviorFrontiers in molecular neuroscience · 2022Article
- Responsible Genes for Neuronal Migration in the Chromosome 17p13.3: BeyondBrain sciences · 2021Review
- AAV9 transduction mediated by systemic delivery of vector via retro-orbital injection in newborn, neonatal and juvenile mice.Experimental animals · 2021Article
- Pathways to Parkinson's disease: a spotlight on 14-3-3 proteins.NPJ Parkinson's disease · 2021Review
- 14-3-3ζ: A suppressor of inflammatory arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Here, we show that deletion of 14-3-3ζ causes neurodevelopmental anomalies similar to those seen in neuropsychiatric disorders such as schizophrenia, autism spectrum disorder and bipolar disorder. 14-3-3ζ-deficient mice displayed striking behavioural and cognitive deficiencies including a reduced capacity to learn and remember, hyperactivity and disrupted sensorimotor gating. These deficits are accompanied by subtle developmental abnormalities of the hippocampus that are underpinned by aberrant neuronal migration. Significantly, 14-3-3ζ-deficient mice exhibited abnormal mossy fibre navigation and glutamatergic synapse formation. The molecular basis of these defects involves the schizophrenia risk factor, DISC1, which interacts isoform specifically with 14-3-3ζ. Our data provide the first evidence of a direct role for 14-3-3ζ deficiency in the aetiology of neurodevelopmental disorders and identifies 14-3-3ζ as a central risk factor in the schizophrenia protein interaction network.
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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.