ArticleExperimental neurobiology2019
14-3-3γ Haploinsufficient Mice Display Hyperactive and Stress-sensitive Behaviors.
Article in Experimental neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- 14-3-3 proteins: Regulators of cardiac excitation-contraction coupling and stress responses.The Journal of physiology · 2026Review
- 14-3-3γ Knockdown promotes matrix mineralization in human mesenchymal stromal cells.Cell death & disease · 2026Article
- Role of the YWHAG gene mutations in Developmental and Epileptic Encephalopathy.Frontiers in neuroscience · 2025Review
- Necessity of an Integrative Animal Model for a Comprehensive Study of Attention-Deficit/Hyperactivity Disorder.Biomedicines · 2023Review
- 14-3-3γ haploinsufficiency leads to altered dopamine pathway and Parkinson's disease-like motor incoordination in mice.Molecular brain · 2023Article
- A heterozygous missense variant in the YWHAG gene causing developmental and epileptic encephalopathy 56 in a Chinese family.BMC medical genomics · 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
- Emerging roles of 14-3-3γ in the brain disorder.BMB reports · 2020Review
- Involvement of the 14-3-3 Gene Family in Autism Spectrum Disorder and Schizophrenia: Genetics, Transcriptomics and Functional Analyses.Journal of clinical medicine · 2020Article
- Social, neurodevelopmental, endocrine, and head size differences associated with atypical deletions in Williams-Beuren syndrome.American journal of medical genetics. Part A · 2020Article
- 14-3-3 Proteins Are on the Crossroads of Cancer, Aging, and Age-Related Neurodegenerative Disease.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
14-3-3γ plays diverse roles in different aspects of cellular processes. Especially in the brain where 14-3-3γ is enriched, it has been reported to be involved in neurological and psychiatric diseases (e.g. Williams-Beuren syndrome and Creutzfeldt-Jakob disease). However, behavioral abnormalities related to 14-3-3γ deficiency are largely unknown. Here, by using 14-3-3γ deficient mice, we found that homozygous knockout mice were prenatally lethal, and heterozygous mice showed developmental delay relative to wild-type littermate mice. In addition, in behavioral analyses, we found that 14-3-3γ heterozygote mice display hyperactive and depressive-like behavior along with more sensitive responses to acute stress than littermate control mice. These results suggest that 14-3-3γ levels may be involved in the developmental manifestation of related neuropsychiatric diseases. In addition, 14-3-3γ heterozygote mice may be a potential model to study the molecular pathophysiology of neuropsychiatric symptoms.
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