ArticlePloS one2015
The Schizophrenia-Related Protein Dysbindin-1A Is Degraded and Facilitates NF-Kappa B Activity in the Nucleus.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Magnesium and Zinc in Schizophrenia.Biomedicines · 2025Review
- DJ-1 inhibits microglial activation and protects dopaminergic neurons in vitro and in vivo through interacting with microglial p65.Cell death & disease · 2021Article
- Modeling Schizophrenia with Glioblastoma Cells: In Vitro Analysis of Risperidone Treatment on Glial Spheroids.Psychiatry and clinical psychopharmacology · 2021Article
- The tumor suppressor OVCA1 is a short half-life protein degraded by the ubiquitin-proteasome pathway.Oncology letters · 2019Article
- Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone.NPJ schizophrenia · 2018Article
- Dysbindin-1 Involvement in the Etiology of Schizophrenia.International journal of molecular sciences · 2017Review
- TRIM24 protein promotes and TRIM32 protein inhibits cardiomyocyte hypertrophy via regulation of dysbindin protein levels.The Journal of biological chemistry · 2017Article
- Gene × Environment Interactions in Schizophrenia: Evidence from Genetic Mouse Models.Neural plasticity · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrobrevin-binding protein 1 (DTNBP1), a gene encoding dysbindin-1, has been identified as a susceptibility gene for schizophrenia. Functioning with partners in synapses or the cytoplasm, this gene regulates neurite outgrowth and neurotransmitter release. Loss of dysbindin-1 affects schizophrenia pathology. Dysbindin-1 is also found in the nucleus, however, the characteristics of dysbindin in the nucleus are not fully understood. Here, we found that dysbindin-1A is degraded in the nucleus via the ubiquitin-proteasome system and that amino acids 2-41 at the N-terminus are required for this process. By interacting with p65, dysbindin-1A promotes the transcriptional activity of NF-kappa B in the nucleus and positively regulates MMP-9 expression. Taken together, the data obtained in this study demonstrate that dysbindin-1A protein levels are highly regulated in the nucleus and that dysbindin-1A regulates transcription factor NF-kappa B activity to promote the expression of MMP-9 and TNF-α.
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Registered trials
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