ArticleHuman molecular genetics2017
Disrupted-in-Schizophrenia-1 (DISC1) protein disturbs neural function in multiple disease-risk pathways.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Peering into the mind: unraveling schizophrenia's secrets using models.Molecular psychiatry · 2025Review
- Decoding the Molecular Mechanisms of miRNAs: Protein Interactions in Schizophrenia Pathogenesis.Current protein & peptide science · 2025Review
- Relevance of interactions between dopamine and glutamate neurotransmission in schizophrenia.Molecular psychiatry · 2022Review
- Article
- Structural interaction between DISC1 and ATF4 underlying transcriptional and synaptic dysregulation in an iPSC model of mental disorders.Molecular psychiatry · 2021Article
- Evaluation of NDEL1 oligopeptidase activity in blood and brain in an animal model of schizophrenia: effects of psychostimulants and antipsychotics.Scientific reports · 2020Article
- Review
- Article
- Altered White Matter and Layer VIb Neurons in HeterozygousFrontiers in neuroanatomy · 2020Article
- Kinase network dysregulation in a human induced pluripotent stem cell model of DISC1 schizophrenia.Molecular omics · 2019Article
- The TRAX, DISC1, and GSK3 complex in mental disorders and therapeutic interventions.Journal of biomedical science · 2018Review
- Genetic interaction of DISC1 and Neurexin in the development of fruit fly glutamatergic synapses.NPJ schizophrenia · 2017Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Although the genetic contribution is under debate, biological studies in multiple mouse models have suggested that the Disrupted-in-Schizophrenia-1 (DISC1) protein may contribute to susceptibility to psychiatric disorders. In the present study, we took the advantages of the Drosophila model to dissect the molecular pathways that can be affected by DISC1 in the context of pathology-related phenotypes. We found that three pathways that include the homologs of Drosophila Dys, Trio, and Shot were downregulated by introducing a C-terminal truncated mutant DISC1. Consistently, these three molecules were downregulated in the induced pluripotent stem cell-derived forebrain neurons from the subjects carrying a frameshift deletion in DISC1 C-terminus. Importantly, the three pathways were underscored in the pathophysiology of psychiatric disorders in bioinformatics analysis. Taken together, our findings are in line with the polygenic theory of psychiatric disorders.
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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.