ArticleHuman molecular genetics2015
Neuronal copper homeostasis susceptibility by genetic defects in dysbindin, a schizophrenia susceptibility factor.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Beyond the Mind-Serum Trace Element Levels in Schizophrenic Patients: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Cellular and subcellular localization of the copper transporter CTR1 in human postmortem hippocampus and striatum.Scientific reports · 2026Article
- A primer on copper biology in the brain.Neurobiology of disease · 2025Review
- Overlapping Machinery in Lysosome-Related Organelle Trafficking: A Lesson from Rare Multisystem Disorders.Cells · 2022Review
- Cortical copper transporter expression in schizophrenia: interactions of risk gene dysbindin-1.Journal of neural transmission (Vienna, Austria : 1996) · 2021Article
- Abnormalities in the copper transporter CTR1 in postmortem hippocampus in schizophrenia: A subregion and laminar analysis.Schizophrenia research · 2021Article
- Markers of copper transport in the cingulum bundle in schizophrenia.Schizophrenia research · 2021Article
- Golgi-Dependent Copper Homeostasis Sustains Synaptic Development and Mitochondrial Content.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Interactions between knockout of schizophrenia risk factor Dysbindin-1 and copper metabolism in mice.Brain research bulletin · 2020Article
- Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches.International journal of molecular sciences · 2020Review
- Impaired copper transport in schizophrenia results in a copper-deficient brain state: A new side to the dysbindin story.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2020Article
- Loss of dysbindin-1 affects GABAergic transmission in the PFC.Psychopharmacology · 2019Article
- Trafficking mechanisms of P-type ATPase copper transporters.Current opinion in cell biology · 2019Review
- The road to lysosome-related organelles: Insights from Hermansky-Pudlak syndrome and other rare diseases.Traffic (Copenhagen, Denmark) · 2019Review
- Article
- The Endolysosomal System and Proteostasis: From Development to Degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Review
- Neurodevelopmental disease mechanisms, primary cilia, and endosomes converge on the BLOC-1 and BORC complexes.Developmental neurobiology · 2018Review
- Article
- Dysbindin Deficiency Modifies the Expression of GABA Neuron and Ion Permeation Transcripts in the Developing Hippocampus.Frontiers in genetics · 2017Article
- Copper and Zinc Homeostasis: Lessons fromFrontiers in genetics · 2017Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Environmental factors and susceptible genomes interact to determine the risk of neurodevelopmental disorders. Although few genes and environmental factors have been linked, the intervening cellular and molecular mechanisms connecting a disorder susceptibility gene with environmental factors remain mostly unexplored. Here we focus on the schizophrenia susceptibility gene DTNBP1 and its product dysbindin, a subunit of the BLOC-1 complex, and describe a neuronal pathway modulating copper metabolism via ATP7A. Mutations in ATP7A result in Menkes disease, a disorder of copper metabolism. Dysbindin/BLOC-1 and ATP7A genetically and biochemically interact. Furthermore, disruption of this pathway causes alteration in the transcriptional profile of copper-regulatory and dependent factors in the hippocampus of dysbindin/BLOC-1-null mice. Dysbindin/BLOC-1 loss-of-function alleles do not affect cell and tissue copper content, yet they alter the susceptibility to toxic copper challenges in both mammalian cells and Drosophila. Our results demonstrate that perturbations downstream of the schizophrenia susceptibility gene DTNBP1 confer susceptibility to copper, a metal that in excess is a neurotoxin and whose depletion constitutes a micronutrient deficiency.
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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.