ArticleNature neuroscience2015
The schizophrenia risk gene product miR-137 alters presynaptic plasticity.
Article in Nature neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 131 papers, 1 of them a synthesis that pooled it.
What it found
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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
131 citing papers in PubMed, 1 synthesis or guideline pooled it, 229 citations in OpenAlex.
- Analyzing the Role of MicroRNAs in Schizophrenia in the Context of Common Genetic Risk Variants.JAMA psychiatry · 2016Pooled it
- Enhanced Therapeutic Effects of Extracellular Vesicles Targeting MiR-137 Contribute to Functional Recovery by Attenuating Neuronal Injury After Ischemic Stroke.Neuroscience bulletin · 2026Article
- Biological underpinnings and genetic predisposition to schizophrenia within microrna-137 regulatory pathways across brain development.Translational psychiatry · 2026Article
- A non-coding RNA risk pathway in schizophrenia: miR-137 enhances the lncRNA GOMAFU through a pathological transcription network.Translational psychiatry · 2025Article
- MicroRNAs and synaptic dysfunction in Parkinson's disease.Molecular therapy. Nucleic acids · 2025Review
- Article
- MicroRNA-138-5p suppresses excitatory synaptic strength at the cerebellar input layer.The Journal of physiology · 2025Article
- Alteration of microRNA expression in lymphocytes in patients with first-episode schizophrenia.BMC psychiatry · 2025Article
- An increased copy number of glycine decarboxylase (GLDC) associated with psychosis reduces extracellular glycine and impairs NMDA receptor function.Molecular psychiatry · 2025Article
- CPLX1 is a novel prognostic biomarker in CRC correlating with immunotherapy resistance and ferroptosis.Frontiers in immunology · 2025Article
- MicroRNAs Fine-Tune Brain and Body Communication in Health and Disease : MicroRNAs in Brain-Body Communication.Advances in experimental medicine and biology · 2025Review
- Schizophrenia risk-associated SNPs affect expression of microRNA 137 host gene: a postmortem study.Human molecular genetics · 2024Article
- Paraventricular hypothalamic RUVBL2 neurons suppress appetite by enhancing excitatory synaptic transmission in distinct neurocircuits.Nature communications · 2024Article
- Endogenous mutant Huntingtin alters the corticogenesis via lowering Golgi recruiting ARF1 in cortical organoid.Molecular psychiatry · 2024Article
- Small Differences and Big Changes: The Many Variables of MicroRNA Expression and Function in the Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
- Generation and transcriptomic characterization of MIR137 knockout miniature pig model for neurodevelopmental disorders.Cell & bioscience · 2024Article
- Article
- The role of synaptic protein NSF in the development and progression of neurological diseases.Frontiers in neuroscience · 2024Review
- miR-137: a potential therapeutic target for lung cancer.Frontiers in cell and developmental biology · 2024Review
- Transition of allele-specific DNA hydroxymethylation at regulatory loci is associated with phenotypic variation in monozygotic twins discordant for psychiatric disorders.BMC medicine · 2023Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
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- Erratum issued
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Noncoding variants in the human MIR137 gene locus increase schizophrenia risk with genome-wide significance. However, the functional consequence of these risk alleles is unknown. Here we examined induced human neurons harboring the minor alleles of four disease-associated single nucleotide polymorphisms in MIR137. We observed increased MIR137 levels compared to those in major allele-carrying cells. microRNA-137 gain of function caused downregulation of the presynaptic target genes complexin-1 (Cplx1), Nsf and synaptotagmin-1 (Syt1), leading to impaired vesicle release. In vivo, miR-137 gain of function resulted in changes in synaptic vesicle pool distribution, impaired induction of mossy fiber long-term potentiation and deficits in hippocampus-dependent learning and memory. By sequestering endogenous miR-137, we were able to ameliorate the synaptic phenotypes. Moreover, reinstatement of Syt1 expression partially restored synaptic plasticity, demonstrating the importance of Syt1 as a miR-137 target. Our data provide new insight into the mechanism by which miR-137 dysregulation can impair synaptic plasticity in the hippocampus.
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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.