ArticleCell death & disease2022
Loss of neurodevelopmental-associated miR-592 impairs neurogenesis and causes social interaction deficits.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Circulating MicroRNAs as Diagnostic and Prognostic Biomarkers for Neuroblastoma: A Systematic Review and Exploratory Re-analysis.Molecular diagnosis & therapy · 2026Pooled it
- Combined Diagnostic Value of Hsa-miR-592 and Hsa-miR-9-3p in Plasma for Methamphetamine Addicts.International journal of molecular sciences · 2024Article
- miR-26 Deficiency Causes Alterations in Lens Transcriptome and Results in Adult-Onset Cataract.Investigative ophthalmology & visual science · 2024Article
- Exosome lncRNA IFNG-AS1 derived from mesenchymal stem cells of human adipose ameliorates neurogenesis and ASD-like behavior in BTBR mice.Journal of nanobiotechnology · 2024Article
- A Young Boy with 21q21.1 Microdeletion Showing Speech Delay, Spastic Diplegia, and MRI Abnormalities: Original Case Report.Global medical genetics · 2023Article
- Astrocytic MicroRNAs and Transcription Factors in Alzheimer's Disease and Therapeutic Interventions.Cells · 2022Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
microRNA-592 (miR-592) has been linked to neurogenesis, but the influence of miR-592 knockout in vivo remains unknown. Here, we report that miR-592 knockout represses IPC-to-mature neuron transition, impairs motor coordination and reduces social interaction. Combining the RNA-seq and tandem mass tagging-based quantitative proteomics analysis (TMT protein quantification) and luciferase reporter assays, we identified MeCP2 as the direct targetgene of miR-592 in the mouse cortex. In Tg(MECP2) mice, lipofection of miR-592 efficiently reduced MECP2 expression in the brains of Tg(MECP2) mice at E14.5. Furthermore, treatment with miR-592 partially ameliorated the autism-like phenotypes observed in adult Tg(MECP2) mice. The findings demonstrate that miR-592 might play a novel role in treating the neurodevelopmental-associated disorder.
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Registered trials
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