ArticleNeurobiology of disease2016
MECP2 impairs neuronal structure by regulating KIBRA.
Article in Neurobiology of disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Revealing function-altering MECP2 mutations in individuals with autism spectrum disorder using yeast and Drosophila.Genetics · 2025Article
- The Role of MeCP2 in Regulating Synaptic Plasticity in the Context of Stress and Depression.Cells · 2022Review
- Neuronal activation modulates enhancer activity of genes for excitatory synaptogenesis through de novo DNA methylation.The Journal of reproduction and development · 2021Article
- Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Using a Drosophila model of MECP2 gain-of-function, we identified memory associated KIBRA as a target of MECP2 in regulating dendritic growth. We found that expression of human MECP2 increased kibra expression in Drosophila, and targeted RNAi knockdown of kibra in identified neurons fully rescued dendritic defects as induced by MECP2 gain-of-function. Validation in mouse confirmed that Kibra is similarly regulated by Mecp2 in a mammalian system. We found that Mecp2 gain-of-function in cultured mouse cortical neurons caused dendritic impairments and increased Kibra levels. Accordingly, Mecp2 loss-of-function in vivo led to decreased Kibra levels in hippocampus, cortex, and cerebellum. Together, our results functionally link two neuronal genes of high interest in human health and disease and highlight the translational utility of the Drosophila model for understanding MECP2 function.
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Registered trials
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