ArticleDevelopmental neurobiology2019
Disruption of MET Receptor Tyrosine Kinase, an Autism Risk Factor, Impairs Developmental Synaptic Plasticity in the Hippocampus.
Article in Developmental neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Article
- Alterations in the Proteome of Developing Neocortical Synaptosomes in the Absence of MET Signaling Revealed by Comparative Proteomics.Developmental neuroscience · 2023Article
- Early impairment of cortical circuit plasticity and connectivity in the 5XFAD Alzheimer's disease mouse model.Translational psychiatry · 2022Article
- Reduced HGF/MET Signaling May Contribute to the Synaptic Pathology in an Alzheimer's Disease Mouse Model.Frontiers in aging neuroscience · 2022Article
- Alterations of the Hippocampal Networks in Valproic Acid-Induced Rat Autism Model.Frontiers in neural circuits · 2022Article
- Time-delimited signaling of MET receptor tyrosine kinase regulates cortical circuit development and critical period plasticity.Molecular psychiatry · 2021Article
- Conditional knockout of MET receptor tyrosine kinase in cortical excitatory neurons leads to enhanced learning and memory in young adult mice but early cognitive decline in older adult mice.Neurobiology of learning and memory · 2021Article
- HGF and MET: From Brain Development to Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- Control of cortical synapse development and plasticity by MET receptor tyrosine kinase, a genetic risk factor for autism.Journal of neuroscience research · 2020Review
- Cyclic Peptide-Based Biologics Regulating HGF-MET.International journal of molecular sciences · 2020Review
- Identification and Functional Analysis of Long Non-coding RNAs in Autism Spectrum Disorders.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
As more genes conferring risks to neurodevelopmental disorders are identified, translating these genetic risk factors into biological mechanisms that impact the trajectory of the developing brain is a critical next step. Here, we report that disrupted signaling mediated MET receptor tyrosine kinase (RTK), an established risk factor for autism spectrum disorders, in the developing hippocampus glutamatergic circuit leads to profound deficits in neural development, synaptic transmission, and plasticity. In cultured hippocampus slices prepared from neonatal mice, pharmacological inhibition of MET kinase activity suppresses dendritic arborization and disrupts normal dendritic spine development. In addition, single-neuron knockdown (RNAi) or overexpression of Met in the developing hippocampal CA1 neurons leads to alterations, opposite in nature, in basal synaptic transmission and long-term plasticity. In forebrain-specific Met conditional knockout mice (Met
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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.