Channelopathies in fragile X syndrome

Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein–protein inter...

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Published inNature reviews. Neuroscience Vol. 22; no. 5; pp. 275 - 289
Main Authors Deng, Pan-Yue, Klyachko, Vitaly A.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.05.2021
Nature Publishing Group
Subjects
631/378/1689/1373
631/378/1689/2115
Animal Genetics and Genomics
Animal models
Animals
Autism
Behavioral Sciences
Biological Techniques
Biomedical and Life Sciences
Biomedicine
Channelopathies
Channelopathies - etiology
Channelopathies - genetics
Channelopathies - physiopathology
Development and progression
Drug therapy
Excitability
FMR1 protein
Fragile X Mental Retardation Protein - genetics
Fragile X syndrome
Fragile X Syndrome - complications
Fragile X Syndrome - genetics
Fragile X Syndrome - physiopathology
Genetic aspects
Health aspects
Humans
Intellectual disabilities
Ion channels
Neurobiology
Neurosciences
Pathophysiology
Phenotypes
Protein interaction
Proteins
Recovery of function
Review Article
United States
Online AccessGet full text

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Abstract Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein–protein interactions and second messenger pathways. Rapidly increasing evidence demonstrates that loss of FMRP leads to numerous ion channel dysfunctions (that is, channelopathies), which in turn contribute significantly to FXS pathophysiology. Consistent with this, pharmacological or genetic interventions that target dysregulated ion channels effectively restore neuronal excitability, synaptic function and behavioural phenotypes in FXS animal models. Recent studies further support a role for direct and rapid FMRP–channel interactions in regulating ion channel function. This Review lays out the current state of knowledge in the field regarding channelopathies and the pathogenesis of FXS, including promising therapeutic implications. Ion channel dysfunctions contribute significantly to fragile X pathophysiology. In this Review, Deng and Klyachko discuss the mechanisms underlying the effects of these channelopathies in fragile X syndrome, and the therapeutic potential of pharmacological interventions that target ion channels.
AbstractList Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein–protein interactions and second messenger pathways. Rapidly increasing evidence demonstrates that loss of FMRP leads to numerous ion channel dysfunctions (that is, channelopathies), which in turn contribute significantly to FXS pathophysiology. Consistent with this, pharmacological or genetic interventions that target dysregulated ion channels effectively restore neuronal excitability, synaptic function and behavioural phenotypes in FXS animal models. Recent studies further support a role for direct and rapid FMRP–channel interactions in regulating ion channel function. This Review lays out the current state of knowledge in the field regarding channelopathies and the pathogenesis of FXS, including promising therapeutic implications.Ion channel dysfunctions contribute significantly to fragile X pathophysiology. In this Review, Deng and Klyachko discuss the mechanisms underlying the effects of these channelopathies in fragile X syndrome, and the therapeutic potential of pharmacological interventions that target ion channels.
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein-protein interactions and second messenger pathways. Rapidly increasing evidence demonstrates that loss of FMRP leads to numerous ion channel dysfunctions (that is, channelopathies), which in turn contribute significantly to FXS pathophysiology. Consistent with this, pharmacological or genetic interventions that target dysregulated ion channels effectively restore neuronal excitability, synaptic function and behavioural phenotypes in FXS animal models. Recent studies further support a role for direct and rapid FMRP-channel interactions in regulating ion channel function. This Review lays out the current state of knowledge in the field regarding channelopathies and the pathogenesis of FXS, including promising therapeutic implications.Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein-protein interactions and second messenger pathways. Rapidly increasing evidence demonstrates that loss of FMRP leads to numerous ion channel dysfunctions (that is, channelopathies), which in turn contribute significantly to FXS pathophysiology. Consistent with this, pharmacological or genetic interventions that target dysregulated ion channels effectively restore neuronal excitability, synaptic function and behavioural phenotypes in FXS animal models. Recent studies further support a role for direct and rapid FMRP-channel interactions in regulating ion channel function. This Review lays out the current state of knowledge in the field regarding channelopathies and the pathogenesis of FXS, including promising therapeutic implications.
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein-protein interactions and second messenger pathways. Rapidly increasing evidence demonstrates that loss of FMRP leads to numerous ion channel dysfunctions (that is, channelopathies), which in turn contribute significantly to FXS pathophysiology. Consistent with this, pharmacological or genetic interventions that target dysregulated ion channels effectively restore neuronal excitability, synaptic function and behavioural phenotypes in FXS animal models. Recent studies further support a role for direct and rapid FMRP-channel interactions in regulating ion channel function. This Review lays out the current state of knowledge in the field regarding channelopathies and the pathogenesis of FXS, including promising therapeutic implications.
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein-protein interactions, and second messenger pathways. Rapidly increasing evidence demonstrates that loss of FMRP leads to numerous ion channel dysfunctions, i.e., channelopathies, which in turn contribute significantly to FXS pathophysiology. Consistent with this, pharmacological or genetic interventions that target dysregulated ion channels effectively restore neuronal excitability, synaptic function, and behavioral phenotypes in FXS animal models. Recent studies further support a role for direct and rapid FMRP-channel interactions in regulating ion channel function. This review lays out the current state of knowledge in the field regarding channelopathies and the pathogenesis of FXS, including promising therapeutic implications.
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss of fragile X mental retardation protein (FMRP), which regulates a wide range of ion channels via translational control, protein–protein interactions and second messenger pathways. Rapidly increasing evidence demonstrates that loss of FMRP leads to numerous ion channel dysfunctions (that is, channelopathies), which in turn contribute significantly to FXS pathophysiology. Consistent with this, pharmacological or genetic interventions that target dysregulated ion channels effectively restore neuronal excitability, synaptic function and behavioural phenotypes in FXS animal models. Recent studies further support a role for direct and rapid FMRP–channel interactions in regulating ion channel function. This Review lays out the current state of knowledge in the field regarding channelopathies and the pathogenesis of FXS, including promising therapeutic implications. Ion channel dysfunctions contribute significantly to fragile X pathophysiology. In this Review, Deng and Klyachko discuss the mechanisms underlying the effects of these channelopathies in fragile X syndrome, and the therapeutic potential of pharmacological interventions that target ion channels.
Audience Academic
Author Deng, Pan-Yue
Klyachko, Vitaly A.
Author_xml – sequence: 1
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  surname: Klyachko
  fullname: Klyachko, Vitaly A.
  email: klyachko@wustl.edu
  organization: Department of Cell Biology and Physiology, Washington University School of Medicine
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33828309$$D View this record in MEDLINE/PubMed
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Snippet Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism. The condition stems from loss...
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StartPage 275
SubjectTerms 631/378/1689/1373
631/378/1689/2115
Animal Genetics and Genomics
Animal models
Animals
Autism
Behavioral Sciences
Biological Techniques
Biomedical and Life Sciences
Biomedicine
Channelopathies
Channelopathies - etiology
Channelopathies - genetics
Channelopathies - physiopathology
Development and progression
Drug therapy
Excitability
FMR1 protein
Fragile X Mental Retardation Protein - genetics
Fragile X syndrome
Fragile X Syndrome - complications
Fragile X Syndrome - genetics
Fragile X Syndrome - physiopathology
Genetic aspects
Health aspects
Humans
Intellectual disabilities
Ion channels
Neurobiology
Neurosciences
Pathophysiology
Phenotypes
Protein interaction
Proteins
Recovery of function
Review Article
Title Channelopathies in fragile X syndrome
URI https://link.springer.com/article/10.1038/s41583-021-00445-9
https://www.ncbi.nlm.nih.gov/pubmed/33828309
https://www.proquest.com/docview/2517102612
https://www.proquest.com/docview/2510251448
https://pubmed.ncbi.nlm.nih.gov/PMC8863066
Volume 22
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