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Distinctive in vitro phenotypes in iPSC-derived neurons from patients with gain- and loss-of-function SCN2A developmental and epileptic encephalopathy

https://doi.org/10.1101/2023.02.14.528217
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Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1002/ana.23897openalex-snapshot
Dravet syndrome patient‐derived neurons suggest a novel epilepsy mechanism
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Electrophysiological features: The next precise step for SCN2A developmental epileptic encephalopathy
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Mutations in the sodium channel gene SCN2A cause neonatal epilepsy with late-onset episodic ataxia
inferredcites →https://doi.org/10.1016/j.bcp.2018.01.003openalex-snapshot
Integration of biological/pathophysiological contexts to help clarify genotype-phenotype mismatches in monogenetic diseases. Childhood epilepsies associated with SCN2A as a case study
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Opposing Effects on Na V 1.2 Function Underlie Differences Between SCN2A Variants Observed in Individuals With Autism Spectrum Disorder or Infantile Seizures
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Synaptic Dysfunction in Human Neurons With Autism-Associated Deletions in PTCHD1-AS
inferredcites →https://doi.org/10.1016/j.braindev.2016.10.015openalex-snapshot
Efficacy of sodium channel blockers in SCN2A early infantile epileptic encephalopathy
inferredcites →https://doi.org/10.1016/j.braindev.2018.03.005openalex-snapshot
SCN2A mutation in an infant presenting with migrating focal seizures and infantile spasm responsive to a ketogenic diet
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A Model for Neural Development and Treatment of Rett Syndrome Using Human Induced Pluripotent Stem Cells
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Molecular Identity of Human Outer Radial Glia during Cortical Development
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Combining NGN2 Programming with Developmental Patterning Generates Human Excitatory Neurons with NMDAR-Mediated Synaptic Transmission
inferredcites →https://doi.org/10.1016/j.celrep.2019.04.058openalex-snapshot
A Single-Cell Model for Synaptic Transmission and Plasticity in Human iPSC-Derived Neurons
inferredcites →https://doi.org/10.1016/j.celrep.2021.109483openalex-snapshot
Paradoxical hyperexcitability from NaV1.2 sodium channel loss in neocortical pyramidal cells
inferredcites →https://doi.org/10.1016/j.mce.2021.111529openalex-snapshot
Glucagon-like peptide-1 analogs mitigate neuroinflammation in Alzheimer's disease by suppressing NLRP2 activation in astrocytes
inferredcites →https://doi.org/10.1016/j.mcn.2011.10.005openalex-snapshot
Rbfox proteins regulate alternative splicing of neuronal sodium channel SCN8A
inferredcites →https://doi.org/10.1016/j.neuron.2013.05.029openalex-snapshot
Rapid Single-Step Induction of Functional Neurons from Human Pluripotent Stem Cells
inferredcites →https://doi.org/10.1016/j.neuron.2018.07.052openalex-snapshot
Sodium Channel SCN3A (NaV1.3) Regulation of Human Cerebral Cortical Folding and Oral Motor Development
inferredcites →https://doi.org/10.1016/j.neuron.2019.05.037openalex-snapshot
The Autism-Associated Gene Scn2a Contributes to Dendritic Excitability and Synaptic Function in the Prefrontal Cortex
inferredcites →https://doi.org/10.1016/j.scr.2021.102386openalex-snapshot
Development of a fully human assay combining NGN2-inducible neurons co-cultured with iPSC-derived astrocytes amenable for electrophysiological studies
inferredcites →https://doi.org/10.1016/j.stemcr.2014.10.015openalex-snapshot
Molecular Mechanisms Regulating the Defects in Fragile X Syndrome Neurons Derived from Human Pluripotent Stem Cells
inferredcites →https://doi.org/10.1016/j.stemcr.2016.07.001openalex-snapshot
A Cas9 Variant for Efficient Generation of Indel-Free Knockin or Gene-Corrected Human Pluripotent Stem Cells
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Complete Disruption of Autism-Susceptibility Genes by Gene Editing Predominantly Reduces Functional Connectivity of Isogenic Human Neurons
inferredcites →https://doi.org/10.1016/j.stemcr.2020.05.015openalex-snapshot
In Vitro Differentiated Human Stem Cell-Derived Neurons Reproduce Synaptic Synchronicity Arising during Neurodevelopment
inferredcites →https://doi.org/10.1016/j.yebeh.2020.107187openalex-snapshot
Neonatal SCN2A encephalopathy: A peculiar recognizable electroclinical sequence
inferredcites →https://doi.org/10.1016/s0140-6736(02)09968-3openalex-snapshot
Sodium-channel defects in benign familial neonatal-infantile seizures
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De novo mutations revealed by whole-exome sequencing are strongly associated with autism
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SHANK3 and IGF1 restore synaptic deficits in neurons from 22q13 deletion syndrome patients
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Assembly of functionally integrated human forebrain spheroids
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CDKL5 ensures excitatory synapse stability by reinforcing NGL-1–PSD95 interaction in the postsynaptic compartment and is impaired in patient iPSC-derived neurons
inferredcites →https://doi.org/10.1038/nrn1430openalex-snapshot
The neurobiology of antiepileptic drugs
inferredcites →https://doi.org/10.1038/s41398-020-01056-1openalex-snapshot
Identification of candidate genetic variants and altered protein expression in neural stem and mature neural cells support altered microtubule function to be an essential component in bipolar disorder
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Discovering the pharmacodynamics of conolidine and cannabidiol using a cultured neuronal network based workflow
inferredcites →https://doi.org/10.1038/s42003-018-0099-2openalex-snapshot
Nav1.2 haplodeficiency in excitatory neurons causes absence-like seizures in mice
inferredcites →https://doi.org/10.1038/tp.2016.284openalex-snapshot
Early onset of inflammation during ontogeny of bipolar disorder: the NLRP2 inflammasome gene distinctly differentiates between patients and healthy controls in the transition between iPS cell and neural stem cell stages
inferredcites →https://doi.org/10.1055/s-0033-1333874openalex-snapshot
Microduplication of 3p26.3 in Nonsyndromic Intellectual Disability Indicates an Important Role of CHL1 for Normal Cognitive Function
inferredcites →https://doi.org/10.1074/jbc.272.38.24008openalex-snapshot
Alternative Splicing of the Sodium Channel SCN8A Predicts a Truncated Two-domain Protein in Fetal Brain and Non-neuronal Cells
inferredcites →https://doi.org/10.1085/jgp.201912442openalex-snapshot
Alternative splicing potentiates dysfunction of early-onset epileptic encephalopathy SCN2A variants
inferredcites →https://doi.org/10.1093/bioinformatics/btp616openalex-snapshot
edgeR : a Bioconductor package for differential expression analysis of digital gene expression data
inferredcites →https://doi.org/10.1093/brain/awx054openalex-snapshot
Genetic and phenotypic heterogeneity suggest therapeutic implications in SCN2A-related disorders
inferredcites →https://doi.org/10.1093/hmg/ddr093openalex-snapshot
Isolation of MECP2-null Rett Syndrome patient hiPS cells and isogenic controls through X-chromosome inactivation
inferredcites →https://doi.org/10.1093/hmg/dds207openalex-snapshot
Signaling defects in iPSC-derived fragile X premutation neurons
inferredcites →https://doi.org/10.1097/ypg.0000000000000110openalex-snapshot
Mutation screening of SCN2A in schizophrenia and identification of a novel loss-of-function mutation
inferredcites →https://doi.org/10.1101/2022.11.19.517191openalex-snapshot
DPYSL2 / CRMP2 isoform B knockout in human iPSC-derived glutamatergic neurons confirms its role in mTOR signaling and neurodevelopmental disorders
inferredcites →https://doi.org/10.1111/epi.13461openalex-snapshot
The SCN8A encephalopathy mutation p.Ile1327Val displays elevated sensitivity to the anticonvulsant phenytoin
inferredcites →https://doi.org/10.1113/jp281834openalex-snapshot
Enhanced slow inactivation contributes to dysfunction of a recurrent SCN2A mutation associated with developmental and epileptic encephalopathy
inferredcites →https://doi.org/10.1152/jn.00195.2015openalex-snapshot
Ca2+ toxicity due to reverse Na+/Ca2+ exchange contributes to degeneration of neurites of DRG neurons induced by a neuropathy-associated Nav1.7 mutation
inferredcites →https://doi.org/10.1172/jci152079openalex-snapshot
Antisense oligonucleotide therapy reduces seizures and extends life span in an SCN2A gain-of-function epilepsy model
inferredcites →https://doi.org/10.1186/1471-2105-10-48openalex-snapshot
GOrilla: a tool for discovery and visualization of enriched GO terms in ranked gene lists
inferredcites →https://doi.org/10.1186/1471-2350-15-35openalex-snapshot
De novo SCN2A splice site mutation in a boy with Autism spectrum disorder
inferredcites →https://doi.org/10.1186/s13039-015-0170-3openalex-snapshot
De novo microduplication of CHL1 in a patient with non-syndromic developmental phenotypes
inferredcites →https://doi.org/10.1186/s13229-019-0265-5openalex-snapshot
Scn2a haploinsufficient mice display a spectrum of phenotypes affecting anxiety, sociability, memory flexibility and ampakine CX516 rescues their hyperactivity
inferredcites →https://doi.org/10.1212/wnl.0000000000001926openalex-snapshot
SCN2A encephalopathy
inferredcites →https://doi.org/10.1212/wnl.0b013e3181f8812eopenalex-snapshot
SCN2A mutation associated with neonatal epilepsy, late-onset episodic ataxia, myoclonus, and pain
inferredcites →https://doi.org/10.1212/wnl.0b013e3182a43e57openalex-snapshot
Clinical spectrum of SCN2A mutations expanding to Ohtahara syndrome
inferredcites →https://doi.org/10.1371/journal.pone.0084547openalex-snapshot
Characterization and Molecular Profiling of PSEN1 Familial Alzheimer's Disease iPSC-Derived Neural Progenitors
inferredcites →https://doi.org/10.1371/journal.pone.0169506openalex-snapshot
Functional Maturation of Human Stem Cell-Derived Neurons in Long-Term Cultures
inferredcites →https://doi.org/10.1523/eneuro.0141-19.2019openalex-snapshot
Resurgent and Gating Pore Currents Induced by De Novo SCN2A Epilepsy Mutations
inferredcites →https://doi.org/10.1523/jneurosci.0564-21.2021openalex-snapshot
Hyperexcitability and Pharmacological Responsiveness of Cortical Neurons Derived from Human iPSCs Carrying Epilepsy-Associated Sodium Channel Nav1.2-L1342P Genetic Variant
inferredcites →https://doi.org/10.1523/jneurosci.3089-03.2004openalex-snapshot
A Nonsense Mutation of the Sodium Channel GeneSCN2Ain a Patient with Intractable Epilepsy and Mental Decline
inferredcites →https://doi.org/10.1684/epd.2018.1001openalex-snapshot
Lacosamide for SCN2A ‐related intractable neonatal and infantile seizures
inferredcites →https://doi.org/10.3389/fncel.2014.00297openalex-snapshot
Molecular identity of axonal sodium channels in human cortical pyramidal cells
inferredcites →https://doi.org/10.7554/elife.13073openalex-snapshot
A deleterious Nav1.1 mutation selectively impairs telencephalic inhibitory neurons derived from Dravet Syndrome patients

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.1080/00207454.2025.2501651openalex-snapshot
Association of SCN2A single nucleotide polymorphisms with Parkinson’s disease: evidence from a case-control study
inferred← citeshttps://doi.org/10.1101/2024.05.09.593441openalex-snapshot
Emerging neurodevelopmental mechanisms in patient induced pluripotent stem cells-derived spheroids modelling SCN1A Dravet Syndrome
inferred← citeshttps://doi.org/10.1101/2025.08.18.670956openalex-snapshot
Epilepsy-Associated SCN2A-L1342P Mutation Drives Network Hyperexcitability and Widespread Transcriptomic Changes in Human Cortical Organoids
inferred← citeshttps://doi.org/10.64898/2026.05.18.725745openalex-snapshot
Excitatory Dysfunction and Phenotypic Rescue in a Human Neuronal Model of SCN2A -Related Disorders
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