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Andrew Escayg

Showing results (41-50 of 60) with videos related to

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Basic & Clinical Pharmacology & Toxicology|June 20, 2023
Generation and initial characterization of mice lacking full-length BAI3 (ADGRB3) expressionFu Hung Shiu, Jennifer C Wong, Debanjan Bhattacharya, et al.
Experimental Neurology|September 10, 2025
ADGRB1 contributes to astrocyte-mediated phagocytosis of excitatory synapsesFu Hung Shiu, Emily J Hill, Yangping Li, et al.
Neurobiology of Disease|February 26, 2017
SCN3A deficiency associated with increased seizure susceptibilityTyra Lamar, Carlos G Vanoye, Jeffrey Calhoun, et al.
Genes, Brain, and Behavior|October 13, 2019
Mutations in the Scn8a DIIS4 voltage sensor reveal new distinctions among hypomorphic and null Na<sub>v</sub> 1.6 sodium channelsGeorge Andrew S Inglis, Jennifer C Wong, Kameryn M Butler, et al.
Human Molecular Genetics|March 4, 2009
Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in miceLigia A Papale, Barbara Beyer, Julie M Jones, et al.
Neurobiology of Disease|May 5, 2009
A BAC transgenic mouse model reveals neuron subtype-specific effects of a Generalized Epilepsy with Febrile Seizures Plus (GEFS+) mutationBin Tang, Karoni Dutt, Ligia Papale, et al.
Experimental Neurology|February 3, 2022
Mice lacking full length Adgrb1 (Bai1) exhibit social deficits, increased seizure susceptibility, and altered brain developmentFu Hung Shiu, Jennifer C Wong, Takahiro Yamamoto, et al.
Frontiers in Pharmacology|December 6, 2021
Pathogenic in-Frame Variants in <i>SCN8A</i>: Expanding the Genetic Landscape of <i>SCN8A-</i>Associated DiseaseJennifer C Wong, Kameryn M Butler, Lindsey Shapiro, et al.
Epilepsia|August 23, 2018
SLC6A1 variants identified in epilepsy patients reduce γ-aminobutyric acid transportKari A Mattison, Kameryn M Butler, George Andrew S Inglis, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|November 8, 2014
Impaired action potential initiation in GABAergic interneurons causes hyperexcitable networks in an epileptic mouse model carrying a human Na(V)1.1 mutationUlrike B S Hedrich, Camille Liautard, Daniel Kirschenbaum, et al.
Pageof 6

Showing results (41-50 of 60) with videos related to

Sort By:
Pageof 6
Basic & Clinical Pharmacology & Toxicology|June 20, 2023
Generation and initial characterization of mice lacking full-length BAI3 (ADGRB3) expressionFu Hung Shiu, Jennifer C Wong, Debanjan Bhattacharya, et al.
Experimental Neurology|September 10, 2025
ADGRB1 contributes to astrocyte-mediated phagocytosis of excitatory synapsesFu Hung Shiu, Emily J Hill, Yangping Li, et al.
Neurobiology of Disease|February 26, 2017
SCN3A deficiency associated with increased seizure susceptibilityTyra Lamar, Carlos G Vanoye, Jeffrey Calhoun, et al.
Genes, Brain, and Behavior|October 13, 2019
Mutations in the Scn8a DIIS4 voltage sensor reveal new distinctions among hypomorphic and null Na<sub>v</sub> 1.6 sodium channelsGeorge Andrew S Inglis, Jennifer C Wong, Kameryn M Butler, et al.
Human Molecular Genetics|March 4, 2009
Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in miceLigia A Papale, Barbara Beyer, Julie M Jones, et al.
Neurobiology of Disease|May 5, 2009
A BAC transgenic mouse model reveals neuron subtype-specific effects of a Generalized Epilepsy with Febrile Seizures Plus (GEFS+) mutationBin Tang, Karoni Dutt, Ligia Papale, et al.
Experimental Neurology|February 3, 2022
Mice lacking full length Adgrb1 (Bai1) exhibit social deficits, increased seizure susceptibility, and altered brain developmentFu Hung Shiu, Jennifer C Wong, Takahiro Yamamoto, et al.
Frontiers in Pharmacology|December 6, 2021
Pathogenic in-Frame Variants in <i>SCN8A</i>: Expanding the Genetic Landscape of <i>SCN8A-</i>Associated DiseaseJennifer C Wong, Kameryn M Butler, Lindsey Shapiro, et al.
Epilepsia|August 23, 2018
SLC6A1 variants identified in epilepsy patients reduce γ-aminobutyric acid transportKari A Mattison, Kameryn M Butler, George Andrew S Inglis, et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience|November 8, 2014
Impaired action potential initiation in GABAergic interneurons causes hyperexcitable networks in an epileptic mouse model carrying a human Na(V)1.1 mutationUlrike B S Hedrich, Camille Liautard, Daniel Kirschenbaum, et al.
Pageof 6