Heun Soh
Affiliations: | Physiology and Neurobiology | University of Connecticut, Storrs, CT, United States |
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| Abreo TJ, Thompson EC, Madabushi A, et al. (2024) Plural molecular and cellular mechanisms of pore domain encephalopathy. Biorxiv : the Preprint Server For Biology |
| Varghese N, Moscoso B, Chavez A, et al. (2023) KCNQ2/3 Gain-of-Function Variants and Cell Excitability: Differential Effects in CA1 vs. L2/3 pyramidal neurons. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience |
| Jing J, Dunbar C, Sonesra A, et al. (2022) Removal of KCNQ2 from parvalbumin-expressing interneurons improves anti-seizure efficacy of retigabine. Experimental Neurology. 114141 |
| Soh H, Springer K, Doci K, et al. (2022) KCNQ2 and KCNQ5 form heteromeric channels independent of KCNQ3. Proceedings of the National Academy of Sciences of the United States of America. 119: e2117640119 |
| Gao X, Bender F, Soh H, et al. (2021) Place fields of single spikes in hippocampus involve Kcnq3 channel-dependent entrainment of complex spike bursts. Nature Communications. 12: 4801 |
| Hou B, Varghese N, Soh H, et al. (2021) Loss of KCNQ2 or KCNQ3 leads to multifocal time-varying activity in the neonatal forebrain . Eneuro |
| Sanders SS, Hernandez LM, Soh H, et al. (2020) The palmitoyl acyltransferase ZDHHC14 controls Kv1-family potassium channel clustering at the axon initial segment. Elife. 9 |
| Kim EC, Patel J, Zhang J, et al. (2019) Heterozygous loss of epilepsy gene KCNQ2 alters social, repetitive, and exploratory behaviors. Genes, Brain, and Behavior. e12599 |
| Soh H, Park S, Ryan K, et al. (2018) Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission. Elife. 7 |
| Soh H, Park S, Ryan K, et al. (2018) Author response: Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission Elife |