Kristen Springer - Publications

Affiliations: 
Physiology and Neurobiology University of Connecticut, Storrs, CT, United States 

6 high-probability publications. We are testing a new system for linking publications to authors. You can help! If you notice any inaccuracies, please sign in and mark papers as correct or incorrect matches. If you identify any major omissions or other inaccuracies in the publication list, please let us know.

Year Citation  Score
2024 Abreo TJ, Thompson EC, Madabushi A, Soh H, Varghese N, Vanoye CG, Springer K, Park KL, Johnson J, Sims S, Ji Z, Chavez AG, Jankovic MJ, Habte B, Zuberi A, et al. Plural molecular and cellular mechanisms of pore domain encephalopathy. Biorxiv : the Preprint Server For Biology. PMID 38260608 DOI: 10.1101/2024.01.04.574177  0.65
2023 Varghese N, Moscoso B, Chavez A, Springer K, Ortiz E, Soh H, Santaniello S, Maheshwari A, Tzingounis AV. 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. PMID 37607817 DOI: 10.1523/JNEUROSCI.0980-23.2023  0.669
2022 Soh H, Springer K, Doci K, Balsbaugh JL, Tzingounis AV. KCNQ2 and KCNQ5 form heteromeric channels independent of KCNQ3. Proceedings of the National Academy of Sciences of the United States of America. 119: e2117640119. PMID 35320039 DOI: 10.1073/pnas.2117640119  0.709
2021 Springer K, Varghese N, Tzingounis AV. Flexible Stoichiometry: Implications for KCNQ2- and KCNQ3-Associated Neurodevelopmental Disorders. Developmental Neuroscience. 1-10. PMID 33794528 DOI: 10.1159/000515495  0.646
2018 Soh H, Park S, Ryan K, Springer K, Maheshwari A, Tzingounis AV. Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission. Elife. 7. PMID 30382937 DOI: 10.7554/Elife.38617  0.62
2018 Soh H, Park S, Ryan K, Springer K, Maheshwari A, Tzingounis AV. Author response: Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission Elife. DOI: 10.7554/Elife.38617.018  0.689
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