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Article

The Sodium Channel B4-Subunits are Dysregulated in Temporal Lobe Epilepsy Drug-Resistant Patients

1
Biomolecular Sciences Research Centre, Sheffield Hallam University, Howard Street, Sheffield S1 1WB, UK
2
Institute of Integrative Biology, University of Liverpool, Biosciences Building, Liverpool L69 7ZB, UK
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(8), 2955; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082955
Received: 15 March 2020 / Revised: 14 April 2020 / Accepted: 21 April 2020 / Published: 22 April 2020
(This article belongs to the Special Issue Genomics of Brain Disorders 2.0)
Temporal lobe epilepsy (TLE) is the most common type of partial epilepsy referred for surgery due to antiepileptic drug (AED) resistance. A common molecular target for many of these drugs is the voltage-gated sodium channel (VGSC). The VGSC consists of four domains of pore-forming α-subunits and two auxiliary β-subunits, several of which have been well studied in epileptic conditions. However, despite the β4-subunits’ role having been reported in some neurological conditions, there is little research investigating its potential significance in epilepsy. Therefore, the purpose of this work was to assess the role of SCN4β in epilepsy by using a combination of molecular and bioinformatics approaches. We first demonstrated that there was a reduction in the relative expression of SCN4B in the drug-resistant TLE patients compared to non-epileptic control specimens, both at the mRNA and protein levels. By analyzing a co-expression network in the neighborhood of SCN4B we then discovered a linkage between the expression of this gene and K+ channels activated by Ca2+, or K+ two-pore domain channels. Our approach also inferred several potential effector functions linked to variation in the expression of SCN4B. These observations support the hypothesis that SCN4B is a key factor in AED-resistant TLE, which could help direct both the drug selection of TLE treatments and the development of future AEDs. View Full-Text
Keywords: temporal lobe epilepsy; hippocampal sclerosis; antiepileptic drug resistance; SCN4B; voltage-gated sodium channels; Nav β4 subunit temporal lobe epilepsy; hippocampal sclerosis; antiepileptic drug resistance; SCN4B; voltage-gated sodium channels; Nav β4 subunit
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MDPI and ACS Style

Sheilabi, M.A.; Takeshita, L.Y.; Sims, E.J.; Falciani, F.; Princivalle, A.P. The Sodium Channel B4-Subunits are Dysregulated in Temporal Lobe Epilepsy Drug-Resistant Patients. Int. J. Mol. Sci. 2020, 21, 2955. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082955

AMA Style

Sheilabi MA, Takeshita LY, Sims EJ, Falciani F, Princivalle AP. The Sodium Channel B4-Subunits are Dysregulated in Temporal Lobe Epilepsy Drug-Resistant Patients. International Journal of Molecular Sciences. 2020; 21(8):2955. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082955

Chicago/Turabian Style

Sheilabi, Mariam A., Louise Y. Takeshita, Edward J. Sims, Francesco Falciani, and Alessandra P. Princivalle. 2020. "The Sodium Channel B4-Subunits are Dysregulated in Temporal Lobe Epilepsy Drug-Resistant Patients" International Journal of Molecular Sciences 21, no. 8: 2955. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082955

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