Potassium KCa3.1 channel overexpression deteriorates functionality and availability of channels at the outer cellular membrane.

ABSTRACT: The engineered expression of K⁺ channels has been proposed as a potential treatment for epilepsy due to their exceptional ability to hyperpolarize neurons. A number of rodent models of gene therapy have yielded promising outcomes. However, the prevailing viral delivery methods for transgenes lack external control over expression, which may lead to the overproduction of K⁺ channel subunits and subsequent adverse effects. AAV-based expression of the KCNN4 gene in excitatory neurons has recently been demonstrated to suppress seizures by decreasing neuronal spiking activity. In this study, we examine the effects of overexpression of KCNN4, a gene encoding a pore-forming subunit of KCa3.1 channels, in neurons and HEK293 cells at the cellular and subcellular levels. We empl

SUBMITTER: Bal NV 

PROVIDER: S-EPMC11811289 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature