Kim, Ajung Bae, Yeonju Gadhe, Changdev G. Jung, Hyun-Gug Yang, Esther Kim, Hyun Lee, Jaekwang Shim, Chanseob Sung, Young Hoon Noh, Junyeol Kim, Eun-Jin Kang, Dawon Pae, Ae Nim Hwang, Eun Mi Park, Jae-Yong 2025-01-23T06:30:12Z 2025-01-23T06:30:12Z 2025-01-23 2025-01 https://pubs.kist.re.kr/handle/201004/151641 TWIK-1 belongs to the two-pore domain K+ (K2P) channel family, which plays an essential role in the background K+ conductance of cells. Despite the development of exon 2-deleted Twik-1 knockout (KO) mice, the physiological role of TWIK-1 has remained largely unknown. Here, we observed that the exon 2-deleted Twik-1 KO mice expressed an internally deleted TWIK-1 (TWIK-1 D Ex2) protein, which unexpectedly acts as a functional K+ channel. The Twik-1 nKO mice in which exon 1 was targeted using the CRISPR-Cas9 technique provides strong evidence that TWIK-1 mediates K+ currents that are responsible for the background passive conductance in astrocytes. Deficiency of TWIK-1-mediated astrocytic passive conductance increased susceptibility to kainic acid-induced seizures. This study paves the way for functional studies on TWIK-1-mediated astrocytic passive conductance. In addition, the exon 1-targeted Twik-1 KO mice would help elucidate the physiological roles of TWIK-1. English CELL PRESS Mice deficient in TWIK-1 are more susceptible to kainic acid-induced seizures Article 10.1016/j.isci.2024.111587 1 iScience, v.28, no.1 iScience 28 1 Y scie scopus 001394599100001 2-s2.0-85212827667 Multidisciplinary Sciences Science & Technology - Other Topics Article CHANNEL POTASSIUM EXPRESSION KCNK