التفاصيل البيبلوغرافية
العنوان: |
Mice deficient in TWIK-1 are more susceptible to kainic acid-induced seizures |
المؤلفون: |
Ajung Kim, Yeonju Bae, Changdev G. Gadhe, Hyun-Gug Jung, Esther Yang, Hyun Kim, Jaekwang Lee, Chanseob Shim, Young Hoon Sung, Junyeol Noh, Eun-Jin Kim, Dawon Kang, Ae Nim Pae, Eun Mi Hwang, Jae-Yong Park |
المصدر: |
iScience, Vol 28, Iss 1, Pp 111587- (2025) |
بيانات النشر: |
Elsevier, 2025. |
سنة النشر: |
2025 |
المجموعة: |
LCC:Science |
مصطلحات موضوعية: |
Biological sciences, Molecular neuroscience, Natural sciences, Neuroscience, Systems neuroscience, Science |
الوصف: |
Summary: 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 ΔEx2) 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. |
نوع الوثيقة: |
article |
وصف الملف: |
electronic resource |
اللغة: |
English |
تدمد: |
2589-0042 |
Relation: |
http://www.sciencedirect.com/science/article/pii/S2589004224028141; https://doaj.org/toc/2589-0042 |
DOI: |
10.1016/j.isci.2024.111587 |
URL الوصول: |
https://doaj.org/article/b42789a175a34a468a4e075a4150f630 |
رقم الانضمام: |
edsdoj.b42789a175a34a468a4e075a4150f630 |
قاعدة البيانات: |
Directory of Open Access Journals |