日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

Coupling of functionality to trafficking of KCNQ2/3 potassium channels at the axon initial segment

轴突起始段KCNQ2/3钾通道的功能与转运的偶联

Yoshioka, Daisuke; Okamura, Yasushi

Chemical and genetic knockout identifies KCNQ2 as the principal background voltage-gated potassium current in human embryonic kidney 293 cells

化学和基因敲除实验表明,KCNQ2是人胚肾293细胞中主要的背景电压门控钾电流。

O'Neill, Matthew J; Yang, Tao; Wada, Yuko; Blair, Marcia A; Glazer, Andrew M

Kcnq2 R213 knock-in mice reveal variant- and region-specific mechanisms underlying self-limited familial neonatal-infantile epilepsy and early infantile developmental and epileptic encephalopathy.

Kcnq2 R213 敲入小鼠揭示了自限性家族性新生儿-婴儿癫痫和早期婴儿发育性癫痫性脑病的变异和区域特异性机制。

Nishijo Takuma, Hamada Nanako, Suliman-Lavie Reut, Tabata Hidenori, Ito Hidenori, Iwamoto Ikuko, Shifman Sagiv, Nagata Koh-Ichi

4-Aminopyridine induced hyperpolarizing oscillations in pediatric human epileptic tissue are network-driven potassium currents that are abolished by activation of KCNQ2-5 (Kv7.2-Kv7.5) channels

4-氨基吡啶诱导的儿童癫痫组织超极化振荡是由网络驱动的钾电流引起的,这种电流可被KCNQ2-5(Kv7.2-Kv7.5)通道的激活所消除。

Kushner, J Keenan; Hoffman, Paige B; Brzezinski, Christine R; O'Neill, Brent R; Hankinson, Todd C; Wilkinson, Charles C; Handler, Michael H; Hoeffer, Charles A; Alexander, Allyson L

Mislocalization of KCNQ2 Channels as a Pathogenic Mechanism in KCNQ2 Developmental and Epileptic Encephalopathy

KCNQ2通道错位是KCNQ2发育性和癫痫性脑病的一种致病机制

Springer, Kristen; Soh, Heun; Paz Zavala, Raquel; Varghese, Nissi; Lutz, Cathleen; Zuberi, Aamir R; Jackson, Alexander C; Tzingounis, Anastasios V

Novel proteolytic post-translational modification in voltage-gated potassium channel KCNQ2

电压门控钾通道KCNQ2中一种新型的蛋白水解翻译后修饰

Kimura, Yuichi; Uchiyama, Hidehiko; Masuda, Koji; Hirose, Shinichi

KCNQ2 Variants in Neonatal Epilepsy: Clinical Characteristics and Neurodevelopmental Outcomes in 30 Patients

KCNQ2变异与新生儿癫痫:30例患者的临床特征和神经发育结局

Li, Yang; Li, Jing'e; Li, Lili; Zhang, Hongwei; Sun, Xiaowei

Neurodevelopmental features in KCNQ2 developmental and epileptic encephalopathy may have limited associations with K(V)7.2 dysfunction

KCNQ2 发育性和癫痫性脑病中的神经发育特征可能与 K(V)7.2 功能障碍的关联有限。

Bidwell, Jessa S; Vanoye, Carlos G; Desai, Reshma R; Berg, Anne T; George, Alfred L Jr

An upstream open reading frame represses translation of the neuronal potassium channel KCNQ2

上游开放阅读框抑制神经元钾通道KCNQ2的翻译

Huey, Dalton J; Guadarrama, Eduardo; DeKeyser, Jean-Marc; Vanoye, Carlos G; Simmons, Christine Q; Li, Qianru; Stroup, Emily K; Ji, Zhe; George, Alfred L

TDP-43-dependent mis-splicing of KCNQ2 triggers intrinsic neuronal hyperexcitability in ALS/FTD.

TDP-43 依赖的 KCNQ2 错误剪接引发 ALS/FTD 中的内在神经元过度兴奋。

Joseph Brian J, Marshall Kelly A, Harley Peter, Mann Jacob R, Alessandrini Francesco, Vanoye Carlos G, Chi Wanhao, Prudencio Mercedes, Simkin Dina, Kao Tzu-Ting, Desai Reshma R, Keuss Matthew J, Barattucci Simone, Zanovello Matteo, Mehta Puja R, DeKeyser Jean-Marc, Limone Francesco, Lee Jonathan, Brown Anna-Leigh, Leyton-Jaimes Marcel F, Nash Leslie A, Juan Irune Guerra San, Aronica Eleonora, Wainger Brian J, Shah Mala, Goswami Anand, Shneider Neil A, Dickson Dennis W, Burrone Juan, Zhang Chaolin, Wichterle Hynek, Petrucelli Leonard, Watts Jonathan K, George Alfred L Jr, Fratta Pietro, Eggan Kevin, Kiskinis Evangelos