Results 101 to 110 of about 2,282 (189)

K+-Channel Openers Suppress Epileptiform Activities Induced by 4-Aminopyridine in Cultured Rat Hippocampal Neurons

Journal of Pharmacological Sciences, 2008
K+ channels are key modulators of neuronal excitability, and mutations in certain types of these channels are known to cause epileptic seizures. Activation of K+ channels is reported to suppress epileptic discharge; however, the types of K+-channel ...
Kiyoaki Kobayashi, Yukio Nishizawa, Kohei Sawada, Hiroo Ogura, Masayuki Miyabe   +4 more
doaj   +1 more source

Uncoupling PIP2-calmodulin regulation of Kv7.2 channels by an assembly destabilizing epileptogenic mutation

Journal of Cell Science, 2015
ABSTRACT We show that the combination of an intracellular bi-partite calmodulin (CaM)-binding site and a distant assembly region affect how an ion channel is regulated by a membrane lipid. Our data reveal that regulation by phosphatidylinositol(4,5)bisphosphate (PIP2) and stabilization of assembled Kv7.2 subunits by intracellular coiled ...
Alberdi, Araitz, Gomis-Perez, Carolina, Bernardo-Seisdedos, Ganeko, Alaimo, Alessandro, Malo, Covadonga, Aldaregia, Juncal, Lopez-Robles, Carlos, Areso, Pilar, Butz, Elisabeth, Wahl-Schott, Christian, Villarroel, Alvaro   +10 more
openaire   +3 more sources

Effects of CXB analogues on Kv7.2/7.3 expressed in HEK293 cells.

, 2013
A, Structures of CXB analogues. (a), Celecoxib (CXB); (b), unmethylated-celecoxib (UM-celecoxib, UMC); (c), 2, 5-Dimethyl-celecoxib (DM-celecoxib, DMC) B, The time course for the effects of CXB, UMC and DMC on the tail currents (−60 mV) of Kv7.2/7.3 ...
Xuan Zhang (56049), Hailin Zhang (48017), Jinlong Qi (287090), Haixia Gao (287091), Dongyang Huang (287093), Xiaona Du (287094), Yao Mi (287089), Li Li (14993), Fan Zhang (46132)   +8 more
core   +1 more source

Tamoxifen inhibited Kv7.2/Kv7.3 channels expressed in HEK-293 cells.

, 2013
A and B, ionic currents recorded in control condition (A) and in presence of 1 µM tamoxifen (B) using voltage protocol shown in the inset. C, Current-voltage relationship in control (square, n = 6) and in presence of 1 µM tamoxifen (circles, n = 6).
Ivan Arael Aréchiga-Figueroa (462495), Martin Tristani-Firouzi (93428), Tania Ferrer (93423), Mark S. Shapiro (53587), José A. Sanchez-Chapula (462496)   +4 more
core   +1 more source

Clinical and genetic analysis of 23 Chinese children with epilepsy associated with KCNQ2 gene mutations

Epilepsia Open
Objective To summarize the clinical features and genetic mutation characteristics of Chinese children with KCNQ2‐related epilepsy. Methods A cohort of children with genetically caused epilepsy was evaluated at Linyi People's Hospital from January 2017 to
Xixi Yu, Fengyuan Che, Xin Zhang, Li Yang, Liping Zhu, Na Xu, Shiyan Qiu, Yufen Li   +7 more
doaj   +1 more source

Developmental expression of Kv potassium channels at the axon initial segment of cultured hippocampal neurons.

PLoS ONE, 2012
Axonal outgrowth and the formation of the axon initial segment (AIS) are early events in the acquisition of neuronal polarity. The AIS is characterized by a high concentration of voltage-dependent sodium and potassium channels.
Diana Sánchez-Ponce, Javier DeFelipe, Juan José Garrido, Alberto Muñoz   +3 more
doaj   +1 more source

Kv7.2 loss-of-function causes early hyperexcitability and network remodelling

Brain
Abstract Loss-of-function (LOF) variants in KCNQ2, encoding the potassium channel subunit Kv7.2, cause a spectrum of neonatal epilepsies ranging from self-limiting familial neonatal epilepsy (SeLFNE) to severe developmental and epileptic encephalopathy (DEE). To dissect the developmental consequences of Kv7.2 LOF, we
Nina Dirkx, Marcus Kaji, Els De Vriendt, Giusy Carleo, Francesco Miceli, Bob Asselbergh, Peter Verstraelen, Noortje Zonnekein, Lidia Carotenuto, Louis T Dang, Vera Sommers, Eve Vlaemynck, Lieven Lagae, Berten Ceulemans, Peter De Jonghe, Winnok H De Vos, Maurizio Taglialatela, Sarah Weckhuysen   +17 more
openaire   +1 more source

Tuning the Wave: Controlling Spreading Depolarization with Activation/Inactivation of Kv7.2 [PDF]

Epilepsy Currents, 2021
openaire   +2 more sources

Study of the in vivo folding of the potassium channel Kv7.2

, 2020
[EN] Arrest peptides were employed as a technique to study the cotranslational folding of cytosolic A and B helices of the potassium channel Kv7.2. The results show the potential of arrest peptides to study cotranslational folding. In the tested conditions, the A and B helices mostly do not cotranslationally fold in the ribosome vestibule.
openaire   +1 more source

A basic residue in the proximal C-terminus is necessary for efficient activation of the M-channel subunit Kv7.2 by PI(4,5)P₂

All Kv7 potassium channels require membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2) for their normal function and hence can be physiologically regulated by neurotransmitters and hormones that stimulate phosphoinositide hydrolysis.
Telezhkin V, Harmer SC, Thomas AM, Tinker A, Brown DA   +4 more
core   +4 more sources