| NEDD4-2 and the CLC-2 channel regulate neuronal excitability in the pathogenesis of mesial temporal lobe epilepsy. | NEDD4-2 and the CLC-2 channel regulate neuronal excitability in the pathogenesis of mesial temporal lobe epilepsy.
Liu Y, Yang H, Zeng R, He L, Xiao T, Peng X, Kuang Z, Wu L., Free PMC Article | 03/4/2024 |
| ClC-2 and caspase-3 were induced by GDM, which resulted in apoptosis and myelination inhibition. The effect was caused by repressing PI3K-Akt signaling pathway. Application of ClC-2 inhibitor DIDS showed protective effects on cerebral white matter damage stimulated by high glucose concentration. | Activated ClC-2 Inhibits p-Akt to Repress Myelination in GDM Newborn Rats.
He F, Peng Y, Yang Z, Ge Z, Tian Y, Ma T, Li H., Free PMC Article | 11/11/2017 |
| ClC-2 is upregulated in pyramidal cells of pilocarpine-treated rats; this involves alpha5 subunit-containing GABA(A) receptor. | ClC-2 contributes to tonic inhibition mediated by α5 subunit-containing GABA(A) receptor in experimental temporal lobe epilepsy.
Ge YX, Liu Y, Tang HY, Liu XG, Wang X. | 02/4/2012 |
| GABAA receptor-mediated synaptic inputs from basket cells were modulated by ClC-2. Our data reveal a previously unknown cell type-specific regulation of intracellular chloride homeostasis in the perisomatic region of hippocampal pyramidal neurons. | Regulation of fast-spiking basket cell synapses by the chloride channel ClC-2.
Földy C, Lee SH, Morgan RJ, Soltesz I., Free PMC Article | 10/23/2010 |
| functional ClC-2-type Cl(-) channel is expressed in rat rectal surface epithelium, but channel activity may be negligible & thus nonessential for controlling electrogenic Na(+) transport in this surface epithelium under basal physiological conditions. | Functional characterization of a ClC-2-like Cl(-) conductance in surface epithelial cells of rat rectal colon.
Inagaki A, Yamaguchi S, Takahashi-Iwanaga H, Iwanaga T, Ishikawa T. | 08/2/2010 |
| The results demonstrate that rat hepatocytes express a ClC-2-like time-dependent inward Cl- channel that could provide a significant depolarizing influence in the hepatocyte. | Contribution of a time-dependent and hyperpolarization-activated chloride conductance to currents of resting and hypotonically shocked rat hepatocytes.
Lan WZ, Abbas H, Lam HD, Lemay AM, Hill CE. | 01/21/2010 |
| novel deletion variants of ClC-2 due to partial exon 15 skipping may be expressed normally in heart and contribute to the formation of endogenous Cl.ir channels in native cardiac cells | Functional characterization of novel alternatively spliced ClC-2 chloride channel variants in the heart.
Britton FC, Wang GL, Huang ZM, Ye L, Horowitz B, Hume JR, Duan D. | 01/21/2010 |
| ClC-2 may be involved in estrogen-induced Cl(-) transport in rat kidney. | Estrogen modulates ClC-2 chloride channel gene expression in rat kidney.
Nascimento DS, Reis CU, Goldenberg RC, Ortiga-Carvalho TM, Pazos-Moura CC, Guggino SE, Guggino WB, Morales MM. | 01/21/2010 |
| effect of an N-terminus deletion on voltage-dependent gating; observations are an argument against a ball-and-chain mechanism for this channel | Effect of an N-terminus deletion on voltage-dependent gating of the ClC-2 chloride channel.
Varela D, Niemeyer MI, Cid LP, Sepúlveda FV., Free PMC Article | 01/21/2010 |
| ClC-2 possesses a common gate, and part of current increase induced by hyperpolarization represents opening of common gate. Protopore gate and common gate of ClC-2 do not appear to be independent. | The voltage-dependent ClC-2 chloride channel has a dual gating mechanism.
Zúñiga L, Niemeyer MI, Varela D, Catalán M, Cid LP, Sepúlveda FV., Free PMC Article | 01/21/2010 |
| the cholesterol environment regulates ClC-2 activity; ClC-2 activity is increased in response to acute oxidative or metabolic stress involving relocalization of this channel to membrane microdomains | Membrane cholesterol content modulates ClC-2 gating and sensitivity to oxidative stress.
Hinzpeter A, Fritsch J, Borot F, Trudel S, Vieu DL, Brouillard F, Baudouin-Legros M, Clain J, Edelman A, Ollero M. | 01/21/2010 |
| Therefore, our findings suggest that the regionally specific alterations in CLC-2 immunoreactivity after SE may determine the properties of paired-pulse responses in the hippocampus of the pilocarpine-induced rat epilepsy model. | Differential paired-pulse responses between the CA1 region and the dentate gyrus are related to altered CLC-2 immunoreactivity in the pilocarpine-induced rat epilepsy model.
Kwak SE, Kim JE, Kim DS, Won MH, Lee HJ, Choi SY, Kwon OS, Kim JS, Kang TC. | 01/21/2010 |
| These results indicate that ClC-2 may not be a Cl- -transporting protein for gastric acid secretion in parietal cells. | Is the ClC-2 chloride channel involved in the Cl- secretory mechanism of gastric parietal cells?
Hori K, Takahashi Y, Horikawa N, Furukawa T, Tsukada K, Takeguchi N, Sakai H. | 01/21/2010 |
| membrane domain boundaries of purified ClC-2 and accessible cysteine residues were determined after its functional reconstitution into proteoliposomes, labelling using a thiol reagent and proteolytic digestion | Evaluation of the membrane-spanning domain of ClC-2.
Ramjeesingh M, Li C, She YM, Bear CE., Free PMC Article | 01/21/2010 |
| CLC-2 is important for fetal lung fluid production and that it may play a role in normal lung morphogenesis. | Inhibition of CLC-2 chloride channel expression interrupts expansion of fetal lung cysts.
Blaisdell CJ, Morales MM, Andrade AC, Bamford P, Wasicko M, Welling P. | 01/21/2010 |