| TRESK channel contributes to depolarization-induced shunting inhibition and modulates epileptic seizures. | TRESK channel contributes to depolarization-induced shunting inhibition and modulates epileptic seizures.
Huang W, Ke Y, Zhu J, Liu S, Cong J, Ye H, Guo Y, Wang K, Zhang Z, Meng W, Gao TM, Luhmann HJ, Kilb W, Chen R. | 02/12/2022 |
| TRESK Regulates Gm11874 to Induce Apoptosis of Spinal Cord Neurons via ATP5i Mediated Oxidative Stress and DNA Damage. | TRESK Regulates Gm11874 to Induce Apoptosis of Spinal Cord Neurons via ATP5i Mediated Oxidative Stress and DNA Damage.
Liu P, Cheng Y, Xu H, Huang H, Tang S, Song F, Zhou J. | 10/23/2021 |
| Upregulation of TRESK Channels Contributes to Motor and Sensory Recovery after Spinal Cord Injury. | Upregulation of TRESK Channels Contributes to Motor and Sensory Recovery after Spinal Cord Injury.
Kim GT, Siregar AS, Kim EJ, Lee ES, Nyiramana MM, Woo MS, Hah YS, Han J, Kang D., Free PMC Article | 03/6/2021 |
| TRESK and TREK-2 two-pore-domain potassium channel subunits form functional heterodimers in primary somatosensory neurons. | TRESK and TREK-2 two-pore-domain potassium channel subunits form functional heterodimers in primary somatosensory neurons.
Lengyel M, Czirják G, Jacobson DA, Enyedi P., Free PMC Article | 01/23/2021 |
| TRESK is a key regulator of nocturnal suprachiasmatic nucleus dynamics and light adaptive responses. | TRESK is a key regulator of nocturnal suprachiasmatic nucleus dynamics and light adaptive responses.
Lalic T, Steponenaite A, Wei L, Vasudevan SR, Mathie A, Peirson SN, Lall GS, Cader MZ., Free PMC Article | 09/26/2020 |
| Findings indicate that endogenous TWIK-related spinal cord K(+) (TRESK) activity regulates trigeminal nociception, likely through controlling the intrinsic excitability of trigeminal ganglia nociceptors. | TRESK K(+) Channel Activity Regulates Trigeminal Nociception and Headache.
Guo Z, Qiu CS, Jiang X, Zhang J, Li F, Liu Q, Dhaka A, Cao YQ., Free PMC Article | 03/7/2020 |
| We compared the kinetics of Ba2+ block when channels were phosphorylated (inhibited) or dephosphorylated (activated) and in different mutants mimicking the two functional states. Neither the phosphorylation/dephosphorylation nor the point mutations influenced the development of Ba2+ block, suggesting that conformational changes of the bundle crossing region do not contribute to phosphorylation-dependent gating of TRESK. | TRESK background potassium channel is not gated at the helix bundle crossing near the cytoplasmic end of the pore.
Lengyel M, Czirják G, Enyedi P., Free PMC Article | 12/22/2018 |
| Migraine-associated TRESK mutation, but not the C110R variant, reduces the endogenous TRESK currents to a degree that affects trigeminal ganglion neuron excitability | Nonmigraine-associated TRESK K+ channel variant C110R does not increase the excitability of trigeminal ganglion neurons.
Guo Z, Liu P, Ren F, Cao YQ., Free PMC Article | 04/11/2015 |
| Identification of blocker binding site in mouse TRESK by molecular modeling and mutational studies | Identification of blocker binding site in mouse TRESK by molecular modeling and mutational studies.
Kim S, Lee Y, Tak HM, Park HJ, Sohn YS, Hwang S, Han J, Kang D, Lee KW. | 04/13/2013 |
| a role for TRESK in the pathogenesis of typical migraine with aura. | A dominant-negative mutation in the TRESK potassium channel is linked to familial migraine with aura.
Lafrenière RG, Cader MZ, Poulin JF, Andres-Enguix I, Simoneau M, Gupta N, Boisvert K, Lafrenière F, McLaughlan S, Dubé MP, Marcinkiewicz MM, Ramagopalan S, Ansorge O, Brais B, Sequeiros J, Pereira-Monteiro JM, Griffiths LR, Tucker SJ, Ebers G, Rouleau GA. | 11/6/2010 |
| single residue of TRESK was found to be glycosylated upon heterologous expression. Signals of the N-glycosylation mutants were reduced by >50% because of inadequate surface expression of the channel. | N-linked glycosylation determines cell surface expression of two-pore-domain K+ channel TRESK.
Egenberger B, Polleichtner G, Wischmeyer E, Döring F. | 03/15/2010 |
| Because 14-3-3 proteins are ubiquitous, they are expected to control the duration of calcineurin-mediated TRESK activation in all the cell types that express the channel, depending on the phosphorylation state of serine 264. | Phosphorylation-dependent binding of 14-3-3 proteins controls TRESK regulation.
Czirják G, Vuity D, Enyedi P., Free PMC Article | 01/21/2010 |
| we found no difference in resting membrane potential between dorsal root ganglia neurones of TRESK[wild type] and TRESK knockout mice | TRESK two-pore-domain K+ channels constitute a significant component of background potassium currents in murine dorsal root ganglion neurones.
Dobler T, Springauf A, Tovornik S, Weber M, Schmitt A, Sedlmeier R, Wischmeyer E, Döring F., Free PMC Article | 01/21/2010 |
| the PQIVID sequence is a docking site for calcineurin, and its occupancy is required for the calcium-dependent regulation of TRESK | Targeting of calcineurin to an NFAT-like docking site is required for the calcium-dependent activation of the background K+ channel, TRESK.
Czirják G, Enyedi P. | 01/21/2010 |
| TRESK-2 is a functional member of the K(2P) channel family and contributes to the background K+ conductance in many types of cells [TRESK-2] | Functional expression of TRESK-2, a new member of the tandem-pore K+ channel family.
Kang D, Mariash E, Kim D. | 01/21/2010 |