scholarly journals NMR-Derived Dynamic Aspects of N-Type Inactivation of a Kv Channel Suggest a Transient Interaction with the T1 Domain

Biochemistry ◽  
2006 ◽  
Vol 45 (6) ◽  
pp. 1663-1672 ◽  
Author(s):  
Kent A. Baker ◽  
Christian Hilty ◽  
Wolfgang Peti ◽  
Alison Prince ◽  
Paul J. Pfaffinger ◽  
...  
Keyword(s):  
Kv Channel ◽  
Transient Interaction ◽  
T1 Domain

scholarly journals Gating Interactions between the Cytoplasmic T1 Domain and Pore of a Kv Channel

2013 ◽  
Vol 104 (2) ◽  
pp. 127a
Author(s):  
Brian Urbani ◽  
Manuel Covarrubias
Keyword(s):  
Kv Channel ◽  
T1 Domain

scholarly journals Role of peroxisome proliferators-activated receptor-gamma in advanced glycation end product-mediated functional loss of voltage-gated potassium channel in rat coronary arteries

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
W Li ◽  
S.D Gao ◽  
B Hua ◽  
Q.B Liu ◽  
H.R Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Funding Source ◽  
Peroxisome Proliferators ◽  
Advanced Glycation ◽  
Coronary Vasodilation ◽  
Voltage Gated ◽  
Kv Channel ◽  
Ppar Γ

Abstract Background Voltage-gated K+ (Kv) channels in coronary artery smooth muscle cells (CSMCs), especially the major specific Kv1 subfamily, contribute to coronary artery vasodilation. Advanced glycation end products (AGEs) have been strongly implicated in diabetes-related cardiovascular complications. Our previous study showed AGEs can impair Kv channel-mediated coronary vasodilation by reducing Kv channel activity. However, its underlying mechanism remains unclear. Purpose Here, we used isolated rat small coronary arteries (RSCAs) and primary CSMCs to investigate the effect of AGEs on Kv channel-mediated coronary vasodilation and the possible involvement of peroxisome proliferators-activated receptor (PPAR)-γ pathway. Methods RSCAs and primary CSMCs were isolated, cultured and treated with bovine serum albumin (BSA), AGE-BSA, alagrebrium (ALA, AGE cross-linking breaker), pioglitazone (PIO) and/or GW9662, and then divided into the following groups: DMEM, BSA, AGE, AGE+ALA, AGE+PIO, and AGE+PIO+GW9662. Kv channel-mediated coronary vasodilation was analyzed using wire myograph. Histology and immunohistochemistry of RSCAs were performed. Western blot was used to detect the protein expression of RAGE, the major Kv1 channel subunits expressed in CSMCs (Kv1.2/1.5), PPAR-γ, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (NOX-2). Results AGEs markedly reduced forskolin-induced Kv channel-mediated vasodilation of RSCAs by interacting with the receptor for AGEs (RAGE), and ALA or PIO significantly reversed this effect. In both RSCAs and primary CSMCs, AGEs decreased Kv1.2 and Kv1.5 channel protein expression, inhibited PPAR-γ expression, increased RAGE and NOX-2 expression. Treatment with ALA or PIO partially reversed the effects of AGEs on Kv1.2/Kv1.5 expression, accompanied by elevation of PPAR-γ level and diminished oxidative stress. Conclusion AGE/RAGE axis-induced inhibition of PPAR-γ pathway and enhancement of oxidative stress may contribute to AGEs-mediated Kv channel dysfunction and coronary vasodilation in RSCAs. Our results may provide new insights into developing therapeutic strategies to manage diabetic vasculature. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): National Natural Science Foundation of China; Natural Science Foundation of Beijing (7172059)

Hanging Gondola Structure of the T1 Domain in a Voltage-Gated K+Channel†

Biochemistry ◽  
2000 ◽  
Vol 39 (34) ◽  
pp. 10347-10352 ◽  
Author(s):  
William R. Kobertz ◽  
Carole Williams ◽  
Christopher Miller
Keyword(s):  
K Channel ◽  
Voltage Gated ◽  
T1 Domain

Poly(Adp-Ribose) Drives Condensation of Fus Via a Transient Interaction

2021 ◽  
Author(s):  
Kevin Rhine ◽  
Morgan Dasovich ◽  
Joseph Yoniles ◽  
Mohsen Badiee ◽  
Sophie Skanchy ◽  
...  
Keyword(s):  
Transient Interaction

scholarly journals The T1 Domain is not the Only Determinant of the Obligatory KV2.1/KV6.4 Heterotetramerization

2011 ◽  
Vol 100 (3) ◽  
pp. 348a
Author(s):  
Elke Bocksteins ◽  
Evy Mayeur ◽  
Tine Bruyns ◽  
Dirk J. Snyders
Keyword(s):  
T1 Domain

scholarly journals Zinc Mediates Assembly of the T1 Domain of the Voltage-gated K Channel 4.2

2002 ◽  
Vol 277 (49) ◽  
pp. 47885-47890 ◽  
Author(s):  
Alex W. Jahng ◽  
Candace Strang ◽  
Don Kaiser ◽  
Thomas Pollard ◽  
Paul Pfaffinger ◽  
...  
Keyword(s):  
K Channel ◽  
Voltage Gated ◽  
T1 Domain

The role of K-channels in the formation of a nociceptive signal in the rat trigeminal nerve

2021 ◽  
Author(s):  
A.D. Buglinina ◽  
T.M. Verkhoturova ◽  
O.Sh. Gafurov ◽  
K.S. Koroleva ◽  
G.F. Sitdikova
Keyword(s):  
Key Words ◽  
Trigeminal Nerve ◽  
Key Words Migraine ◽  
K Channels ◽  
Kv Channel ◽  
Inflammatory Agent ◽  
Kv Channels ◽  
Pain Signal ◽  
Isolated Rat

The central problem of this work is to elucidate the mechanisms of pain in migraine and to establish the role of Kv channels in regulating the excitability of meningeal afferents of the trigeminal nerve that form a pain signal in migraine. The study was conducted on a preparation of an isolated rat skull. It was found that Kv-channel inhibitors 4-aminopyridine (100 microns and 1 mM) and tetraethylammonium (5mm) lead to an increase in the excitability of trigeminal nerve afferents, at the same time, this effect was partially removed by a nonsteroidal anti–inflammatory agent - naproxen, and was not sensitive to sumatriptan, a classic anti-migraine drug. Key words: migraine, K-channels, trigeminal nerve, 4-aminopyridine, tetraethylammonium, naproxen, sumatriptan.

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