scholarly journals A Novel Leg-Shaking Drosophila Mutant Defective in a Voltage-Gated K+ Current and Hypersensitive to Reactive Oxygen Species

2000 ◽  
Vol 20 (16) ◽  
pp. 5958-5964 ◽  
Author(s):  
Jing W. Wang ◽  
James M. Humphreys ◽  
John P. Phillips ◽  
Arthur J. Hilliker ◽  
Chun-Fang Wu
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Voltage Gated ◽  
K Current ◽  
Drosophila Mutant

scholarly journals Extracellular Phosphate Is an Endogenous Regulator for Voltage-Gated Proton Channels and Production of Reactive Oxygen Species in Osteoclasts

2018 ◽  
Vol 114 (3) ◽  
pp. 305a
Author(s):  
Guangshuai Li ◽  
Katsuuki Miura ◽  
Yoshiko Hino ◽  
Yoshie Moriura ◽  
Junko Kawawaki ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Proton Channels ◽  
Voltage Gated ◽  
Endogenous Regulator

scholarly journals Sphingosylphosphorylcholine potentiates vasoreactivity and voltage-gated Ca2+ entry via NOX1 and reactive oxygen species

2015 ◽  
Vol 106 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Yasin Shaifta ◽  
Vladimir A. Snetkov ◽  
Jesus Prieto-Lloret ◽  
Greg A. Knock ◽  
Sergey V. Smirnov ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Voltage Gated

scholarly journals Kv1.3 voltage-gated potassium channels link cellular respiration to proliferation through a non-conducting mechanism

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Faye L. Styles ◽  
Moza M. Al-Owais ◽  
Jason L. Scragg ◽  
Eulashini Chuntharpursat-Bon ◽  
Nishani T. Hettiarachchi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cellular Proliferation ◽  
Reactive Oxygen ◽  
High Energy ◽  
Metabolic Reprogramming ◽  
Cellular Respiration ◽  
Oxygen Species ◽  
Voltage Gated ◽  
Conducting Mechanism ◽  
Kv1.3 Channels

AbstractCellular energy metabolism is fundamental for all biological functions. Cellular proliferation requires extensive metabolic reprogramming and has a high energy demand. The Kv1.3 voltage-gated potassium channel drives cellular proliferation. Kv1.3 channels localise to mitochondria. Using high-resolution respirometry, we show Kv1.3 channels increase oxidative phosphorylation, independently of redox balance, mitochondrial membrane potential or calcium signalling. Kv1.3-induced respiration increased reactive oxygen species production. Reducing reactive oxygen concentrations inhibited Kv1.3-induced proliferation. Selective Kv1.3 mutation identified that channel-induced respiration required an intact voltage sensor and C-terminal ERK1/2 phosphorylation site, but is channel pore independent. We show Kv1.3 channels regulate respiration through a non-conducting mechanism to generate reactive oxygen species which drive proliferation. This study identifies a Kv1.3-mediated mechanism underlying the metabolic regulation of proliferation, which may provide a therapeutic target for diseases characterised by dysfunctional proliferation and cell growth.

scholarly journals Endogenous reactive oxygen species modulates voltage-gated sodium channels in dorsal root ganglia of rats

2011 ◽  
Vol 110 (5) ◽  
pp. 1439-1447 ◽  
Author(s):  
Han-Jun Wang ◽  
Yu-Long Li ◽  
Li-Bin Zhang ◽  
Irving H. Zucker ◽  
Lie Gao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Pressor Response ◽  
Reactive Oxygen ◽  
Muscle Afferents ◽  
Transient Receptor Potential Vanilloid ◽  
Oxygen Species ◽  
Patch Clamp Technique ◽  
Voltage Gated

We recently reported that reactive oxygen species (ROS) plays an excitatory role in modulation of the exercise pressor reflex (EPR) in normal rats. In this study, we further tested two independent hypotheses: 1) ROS interacts with EPR-related ionotropic receptors such as the purinergic receptors (P2) and transient receptor potential vanilloid 1 receptors (TRPV1) to indirectly modulate the EPR function; 2) ROS directly affects excitability of muscle afferents by modulating the voltage-gated sodium (Nav) channels. To test the first hypothesis, we performed animal experiments to investigate the effect of the SOD mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidine 1-oxyl (Tempol) on the pressor response to hindlimb intra-arterial (IA) injection of either α,β-methylene ATP (a P2X agonist) or capsaicin (a TRPV1 agonist) in decerebrate rats. To test the second hypothesis, we used the patch-clamp technique to determine the effect of ROS on Nav channels on the soma of muscle afferents. We also performed local microinjection of a sodium channel blocker, tetrodotoxin (TTX), into ipsilateral L4/L5 dorsal root ganglia (DRGs) to investigate whether the blockade of Nav channels by TTX affects the EPR function. We found that Tempol did not affect the pressor response to injection of either capsaicin or α,β-methylene ATP but significantly decreased the Nav current in small and medium-sized 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate (DiI)-labeled DRG neurons. A membrane-permeant superoxide dismutase, polyethylene glycol (PEG)-SOD, had an effect on the Nav current in these neurons similar to that of Tempol. Microinjection of TTX into L4/L5 DRGs dramatically attenuated the pressor response to static contraction induced by electrical stimulation of L4/L5 ventral roots. These data suggest that ROS modulates the EPR by affecting the activity of the Nav channels on muscle afferents.

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