scholarly journals Regulation of Kvl channel trafficking by the mamba snake neurotoxin dendrotoxin K

2006 ◽  
Vol 21 (3) ◽  
pp. 906-914 ◽  
Author(s):  
Helene Vacher ◽  
Durga P. Mohapatra ◽  
Hiroaki Misonou ◽  
James S. Trimmer
Keyword(s):  
Channel Trafficking ◽  
Snake Neurotoxin

scholarly journals Synthetic Alkyl-Ether-lipid promotes TRPV2 Channel trafficking trough PI3K/Akt-Girdin Axis in cancer cells and increases mammary tumor volume

Cell Calcium ◽  
2021 ◽  
pp. 102435
Author(s):  
Maxime Guéguinou ◽  
Romain Felix ◽  
Séverine Marionneau-Lambot ◽  
Thibault Oullier ◽  
Aubin Penna ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Mammary Tumor ◽  
Tumor Volume ◽  
Ether Lipid ◽  
Alkyl Ether ◽  
Channel Trafficking

scholarly journals AKAP79/150 coordinates leptin-induced PKA signaling to regulate KATP channel trafficking in pancreatic β-cells

2021 ◽  
pp. 100442
Author(s):  
Veronica A. Cochrane ◽  
Zhongying Yang ◽  
Mark L. Dell’Acqua ◽  
Show-Ling Shyng
Keyword(s):  
Katp Channel ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Channel Trafficking

scholarly journals Long-QT founder variant T309I-Kv7.1 with dominant negative pattern may predispose delayed afterdepolarizations under β-adrenergic stimulation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Iva Synková ◽  
Markéta Bébarová ◽  
Irena Andršová ◽  
Larisa Chmelikova ◽  
Olga Švecová ◽  
...  
Keyword(s):  
Calcium Current ◽  
Cell Model ◽  
Dominant Negative ◽  
Qtc Interval ◽  
Adrenergic Stimulation ◽  
Patch Clamp Technique ◽  
Long Qt ◽  
Channel Trafficking ◽  
Whole Cell Patch Clamp ◽  
Delayed Afterdepolarizations

AbstractThe variant c.926C > T (p.T309I) in KCNQ1 gene was identified in 10 putatively unrelated Czech families with long QT syndrome (LQTS). Mutation carriers (24 heterozygous individuals) were more symptomatic compared to their non-affected relatives (17 individuals). The carriers showed a mild LQTS phenotype including a longer QTc interval at rest (466 ± 24 ms vs. 418 ± 20 ms) and after exercise (508 ± 32 ms vs. 417 ± 24 ms), 4 syncopes and 2 aborted cardiac arrests. The same haplotype associated with the c.926C > T variant was identified in all probands. Using the whole cell patch clamp technique and confocal microscopy, a complete loss of channel function was revealed in the homozygous setting, caused by an impaired channel trafficking. Dominant negativity with preserved reactivity to β-adrenergic stimulation was apparent in the heterozygous setting. In simulations on a human ventricular cell model, the dysfunction resulted in delayed afterdepolarizations (DADs) and premature action potentials under β-adrenergic stimulation that could be prevented by a slight inhibition of calcium current. We conclude that the KCNQ1 variant c.926C > T is the first identified LQTS-related founder mutation in Central Europe. The dominant negative channel dysfunction may lead to DADs under β-adrenergic stimulation. Inhibition of calcium current could be possible therapeutic strategy in LQTS1 patients refractory to β-blocker therapy.

CACNA1A mutations causing episodic and progressive ataxia alter channel trafficking and kinetics

Neurology ◽  
2005 ◽  
Vol 64 (12) ◽  
pp. 2090-2097 ◽  
Author(s):  
J. Wan ◽  
R. Khanna ◽  
M. Sandusky ◽  
D. M. Papazian ◽  
J. C. Jen ◽  
...  
Keyword(s):  
Channel Trafficking ◽  
Progressive Ataxia

Abstract 63: Potential Genetic and Pharmacological Protection from Virus-induced Ventricular Arrhythmias and Sudden Cardiac Death

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Nathalie Strutz-eebohm ◽  
Katja Steinke ◽  
Ulrike Henrion ◽  
Matthias Rohbeck ◽  
Karin Klingel ◽  
...  
Keyword(s):  
Ion Channels ◽  
Sudden Cardiac Death ◽  
Action Potentials ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Proper Function ◽  
Channel Trafficking ◽  
Cardiac Ion Channels ◽  
Evolutionary Advantage ◽  
Group B

In patients as well as in mouse models, enteroviral infections, especially Coxsackie group B viruses (CVB1-6), frequently induce ventricular arrhythmias and sudden cardiac death. The cardiac action potential requires proper function of cardiac ion channels. CVB3 alters Kv7.1 channel trafficking potentially leading to changes in action potentials and increasing likelihood of arrhythmias. Genetic variants of cardiac ion channels can cause changes in channel trafficking that may preserve from CVB3 modulations and present an evolutionary advantage. Here, we show that a common polymorphic Kv7.1 channel variant uses alternative trafficking pathways and may thus exert a benefit during CVB3 infections. Genetic and pharmacological disruption of a CVB3-stimulated Serum- and Glucocorticoid inducible Kinase 1 (SGK1) pathways blunts Kv7.1 channel dysfunctions. Our results suggest that escape from CVB3-induced SGK1-stimulation by genetic variation in Kv7.1 may be protective and inhibition of SGK1 may present a pharmacological approach to reduce the pro-arrhythmic risk associated with acute coxsackievirus infections.

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