UB Paderborn / Katalog / Suche / in CDI

1 – 25 von 116

Sortiert nach

Safety and efficacy of a Nav1.7 selective sodium channel blocker in patients with trigeminal neuralgia: a double-blind, placebo-controlled, randomised withdrawal phase 2a trial

Lancet neurology, 2017-04, Vol.16 (4), p.291-300

2017

Link zum Volltext

Verfügbarkeit prüfen

Gain-of-function mutations in sodium channel Nav1.9 in painful neuropathy

Brain (London, England : 1878), 2014-06, Vol.137 (6), p.1627-1642

2014

Link zum Volltext

Verfügbarkeit prüfen

Inhibition of sodium conductance by cannabigerol contributes to a reduction of dorsal root ganglion neuron excitability

British journal of pharmacology, 2022-08, Vol.179 (15), p.4010-4030

2022

Link zum Volltext

Verfügbarkeit prüfen

Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy

Annals of neurology, 2012-01, Vol.71 (1), p.26-39

2012

Link zum Volltext

Verfügbarkeit prüfen

Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models

Pain (Amsterdam), 2020-04, Vol.161 (4), p.831-841

2020

Link zum Volltext

Verfügbarkeit prüfen

A novel de novo mutation of SCN8A (Nav 1.6) with enhanced channel activation in a child with epileptic encephalopathy

Neurobiology of disease, 2014-09, Vol.69, p.117-123

2014

Link zum Volltext

Verfügbarkeit prüfen

Kv7-specific activators hyperpolarize resting membrane potential and modulate human iPSC-derived sensory neuron excitability

Frontiers in pharmacology, 2023-02, Vol.14, p.1138556-1138556

2023

Link zum Volltext

Verfügbarkeit prüfen

Contributions of NaV1.8 and NaV1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons

Scientific reports, 2021-12, Vol.11 (1), p.24283-24283, Article 24283

2021

Link zum Volltext

Verfügbarkeit prüfen

A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons

Experimental neurology, 2010-08, Vol.224 (2), p.362-368

2010

Link zum Volltext

Verfügbarkeit prüfen

A Novel Gain-of-Function Nav1.9 Mutation in a Child With Episodic Pain

Frontiers in neuroscience, 2019-09, Vol.13, p.918-918

2019

Link zum Volltext

Verfügbarkeit prüfen

Lacosamide Inhibition of NaV1.7 Channels Depends on its Interaction With the Voltage Sensor Domain and the Channel Pore

Frontiers in pharmacology, 2021-12, Vol.12, p.791740-791740

2021

Link zum Volltext

Verfügbarkeit prüfen

Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation

Scientific reports, 2018-01, Vol.8 (1), p.1-13, Article 1811

2018

Link zum Volltext

Verfügbarkeit prüfen

Identification and localization of TRPC channels in the rat kidney

American journal of physiology. Renal physiology, 2006-05, Vol.290 (5), p.F1241-F1252

2006

Link zum Volltext

Verfügbarkeit prüfen

Human TRPC6 expressed in HEK 293 cells forms non-selective cation channels with limited Ca2+ permeability

The Journal of physiology, 2006-04, Vol.572 (2), p.359-377

2006

Link zum Volltext

Verfügbarkeit prüfen

Association of Immunophilins with Mammalian TRPC Channels

The Journal of biological chemistry, 2004-08, Vol.279 (33), p.34521-34529

2004

Link zum Volltext

Verfügbarkeit prüfen

Effects of Ranolazine on Wild-Type and Mutant hNav1.7 Channels and on DRG Neuron Excitability

Molecular pain, 2010-06, Vol.6 (1), p.35-35

2010

Link zum Volltext

Verfügbarkeit prüfen

Palytoxin-induced cell death cascade in bovine aortic endothelial cells

American Journal of Physiology: Cell Physiology, 2006-10, Vol.291 (4), p.C657-C667

2006

Link zum Volltext

Verfügbarkeit prüfen

Activation of Human TRPC6 Channels by Receptor Stimulation

The Journal of biological chemistry, 2004-05, Vol.279 (21), p.22047-22056

2004

Link zum Volltext

Verfügbarkeit prüfen

Regulation of Drosophila transient receptor potential-like (TrpL) channels by phospholipase C-dependent mechanisms

The Journal of physiology, 2001-01, Vol.530 (1), p.1-19

2001

Link zum Volltext

Verfügbarkeit prüfen

Cannabigerol inhibits sodium conductance to reduce neuronal dorsal root ganglion excitability

Biophysical journal, 2022-02, Vol.121 (3), p.93a-93a

2022

Link zum Volltext

Verfügbarkeit prüfen

Regulation of Drosophila TRPL Channels by Immunophilin FKBP59

The Journal of biological chemistry, 2001-10, Vol.276 (42), p.38762-38773

2001

Link zum Volltext

Verfügbarkeit prüfen

Gain-of-function mutations in sodium channel Na(v)1.9 in painful neuropathy

Brain (London, England : 1878), 2014-06, Vol.137 (Pt 6), p.1627-1642

2014

Link zum Volltext

Verfügbarkeit prüfen

Nonlinear effects of hyperpolarizing shifts in activation of mutant Nav1.7 channels on resting membrane potential

Journal of neurophysiology, 2017-04, Vol.117 (4), p.1702-1712

2017

Link zum Volltext

Verfügbarkeit prüfen

Fibroblast growth factor homologous factor 2 attenuates excitability of DRG neurons

Journal of neurophysiology, 2022-11, Vol.128 (5), p.1258-1266

2022

Link zum Volltext

Verfügbarkeit prüfen

1 – 25 von 116

Suche als RSS-Feed

Suchergebnisse filtern

Filter anzeigen

Nur zeigen

Geprüft (Peer-Review)
(115)
Mit Volltextzugriff
(111)

Publikationsform

Artikel
(115)
Dissertationen
(1)

Sprache

Englisch
(116)
Japanisch
(14)

Erscheinungsjahr

n.n

Thema

Science & Technology
(44)
Life Sciences & Biomedicine
(41)
Humans
(40)
Animals
(37)
Pain
(22)
Neurosciences
(21)
Mutation
(19)
Neurosciences & Neurology
(19)
Patch-Clamp Techniques
(19)
Mice
(15)
Sodium Channels
(15)
Physiology
(14)
Rats
(14)
Nav1.7 Voltage-Gated Sodium Channel - Genetics
(13)
Biochemistry & Molecular Biology
(12)
Biological And Medical Sciences
(12)
Cell Line
(12)
Electrophysiology
(12)
Female
(12)
Hek293 Cells
(12)

15 weitere anzeigen...

Weniger anzeigen...

Menü

Weitere Dienste

Einstellungen

Safety and efficacy of a Nav1.7 selective sodium channel blocker in patients with trigeminal neuralgia: a double-blind, placebo-controlled, randomised withdrawal phase 2a trial

Gain-of-function mutations in sodium channel Nav1.9 in painful neuropathy

Inhibition of sodium conductance by cannabigerol contributes to a reduction of dorsal root ganglion neuron excitability

Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy

Subtype-Selective Small Molecule Inhibitors Reveal a Fundamental Role for Nav1.7 in Nociceptor Electrogenesis, Axonal Conduction and Presynaptic Release

Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models

A novel de novo mutation of SCN8A (Nav 1.6) with enhanced channel activation in a child with epileptic encephalopathy

Kv7-specific activators hyperpolarize resting membrane potential and modulate human iPSC-derived sensory neuron excitability

Contributions of NaV1.8 and NaV1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons

A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons

A Novel Gain-of-Function Nav1.9 Mutation in a Child With Episodic Pain

Lacosamide Inhibition of NaV1.7 Channels Depends on its Interaction With the Voltage Sensor Domain and the Channel Pore

Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation

Identification and localization of TRPC channels in the rat kidney

Human TRPC6 expressed in HEK 293 cells forms non-selective cation channels with limited Ca2+ permeability

Association of Immunophilins with Mammalian TRPC Channels

Effects of Ranolazine on Wild-Type and Mutant hNav1.7 Channels and on DRG Neuron Excitability

Palytoxin-induced cell death cascade in bovine aortic endothelial cells

Activation of Human TRPC6 Channels by Receptor Stimulation

Regulation of Drosophila transient receptor potential-like (TrpL) channels by phospholipase C-dependent mechanisms

Cannabigerol inhibits sodium conductance to reduce neuronal dorsal root ganglion excitability

Regulation of Drosophila TRPL Channels by Immunophilin FKBP59

Gain-of-function mutations in sodium channel Na(v)1.9 in painful neuropathy

Nonlinear effects of hyperpolarizing shifts in activation of mutant Nav1.7 channels on resting membrane potential

Fibroblast growth factor homologous factor 2 attenuates excitability of DRG neurons

Suchergebnisse filtern