| P2093 | author name string | Frank Lehmann-Horn | |
| | Karin Jurkat-Rott | |
| | James R Groome | |
| | Vern Winston | |
| | Landon Bayless-Edwards | |
| | Paula Arinze | |
| P2860 | cites work | A quantitative description of membrane current and its application to conduction and excitation in nerve | Q22337072 |
| | Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels | Q24531491 |
| | Water wires in atomistic models of the Hv1 proton channel | Q24618339 |
| | A Gating Charge Transfer Center in Voltage Sensors | Q27660396 |
| | Channelopathies of skeletal muscle excitability | Q28082428 |
| | A calcium channel mutation causing hypokalemic periodic paralysis | Q28242375 |
| | Hypokalemic periodic paralysis: In vitro investigation of muscle fiber membrane parameters | Q28265960 |
| | Voltage sensor charge loss accounts for most cases of hypokalemic periodic paralysis | Q33763782 |
| | Extracellular potassium homeostasis: insights from hypokalemic periodic paralysis | Q34039490 |
| | An atypical phenotype of hypokalemic periodic paralysis caused by a mutation in the sodium channel gene SCN4A. | Q34417442 |
| | An expanding view for the molecular basis of familial periodic paralysis | Q34738564 |
| | Leaky sodium channels from voltage sensor mutations in periodic paralysis, but not paramyotonia | Q34999202 |
| | Gating pore currents are defects in common with two Nav1.5 mutations in patients with mixed arrhythmias and dilated cardiomyopathy | Q35014373 |
| | Voltage-sensor sodium channel mutations cause hypokalemic periodic paralysis type 2 by enhanced inactivation and reduced current | Q35208537 |
| | Defective fast inactivation recovery of Nav 1.4 in congenital myasthenic syndrome. | Q35878466 |
| | Pathophysiological role of omega pore current in channelopathies | Q36022793 |
| | A Na+ channel mutation linked to hypokalemic periodic paralysis exposes a proton-selective gating pore | Q36299707 |
| | Coupling interactions between voltage sensors of the sodium channel as revealed by site-specific measurements | Q36412534 |
| | Gating pore currents and the resting state of Nav1.4 voltage sensor domains | Q36436974 |
| | Resting potential-dependent regulation of the voltage sensitivity of sodium channel gating in rat skeletal muscle in vivo | Q36493507 |
| | A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis. | Q36516769 |
| | Gating pore currents in DIIS4 mutations of NaV1.4 associated with periodic paralysis: saturation of ion flux and implications for disease pathogenesis | Q36908941 |
| | Depolarization-activated gating pore current conducted by mutant sodium channels in potassium-sensitive normokalemic periodic paralysis | Q37018940 |
| | Domain IV voltage-sensor movement is both sufficient and rate limiting for fast inactivation in sodium channels. | Q37055488 |
| | K+-dependent paradoxical membrane depolarization and Na+ overload, major and reversible contributors to weakness by ion channel leaks | Q37102151 |
| | A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation | Q37301303 |
| | NaV1.4 mutations cause hypokalaemic periodic paralysis by disrupting IIIS4 movement during recovery | Q37647775 |
| | Voltage-sensor mutations in channelopathies of skeletal muscle | Q37692699 |
| | Biophysics, pathophysiology, and pharmacology of ion channel gating pores | Q38207583 |
| | Sodium channel inactivation defects are associated with acetazolamide-exacerbated hypokalemic periodic paralysis | Q40780362 |
| | Mutant channels contribute <50% to Na+ current in paramyotonia congenita muscle | Q40950898 |
| | Sodium channel mutations in paramyotonia congenita uncouple inactivation from activation | Q41491359 |
| | Mechanisms Responsible for ω-Pore Currents in Cav Calcium Channel Voltage-Sensing Domains. | Q47131974 |
| | In situ immune response and mechanisms of cell damage in central nervous system of fatal cases microcephaly by Zika virus | Q47557035 |
| | Substitutions of the S4DIV R2 residue (R1451) in NaV1.4 lead to complex forms of paramyotonia congenita and periodic paralyses | Q48120363 |
| | Structure of a eukaryotic voltage-gated sodium channel at near-atomic resolution | Q48255148 |
| | Gating pore current in an inherited ion channelopathy | Q48799799 |
| | Human Na+ channel fast and slow inactivation in paramyotonia congenita mutants expressed in Xenopus laevis oocytes | Q48960709 |
| | Spider toxin inhibits gating pore currents underlying periodic paralysis. | Q52325902 |
| | A novel Ile1455Thr variant in the skeletal muscle sodium channel alpha-subunit in a patient with a severe adult-onset proximal myopathy with electrical myotonia and a patient with mild paramyotonia phenotype. | Q52809834 |
| | Paradoxical depolarization of BA2+- treated muscle exposed to low extracellular K+: insights into resting potential abnormalities in hypokalemic paralysis. | Q53556880 |
| | Putting the squeeze on superconductivity. | Q53752232 |
| | A defect in skeletal muscle sodium channel deactivation exacerbates hyperexcitability in human paramyotonia congenita | Q74315934 |
| | [The mutation R672H in SCN4A gene exists in Chinese patients with hypokalaemic periodic paralysis] | Q83303458 |
| P433 | issue | 1 | |
| P921 | main subject | periodic paralysis | Q1788314 |
| P304 | page(s) | 10372 | |
| P577 | publication date | 2018-07-10 | |
| P1433 | published in | Scientific Reports | Q2261792 |
| P1476 | title | NaV1.4 DI-S4 periodic paralysis mutation R222W enhances inactivation and promotes leak current to attenuate action potentials and depolarize muscle fibers | |
| P478 | volume | 8 | |