| scholarly article | Q13442814 |
| P50 | author | Theodore R Cummins | Q90928923 |
| P2093 | author name string | Patrick L Sheets | |
| Yucheng Xiao | |||
| Brian W Jarecki | |||
| James O Jackson | |||
| P2860 | cites work | Exon organization, coding sequence, physical mapping, and polymorphic intragenic markers for the human neuronal sodium channel gene SCN8A | Q22008052 |
| The Structure of the Potassium Channel: Molecular Basis of K+ Conduction and Selectivity | Q22337058 | ||
| Structure and functional expression of a new member of the tetrodotoxin-sensitive voltage-activated sodium channel family from human neuroendocrine cells | Q24314768 | ||
| A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons | Q24546007 | ||
| SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes | Q28118877 | ||
| Molecular basis of an inherited epilepsy | Q28207595 | ||
| Paroxysmal extreme pain disorder (previously familial rectal pain syndrome) | Q28239536 | ||
| Currents related to movement of the gating particles of the sodium channels | Q28244673 | ||
| From genes to pain: Na v 1.7 and human pain disorders | Q28254063 | ||
| Expression of alternatively spliced sodium channel alpha-subunit genes. Unique splicing patterns are observed in dorsal root ganglia | Q28276370 | ||
| Functional analysis of novel KCNQ2 and KCNQ3 gene variants found in a large pedigree with benign familial neonatal convulsions (BFNC) | Q28277873 | ||
| International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels | Q28289125 | ||
| Mouse heart Na+ channels: primary structure and function of two isoforms and alternatively spliced variants | Q28504505 | ||
| Functional analysis of a voltage-gated sodium channel and its splice variant from rat dorsal root ganglia | Q28574189 | ||
| Expression pattern of neuronal and skeletal muscle voltage-gated Na+ channels in the developing mouse heart | Q28588673 | ||
| Alternative splicing within the I-II loop controls surface expression of T-type Ca(v)3.1 calcium channels | Q30437894 | ||
| Roles of tetrodotoxin (TTX)-sensitive Na+ current, TTX-resistant Na+ current, and Ca2+ current in the action potentials of nociceptive sensory neurons. | Q34160850 | ||
| Na+ channels must deactivate to recover from inactivation | Q48143852 | ||
| Ca(V)2.1 P/Q-type calcium channel alternative splicing affects the functional impact of familial hemiplegic migraine mutations: implications for calcium channelopathies | Q48727038 | ||
| Molecular determinants of emerging excitability in rat embryonic motoneurons | Q49122226 | ||
| Expression and functional characterization of the human ether-à-go-go-related gene (HERG) K+ channel cardiac splice variant in Xenopus laevis oocytes. | Q50643777 | ||
| Structural parts involved in activation and inactivation of the sodium channel | Q59072056 | ||
| Evidence for voltage-dependent S4 movement in sodium channels | Q71909065 | ||
| Alternative splicing of the Ca(v)1.3 channel IQ domain, a molecular switch for Ca2+-dependent inactivation within auditory hair cells | Q79271849 | ||
| A physical model of potassium channel activation: from energy landscape to gating kinetics | Q34181428 | ||
| Smooth muscle-selective alternatively spliced exon generates functional variation in Cav1.2 calcium channels | Q34350275 | ||
| Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. | Q34350866 | ||
| SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels | Q34426317 | ||
| Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons | Q34426737 | ||
| Alternative splicing of an insect sodium channel gene generates pharmacologically distinct sodium channels | Q34708118 | ||
| Alteration of voltage-dependence of Shaker potassium channel by mutations in the S4 sequence | Q34776692 | ||
| Inherited neuronal ion channelopathies: new windows on complex neurological diseases | Q35226085 | ||
| Evolutionary convergence of alternative splicing in ion channels | Q35752648 | ||
| Some kinetic and steady-state properties of sodium channels after removal of inactivation | Q36408465 | ||
| Deletion of the S3-S4 linker in the Shaker potassium channel reveals two quenching groups near the outside of S4 | Q36412133 | ||
| Structural implications of fluorescence quenching in the Shaker K+ channel | Q36436115 | ||
| Tracking voltage-dependent conformational changes in skeletal muscle sodium channel during activation. | Q36436547 | ||
| Histidine scanning mutagenesis of basic residues of the S4 segment of the shaker k+ channel | Q36444662 | ||
| Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade | Q36487377 | ||
| Voltage-gated sodium channels: action players with many faces | Q36652537 | ||
| Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons | Q36678533 | ||
| Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable | Q36916035 | ||
| A novel Na+ channel splice form contributes to the regulation of an androgen-dependent social signal | Q37042444 | ||
| A catalog of SCN1A variants | Q37274545 | ||
| A quantitative description of membrane current and its application to conduction and excitation in nerve. 1952. | Q37920788 | ||
| Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation | Q39965463 | ||
| Alternative splicing of Nav1.5: an electrophysiological comparison of 'neonatal' and 'adult' isoforms and critical involvement of a lysine residue. | Q39994623 | ||
| Biophysical properties of human Na v1.7 splice variants and their regulation by protein kinase A. | Q40003069 | ||
| Differential splicing patterns of L-type calcium channel Cav1.2 subunit in hearts of Spontaneously Hypertensive Rats and Wistar Kyoto Rats | Q40037183 | ||
| Voltage-gated sodium channel expression and potentiation of human breast cancer metastasis. | Q40390262 | ||
| Developmentally regulated alternative RNA splicing of rat brain sodium channel mRNAs | Q40507940 | ||
| Voltage sensors in domains III and IV, but not I and II, are immobilized by Na+ channel fast inactivation | Q41608443 | ||
| Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons | Q42169958 | ||
| Differential role of N-type calcium channel splice isoforms in pain. | Q42514056 | ||
| Slow closed-state inactivation: a novel mechanism underlying ramp currents in cells expressing the hNE/PN1 sodium channel. | Q42686664 | ||
| A fluorometric approach to local electric field measurements in a voltage-gated ion channel | Q44288096 | ||
| A mutant KcsA K(+) channel with altered conduction properties and selectivity filter ion distribution | Q44852946 | ||
| Voltage-sensing residues in the S2 and S4 segments of the Shaker K+ channel | Q46299178 | ||
| NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders. | Q46301976 | ||
| Roles of alternative splicing in the functional properties of inner ear-specific KCNQ4 channels | Q46398878 | ||
| Transmembrane movement of the shaker K+ channel S4. | Q46456961 | ||
| Calibrated measurement of gating-charge arginine displacement in the KvAP voltage-dependent K+ channel | Q46790301 | ||
| A smooth muscle Cav1.2 calcium channel splice variant underlies hyperpolarized window current and enhanced state-dependent inhibition by nifedipine | Q46966343 | ||
| Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation | Q48001757 | ||
| P433 | issue | 4 | |
| P921 | main subject | paroxysmal extreme pain disorder | Q7139588 |
| alternative mRNA splicing, via spliceosome | Q21114084 | ||
| P304 | page(s) | 259-267 | |
| P577 | publication date | 2009-07-23 | |
| P1433 | published in | Channels | Q15764469 |
| P1476 | title | Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T. | |
| P478 | volume | 3 |
| Q26744085 | Alternative RNA splicing: contribution to pain and potential therapeutic strategy |
| Q35378377 | Alternative splicing modulates inactivation of type 1 voltage-gated sodium channels by toggling an amino acid in the first S3-S4 linker |
| Q38722862 | Conservation of alternative splicing in sodium channels reveals evolutionary focus on release from inactivation and structural insights into gating |
| Q35650543 | Dissection of voltage-gated sodium channels in developing cochlear sensory epithelia |
| Q38090292 | Genes, molecules and patients--emerging topics to guide clinical pain research |
| Q24622323 | Pain as a channelopathy |
| Q42088430 | SCN1A splice variants exhibit divergent sensitivity to commonly used antiepileptic drugs |
| Q37681340 | Sodium channelopathies and pain |
| Q28728868 | Splice variants of Na(V)1.7 sodium channels have distinct β subunit-dependent biophysical properties |
| Q58764681 | The Na1.7 Channel Subtype as an Antinociceptive Target for Spider Toxins in Adult Dorsal Root Ganglia Neurons |
Search more.