Pages that link to "Q34426317"
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The following pages link to SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels (Q34426317):
Displaying 50 items.
- Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7 (Q21203947) (← links)
- A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons (Q24546007) (← links)
- A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity (Q24679655) (← links)
- Genetic predictors of human chronic pain conditions (Q26753046) (← links)
- Pain perception is altered by a nucleotide polymorphism in SCN9A (Q33739909) (← links)
- Association of rare missense variants in the second intracellular loop of NaV1.7 sodium channels with familial autism (Q33790438) (← links)
- Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T. (Q33796526) (← links)
- Challenges in the development of novel treatment strategies for neuropathic pain (Q33947001) (← links)
- A nonsense mutation in the SCN9A gene in congenital insensitivity to pain (Q34263684) (← links)
- Size matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating (Q34569783) (← links)
- A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers (Q34576217) (← links)
- Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders (Q34585790) (← links)
- Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons. (Q34585853) (← links)
- The roles of sodium channels in nociception: Implications for mechanisms of pain (Q34674268) (← links)
- Massage therapy techniques as pain management for erythromelalgia: a case report (Q34936531) (← links)
- Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7. (Q35642815) (← links)
- Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons (Q36091952) (← links)
- Imaging the neural correlates of neuropathic pain and pleasurable relief associated with inherited erythromelalgia in a single subject with quantitative arterial spin labelling. (Q36223860) (← links)
- Network topology of NaV1.7 mutations in sodium channel-related painful disorders. (Q36290427) (← links)
- Human monogenic disorders - a source of novel drug targets (Q36420699) (← links)
- Infrequent SCN9A mutations in congenital insensitivity to pain and erythromelalgia. (Q36674682) (← links)
- Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons (Q36678533) (← links)
- Compound heterozygosity in sodium channel Nav1.7 in a family with hereditary erythermalgia (Q36727094) (← links)
- Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable (Q36916035) (← links)
- Advanced Genetic Testing Comes to the Pain Clinic to Make a Diagnosis of Paroxysmal Extreme Pain Disorder (Q37150552) (← links)
- Nature and nurture of human pain (Q37287580) (← links)
- Genetics and molecular pathophysiology of Na(v)1.7-related pain syndromes (Q37382551) (← links)
- Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation. (Q37511682) (← links)
- Sodium channelopathies and pain (Q37681340) (← links)
- Pain Disorders and Erythromelalgia Caused by Voltage-Gated Sodium Channel Mutations (Q37943756) (← links)
- Advances in targeting voltage-gated sodium channels with small molecules (Q38040330) (← links)
- Validating therapeutic targets through human genetics (Q38122628) (← links)
- Mutational consequences of aberrant ion channels in neurological disorders (Q38239544) (← links)
- The role of sodium channels in painful diabetic and idiopathic neuropathy. (Q38241746) (← links)
- Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use. (Q38260278) (← links)
- Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation (Q39965463) (← links)
- Distribution of the voltage-gated sodium channel Na(v)1.7 in the rat: expression in the autonomic and endocrine systems. (Q40089012) (← links)
- A stop codon mutation in SCN9A causes lack of pain sensation (Q40114322) (← links)
- Extending the clinical spectrum of pain channelopathies (Q41210428) (← links)
- Sodium channel slow inactivation interferes with open channel block (Q41505443) (← links)
- Expression of Nav1.7 in DRG neurons extends from peripheral terminals in the skin to central preterminal branches and terminals in the dorsal horn (Q41901986) (← links)
- Hansen's disease associated with erythromelalgia mimicking Lupus erythematosus (Q41983879) (← links)
- Erythromelalgia mutation Q875E Stabilizes the activated state of sodium channel Nav1.7. (Q42249654) (← links)
- Genistein inhibits voltage-gated sodium currents in SCG neurons through protein tyrosine kinase-dependent and kinase-independent mechanisms (Q42524127) (← links)
- 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) (← links)
- Autonomic dysfunction in SCN9A-associated primary erythromelalgia (Q46980912) (← links)
- Depolarized inactivation overcomes impaired activation to produce DRG neuron hyperexcitability in a Nav1.7 mutation in a patient with distal limb pain. (Q48215989) (← links)
- Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy. (Q48430447) (← links)
- A case of primary erythermalgia with encephalopathy (Q48567290) (← links)
- Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation. (Q48686306) (← links)