Pages that link to "Q28569751"
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The following pages link to Identification of PN1, a predominant voltage-dependent sodium channel expressed principally in peripheral neurons (Q28569751):
Displaying 50 items.
- Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7 (Q21203947) (← links)
- Overview of the voltage-gated sodium channel family (Q21999779) (← links)
- Exon organization, coding sequence, physical mapping, and polymorphic intragenic markers for the human neuronal sodium channel gene SCN8A (Q22008052) (← links)
- Where is the spike generator of the cochlear nerve? Voltage-gated sodium channels in the mouse cochlea. (Q24540329) (← links)
- Fibroblast growth factor 14 is an intracellular modulator of voltage-gated sodium channels (Q24544162) (← links)
- A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons (Q24546007) (← links)
- Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain (Q24562888) (← links)
- Pain as a channelopathy (Q24622323) (← links)
- Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons (Q24632552) (← links)
- Sodium channel Na(v)1.6 is localized at nodes of ranvier, dendrites, and synapses (Q24653551) (← links)
- Synthetic ciguatoxins selectively activate Nav1.8-derived chimeric sodium channels expressed in HEK293 cells (Q24655470) (← links)
- A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity (Q24679655) (← links)
- Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8. (Q24814946) (← links)
- Primary erythromelalgia: a review (Q26784432) (← links)
- Cellular hyper-excitability caused by mutations that alter the activation process of voltage-gated sodium channels (Q27008161) (← links)
- Changing channels in pain and epilepsy: Exploiting ion channel gene therapy for disorders of neuronal hyperexcitability (Q28081164) (← links)
- Neurobiology: a channel sets the gain on pain (Q28278802) (← links)
- An SCN9A channelopathy causes congenital inability to experience pain (Q28278844) (← links)
- Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain (Q28542818) (← links)
- Sodium voltage-gated channel alpha subunit 9 (Q28561892) (← links)
- Expression of skeletal muscle-type voltage-gated Na+ channel in rat and human prostate cancer cell lines (Q28573941) (← links)
- The role of voltage-gated sodium channels in neuropathic pain (Q29543085) (← links)
- Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ. (Q30354178) (← links)
- Voltage-gated Na+ channels in neuropathic pain (Q30443511) (← links)
- Fluorescent saxitoxins for live cell imaging of single voltage-gated sodium ion channels beyond the optical diffraction limit (Q30542058) (← links)
- Gating properties of Na(v)1.7 and Na(v)1.8 peripheral nerve sodium channels. (Q30730215) (← links)
- Ankyrin G and voltage gated sodium channels colocalize in human neuroma--key proteins of membrane remodeling after axonal injury (Q31048324) (← links)
- Progesterone treatment abolishes exogenously expressed ionic currents in Xenopus oocytes (Q31919524) (← links)
- Distribution of the tetrodotoxin-resistant sodium channel PN3 in rat sensory neurons in normal and neuropathic conditions. (Q32108845) (← links)
- Sodium channel Nav1.6 accumulates at the site of infraorbital nerve injury (Q33292270) (← links)
- Nav1.7 expression is increased in painful human dental pulp (Q33329730) (← links)
- Sodium channel expression and localization at demyelinated sites in painful human dental pulp (Q33475316) (← links)
- Upregulation of nav1.7 through high salt loading: (mol pain 2013;9:39) (Q33586810) (← links)
- Regulation of ion channel expression in neural cells by hormones and growth factors (Q33595739) (← links)
- Burning pain: axonal dysfunction in erythromelalgia. (Q33595891) (← links)
- Sodium channel Na v 1.7 immunoreactivity in painful human dental pulp and burning mouth syndrome (Q33596969) (← links)
- Sodium channels and pain (Q33679468) (← links)
- A comparison of the potential role of the tetrodotoxin-insensitive sodium channels, PN3/SNS and NaN/SNS2, in rat models of chronic pain (Q33679477) (← links)
- Diversity of mammalian voltage-gated sodium channels. (Q33691479) (← links)
- The neuron as a dynamic electrogenic machine: modulation of sodium-channel expression as a basis for functional plasticity in neurons (Q33867569) (← links)
- Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders (Q33875626) (← links)
- Vasomotor sympathetic neurons are more excitable than secretomotor sympathetic neurons in bullfrog paravertebral ganglia. (Q33886624) (← links)
- Blockade of persistent sodium currents contributes to the riluzole-induced inhibition of spontaneous activity and oscillations in injured DRG neurons (Q33889459) (← links)
- A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia (Q33918510) (← links)
- Regional differences in nerve terminal Na+ channel subtype expression and Na+ channel-dependent glutamate and GABA release in rat CNS. (Q34039148) (← links)
- Sodium channels and the molecular pathophysiology of pain (Q34093984) (← links)
- Modulation of neuronal sodium channels by the sea anemone peptide BDS-I. (Q34263269) (← links)
- Two novel mutations of SCN9A (Nav1.7) are associated with partial congenital insensitivity to pain (Q34300278) (← links)
- Regulation of Na+ channel distribution in the nervous system (Q34321652) (← links)
- Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. (Q34350866) (← links)