NAV1Network Analyzer Version 1
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Two types of "gain-of-function" mutations in Nav1.7 produce severe chronic pain in humans, while "loss-of-function" mutations produce inability to sense pain.
STK-001 is designed to upregulate NaV1.1 protein expression from the non-mutant (wild-type) copy of the SCN1A gene to restore physiological NaV1.1 levels, thereby reducing both occurrence of seizures and significant non-seizure comorbidities.
This study is the third positive proof-of-concept study of VX-150 and further validates the potential role of NaV1.8 inhibition in the treatment of pain.
Amgen, a biotech company, is currently developing a medication from the tarantula venom that targets NaV1.7.
Because both Nav1.7 and Nav1.8 are responsible for the initial depolarization phase involved in the generation of APs [23], we examined whether dexmedetomidine could modulate [I.sub.Na] and APs in small-sized TG neurons.
Recently, autosomal dominant mutations in SCN11A, which encodes Nav1.9, a voltage-gated sodium channel subunit alpha type 9, have been found in pain syndromes, including episodic familial pain syndrome [11-13].
Although inhibition of the hERG channel (human ether-a-go-go-related gene) regulating the major repolarizing current in the heart, IKr (delayed inward potassium current), is the most common mechanism of QT prolongation [4, 5], it can also be caused by the drug triggered inhibition of other channels, that is, potassium (Kv7.1), sodium (Nav1.5), or calcium (Cav1.2) [6-9].
Since nerve damage from diabetic hyperglycemia causes pain, several existing and potential pain drugs and Chromocell novel NaV1.7 blocker compound were evaluated as pain treatments in the subject animals.
Vijayalakshmi et al., "Exposure to cerebrospinal fluid of sporadic amyotrophic lateral sclerosis patients alters Nav1.6 and Kv1.6 channel expression in rat spinal motor neurons," Brain Research, vol.
Defective polysialylation and sialylation induce opposite effects on gating of the skeletal Na+ channel NaV1.4 in Chinese hamster ovary cells.
Further phylogenetic analysis determined that the isolate belonged to ST25 clade NAV1 (Figure), which is common among diseased swine in Canada (6,7) but heretofore not associated with human disease.
You're displaying DME off NAV1, you should be using it off NAV2.