Associated Papers
Parental segregation study reveals rare benign and likely benign variants in a Brazilian cohort of rare diseases.
Quaio CRD'C et al.
Scientific Reports, 2022
35546177 (PubMed )
Supplement: 41598_2022_11932_MOESM1_ESM.xlsx › Supplementary_Table_-_Data
Hydropathicity-based prediction of pain-causing NaV1.7 variants.
Xenakis MN et al.
Bmc Bioinformatics, 2021
33892629 (PubMed )
Supplement: 12859_2021_4119_MOESM1_ESM.pdf
Computational pipeline to probe NaV1.7 gain-of-function variants in neuropathic painful syndromes.
Toffano AA et al.
Scientific Reports, 2020
33087732 (PubMed )
Supplement: 41598_2020_74591_MOESM1_ESM.pdf
Distribution and Functional Characteristics of Voltage-Gated Sodium Channels in Immature Cochlear Hair Cells.
Zhou Y et al.
Neuroscience Bulletin, 2020
Network topology of NaV1.7 mutations in sodium channel-related painful disorders.
Kapetis D et al.
Bmc Systems Biology, 2017
The tarantula toxins ProTx-II and huwentoxin-IV differentially interact with human Nav1.7 voltage sensors to inhibit channel activation and inactivation.
Xiao Y et al.
Molecular Pharmacology, 2010
Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia.
Choi JS et al.
Brain : a Journal of Neurology, 2010
Biophysical properties of human Na v1.7 splice variants and their regulation by protein kinase A.
Chatelier A et al.
Journal of Neurophysiology, 2008
Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T.
Jarecki BW et al.
Channels (austin, Tex.), 0
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