ArticleBMC systems biology2017
Network topology of NaV1.7 mutations in sodium channel-related painful disorders.
Article in BMC systems biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Learning molecular traits of human pain disease via voltage-gated sodium channel structure renormalization.Computational and structural biotechnology journal · 2025Article
- Calculation of centralities in protein kinase A.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Dissecting mutational allosteric effects in alkaline phosphatases associated with different Hypophosphatasia phenotypes: An integrative computational investigation.PLoS computational biology · 2022Article
- Assessing the impact of pain-linked Nav1.7 variants: An example of two variants with no biophysical effect.Channels (Austin, Tex.) · 2021Article
- Hydropathicity-based prediction of pain-causing NaV1.7 variants.BMC bioinformatics · 2021Article
- Non-extensitivity and criticality of atomic hydropathicity around a voltage-gated sodium channel's pore: a modeling study.Journal of biological physics · 2021Article
- Computational pipeline to probe NaV1.7 gain-of-function variants in neuropathic painful syndromes.Scientific reports · 2020Article
- Differential effect of lacosamide on Nav1.7 variants from responsive and non-responsive patients with small fibre neuropathy.Brain : a journal of neurology · 2020Article
- A bioinformatics investigation into the pharmacological mechanisms of the effect of the Yinchenhao decoction on hepatitis C based on network pharmacology.BMC complementary medicine and therapies · 2020Article
- Probing Carbon Utilization ofCells · 2020Article
- Association of small-fiber polyneuropathy with three previously unassociated rare missense SCN9A variants.Canadian journal of pain = Revue canadienne de la douleur · 2020Article
- Review
- A Mixed Periodic Paralysis & Myotonia Mutant, P1158S, Imparts pH-Sensitivity in Skeletal Muscle Voltage-gated Sodium Channels.Scientific reports · 2018Article
- Identification of diverse target RNAs that are functionally regulated by human Pumilio proteins.Nucleic acids research · 2018Article
- Article
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Authors and funding
16 authors.
Funding
Abstract
backgroundGain-of-function mutations in SCN9A gene that encodes the voltage-gated sodium channel NaV1.7 have been associated with a wide spectrum of painful syndromes in humans including inherited erythromelalgia, paroxysmal extreme pain disorder and small fibre neuropathy. These mutations change the biophysical properties of NaV1.7 channels leading to hyperexcitability of dorsal root ganglion nociceptors and pain symptoms. There is a need for better understanding of how gain-of-function mutations alter the atomic structure of Nav1.7.
resultsWe used homology modeling to build an atomic model of NaV1.7 and a network-based theoretical approach, which can predict interatomic interactions and connectivity arrangements, to investigate how pain-related NaV1.7 mutations may alter specific interatomic bonds and cause connectivity rearrangement, compared to benign variants and polymorphisms. For each amino acid substitution, we calculated the topological parameters betweenness centrality (B
conclusionsOur in-silico analyses predict that pain-related pathogenic NaV1.7 mutations may affect the network topological properties of the protein and suggest |ΔB
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