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Article

Loss-of-function mutations in sodium channel Nav1.7 cause anosmia.

Nature - 14 Apr 2011

Weiss Jan, Pyrski Martina, Jacobi Eric, Bufe Bernd, Willnecker Vivienne, Schick Bernhard, Zizzari Philippe, Gossage Samuel J, Greer Charles A, Leinders-Zufall Trese, Woods C Geoffrey, Wood John N, Zufall Frank

Abstract excerpt

Loss of function of the gene SCN9A, encoding the voltage-gated sodium channel Na(v)1.7, causes a congenital inability to experience pain in humans. Here we show that Na(v)1.7 is not only necessary for pain sensation but is also an essential requirement for odour perception in both mice and humans. We examined human patients with loss-of-function mutations in SCN9A and show that they are unable to sense odours. To...

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Identifiers

PMID: 21441906
DOI: 10.1038/nature09975
PMCID: PMC3674497

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

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Loss-of-function mutations in sodium channel Nav1.7 cause anosmia.PMID 21441906Read ↗

The mechanism of analgesia in Na <sub>V</sub> 1.7 null mutantsSemantic proximity Read ↗

Nociceptor-specific gene deletion reveals a major role for Na <sub>v</sub> 1.7 (PN1) in acute and inflammatory painSemantic proximity Read ↗

Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain.Semantic proximity Read ↗

Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disordersSemantic proximity Read ↗

Two distinct mechanisms for Na <sub>v</sub> 1.7 null analgesiaSemantic proximity Read ↗

Novel SCN9A missense mutations contribute to congenital insensitivity to pain: Unexpected correlation between electrophysiological characterization and clinical phenotype.Semantic proximity Read ↗

A stop codon mutation in SCN9A causes lack of pain sensation.Semantic proximity Read ↗

Functional confirmation that the R1488* variant in SCN9A results in complete loss-of-function of Nav1.7.Semantic proximity Read ↗

Painless Na <sub>v</sub> 1.7 mutations reveal function-critical residues in the outer vestibule and N-terminusSemantic proximity Read ↗

An SCN9A channelopathy causes congenital inability to experience pain.Semantic proximity Read ↗

Pain behavior in SCN9A (Nav1.7) and SCN10A (Nav1.8) mutant rodent modelsSemantic proximity Read ↗

From genes to pain: Na v 1.7 and human pain disorders.Semantic proximity Read ↗

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