(Q50346081)

5 March 2018

title

Pain insensitivity: distal S6-segment mutations in NaV1.9 emerge as critical hotspot. (English)

1 reference

5 March 2018

Ingo Kurth

4

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author name string

Margaret K King

1

1 reference

5 March 2018

Enrico Leipold

2

1 reference

5 March 2018

Jessica M Goehringer

3

1 reference

5 March 2018

Thomas D Challman

5

1 reference

5 March 2018

publication date

13 March 2017

1 reference

5 March 2018

published in

Neurogenetics

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5 March 2018

volume

18

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5 March 2018

issue

3

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5 March 2018

page(s)

179-181

1 reference

5 March 2018

https://scigraph.springernature.com/pub.10.1007/s10048-017-0513-9

exact match

0 references

cites work

NaV1.9: a sodium channel linked to human pain

1 reference

https://api.crossref.org/works/10.1007%2FS10048-017-0513-9

Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use.

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10048-017-0513-9

A de novo gain-of-function mutation in SCN11A causes loss of pain perception

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10048-017-0513-9

Congenital insensitivity to pain: Fracturing without apparent skeletal pathobiology caused by an autosomal dominant, second mutation in SCN11A encoding voltage-gated sodium channel 1.9.

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10048-017-0513-9

Cold-aggravated pain in humans caused by a hyperactive NaV1.9 channel mutant

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10048-017-0513-9

Gain-of-function mutations in SCN11A cause familial episodic pain

21 January 2018

1 reference

https://api.crossref.org/works/10.1007%2FS10048-017-0513-9

10.1007/S10048-017-0513-9

21 January 2018

Identifiers

DOI

1 reference

5 March 2018

PubMed ID

28289907

1 reference

5 March 2018