-
1
-
-
77953684015
-
Sodium channels in normal and pathological pain
-
Dib-Hajj S.D., et al. Sodium channels in normal and pathological pain. Annu. Rev. Neurosci. 2010, 33:325-347.
-
(2010)
Annu. Rev. Neurosci.
, vol.33
, pp. 325-347
-
-
Dib-Hajj, S.D.1
-
2
-
-
84866372487
-
Neurological perspectives on voltage-gated sodium channels
-
Eijkelkamp N., et al. Neurological perspectives on voltage-gated sodium channels. Brain 2012, 135:2585-2612.
-
(2012)
Brain
, vol.135
, pp. 2585-2612
-
-
Eijkelkamp, N.1
-
3
-
-
0035023041
-
The primary erythermalgia-susceptibility gene is located on chromosome 2q31-32
-
Drenth J.P., et al. The primary erythermalgia-susceptibility gene is located on chromosome 2q31-32. Am. J. Hum. Genet. 2001, 68:1277-1282.
-
(2001)
Am. J. Hum. Genet.
, vol.68
, pp. 1277-1282
-
-
Drenth, J.P.1
-
4
-
-
12144288410
-
Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia
-
Yang Y., et al. Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia. J. Med. Genet. 2004, 41:171-174.
-
(2004)
J. Med. Genet.
, vol.41
, pp. 171-174
-
-
Yang, Y.1
-
5
-
-
4644268452
-
Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy
-
Cummins T.R., et al. Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. J. Neurosci. 2004, 24:8232-8236.
-
(2004)
J. Neurosci.
, vol.24
, pp. 8232-8236
-
-
Cummins, T.R.1
-
6
-
-
23444443202
-
Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons
-
Dib-Hajj S.D., et al. Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons. Brain 2005, 128:1847-1854.
-
(2005)
Brain
, vol.128
, pp. 1847-1854
-
-
Dib-Hajj, S.D.1
-
7
-
-
84871443483
-
The Na(V)1.7 sodium channel: from molecule to man
-
Dib-Hajj S.D., et al. The Na(V)1.7 sodium channel: from molecule to man. Nat. Rev. Neurosci. 2012, 14:49-62.
-
(2012)
Nat. Rev. Neurosci.
, vol.14
, pp. 49-62
-
-
Dib-Hajj, S.D.1
-
8
-
-
36849036949
-
Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders
-
Drenth J.P., Waxman S.G. Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders. J. Clin. Invest. 2007, 117:3603-3609.
-
(2007)
J. Clin. Invest.
, vol.117
, pp. 3603-3609
-
-
Drenth, J.P.1
Waxman, S.G.2
-
9
-
-
33847168937
-
SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes
-
Fertleman C.R., et al. SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron 2006, 52:767-774.
-
(2006)
Neuron
, vol.52
, pp. 767-774
-
-
Fertleman, C.R.1
-
10
-
-
58149154859
-
NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders
-
Estacion M., et al. NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders. J. Neurosci. 2008, 28:11079-11088.
-
(2008)
J. Neurosci.
, vol.28
, pp. 11079-11088
-
-
Estacion, M.1
-
11
-
-
34548419652
-
A stop codon mutation in SCN9A causes lack of pain sensation
-
Ahmad S., et al. A stop codon mutation in SCN9A causes lack of pain sensation. Hum. Mol. Genet. 2007, 16:2114-2121.
-
(2007)
Hum. Mol. Genet.
, vol.16
, pp. 2114-2121
-
-
Ahmad, S.1
-
12
-
-
33845901486
-
An SCN9A channelopathy causes congenital inability to experience pain
-
Cox J.J., et al. An SCN9A channelopathy causes congenital inability to experience pain. Nature 2006, 444:894-898.
-
(2006)
Nature
, vol.444
, pp. 894-898
-
-
Cox, J.J.1
-
13
-
-
34247874778
-
Loss-of-function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations
-
Goldberg Y.P., et al. Loss-of-function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations. Clin. Genet. 2007, 71:311-319.
-
(2007)
Clin. Genet.
, vol.71
, pp. 311-319
-
-
Goldberg, Y.P.1
-
14
-
-
33744454923
-
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons
-
Rush A.M., et al. A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons. Proc. Natl. Acad. Sci. U.S.A. 2006, 103:8245-8250.
-
(2006)
Proc. Natl. Acad. Sci. U.S.A.
, vol.103
, pp. 8245-8250
-
-
Rush, A.M.1
-
15
-
-
12644288297
-
Identification of PN1, a predominant voltage-dependent sodium channel expressed principally in peripheral neurons
-
Toledo-Aral J.J., et al. Identification of PN1, a predominant voltage-dependent sodium channel expressed principally in peripheral neurons. Proc. Natl. Acad. Sci. U.S.A. 1997, 94:1527-1532.
-
(1997)
Proc. Natl. Acad. Sci. U.S.A.
, vol.94
, pp. 1527-1532
-
-
Toledo-Aral, J.J.1
-
16
-
-
79954495540
-
Loss-of-function mutations in sodium channel Nav1.7 cause anosmia
-
Weiss J., et al. Loss-of-function mutations in sodium channel Nav1.7 cause anosmia. Nature 2011, 472:186-190.
-
(2011)
Nature
, vol.472
, pp. 186-190
-
-
Weiss, J.1
-
17
-
-
79955737978
-
Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons
-
Ahn H.S., et al. Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons. Mol. Pain 2011, 7:32.
-
(2011)
Mol. Pain
, vol.7
, pp. 32
-
-
Ahn, H.S.1
-
18
-
-
84863715581
-
Small-fibre neuropathies - advances in diagnosis, pathophysiology and management
-
Hoeijmakers J.G., et al. Small-fibre neuropathies - advances in diagnosis, pathophysiology and management. Nat. Rev. Neurol. 2012, 8:369-379.
-
(2012)
Nat. Rev. Neurol.
, vol.8
, pp. 369-379
-
-
Hoeijmakers, J.G.1
-
19
-
-
84856143604
-
Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy
-
Faber C.G., et al. Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy. Ann. Neurol. 2012, 71:26-39.
-
(2012)
Ann. Neurol.
, vol.71
, pp. 26-39
-
-
Faber, C.G.1
-
20
-
-
84857229966
-
Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation
-
Hoeijmakers J.G., et al. Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation. Brain 2012, 135:345-358.
-
(2012)
Brain
, vol.135
, pp. 345-358
-
-
Hoeijmakers, J.G.1
-
21
-
-
84869795443
-
Gain-of-function Nav1.8 mutations in painful neuropathy
-
Faber C.G., et al. Gain-of-function Nav1.8 mutations in painful neuropathy. Proc. Natl. Acad. Sci. U.S.A. 2012, 109:19444-19449.
-
(2012)
Proc. Natl. Acad. Sci. U.S.A.
, vol.109
, pp. 19444-19449
-
-
Faber, C.G.1
-
22
-
-
40449087926
-
Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade
-
Cheng X., et al. Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade. Mol. Pain 2008, 4:1.
-
(2008)
Mol. Pain
, vol.4
, pp. 1
-
-
Cheng, X.1
-
23
-
-
67650066369
-
Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation
-
Han C., et al. Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation. Brain 2009, 132:1711-1722.
-
(2009)
Brain
, vol.132
, pp. 1711-1722
-
-
Han, C.1
-
24
-
-
84866147238
-
Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy
-
Han C., et al. Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy. Brain 2012, 135:2613-2628.
-
(2012)
Brain
, vol.135
, pp. 2613-2628
-
-
Han, C.1
-
25
-
-
82455171777
-
Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7
-
Estacion M., et al. Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7. Mol. Pain 2011, 7:92.
-
(2011)
Mol. Pain
, vol.7
, pp. 92
-
-
Estacion, M.1
-
26
-
-
73549101494
-
A sodium channel gene SCN9A polymorphism that increases nociceptor excitability
-
Estacion M., et al. A sodium channel gene SCN9A polymorphism that increases nociceptor excitability. Ann. Neurol. 2009, 66:862-866.
-
(2009)
Ann. Neurol.
, vol.66
, pp. 862-866
-
-
Estacion, M.1
-
27
-
-
77950429077
-
Pain perception is altered by a nucleotide polymorphism in SCN9A
-
Reimann F., et al. Pain perception is altered by a nucleotide polymorphism in SCN9A. Proc. Natl. Acad. Sci. U.S.A. 2010, 107:5148-5153.
-
(2010)
Proc. Natl. Acad. Sci. U.S.A.
, vol.107
, pp. 5148-5153
-
-
Reimann, F.1
-
28
-
-
58149232445
-
Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas
-
Black J.A., et al. Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas. Ann. Neurol. 2008, 64:644-653.
-
(2008)
Ann. Neurol.
, vol.64
, pp. 644-653
-
-
Black, J.A.1
-
29
-
-
79960621367
-
The crystal structure of a voltage-gated sodium channel
-
Payandeh J., et al. The crystal structure of a voltage-gated sodium channel. Nature 2011, 475:353-358.
-
(2011)
Nature
, vol.475
, pp. 353-358
-
-
Payandeh, J.1
-
30
-
-
84870798937
-
Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(v)1.7 mutant channel
-
Yang Y., et al. Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(v)1.7 mutant channel. Nat. Commun. 2012, 3:1186.
-
(2012)
Nat. Commun.
, vol.3
, pp. 1186
-
-
Yang, Y.1
-
31
-
-
67650090921
-
A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia
-
Fischer T.Z., et al. A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia. Ann. Neurol. 2009, 65:733-741.
-
(2009)
Ann. Neurol.
, vol.65
, pp. 733-741
-
-
Fischer, T.Z.1
-
32
-
-
78049357954
-
Isoform-specific and pan-channel partners regulate trafficking and plasma membrane stability; and alter sodium channel gating properties
-
Dib-Hajj S.D., Waxman S.G. Isoform-specific and pan-channel partners regulate trafficking and plasma membrane stability; and alter sodium channel gating properties. Neurosci. Lett. 2010, 486:84-91.
-
(2010)
Neurosci. Lett.
, vol.486
, pp. 84-91
-
-
Dib-Hajj, S.D.1
Waxman, S.G.2
|