Nav1.9

1

Murenzi E et al. Evaluation of microtransplantation of rat brain neurolemma into Xenopus laevis oocytes as a technique to study the effect of neurotoxicants on endogenous voltage-sensitive ion channels.
Neurotoxicology, 2016 Apr 7 , ().

2

Coll M et al. Genetic investigation of sudden unexpected death in epilepsy cohort by panel target resequencing.
Int. J. Legal Med., 2015 Sep 30 , ().

3

Nutter TJ et al. A delayed chronic pain like condition with decreased Kv channel activity in a rat model of Gulf War Illness pain syndrome.
Neurotoxicology, 2015 Sep 26 , 51 (67-79).

4

Remacle AG et al. Matrix Metalloproteinase (MMP) Proteolysis of the Extracellular Loop of Voltage-gated Sodium Channels and Potential Alterations in Pain Signaling.
J. Biol. Chem., 2015 Sep 18 , 290 (22939-44).

5

Kurowski P et al. Muscarinic receptor control of pyramidal neuron membrane potential in the medial prefrontal cortex (mPFC) in rats.
Neuroscience, 2015 Sep 10 , 303 (474-88).

6

Dib-Hajj SD et al. NaV1.9: a sodium channel linked to human pain.
Nat. Rev. Neurosci., 2015 Sep , 16 (511-9).

7

Li G et al. Positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury.
Mol Med Rep, 2015 Sep , 12 (3583-90).

8

Lolignier S et al. The Nav1.9 channel is a key determinant of cold pain sensation and cold allodynia.
Cell Rep, 2015 May 19 , 11 (1067-78).

9

Wildburger NC et al. Quantitative proteomics reveals protein-protein interactions with fibroblast growth factor 12 as a component of the voltage-gated sodium channel 1.2 (nav1.2) macromolecular complex in Mammalian brain.
Mol. Cell Proteomics, 2015 May , 14 (1288-300).

10

Woods CG et al. The phenotype of congenital insensitivity to pain due to the NaV1.9 variant p.L811P.
Eur. J. Hum. Genet., 2015 May , 23 (561-3).

11

Yan Z et al. Expression and functional role of Nav1.9 sodium channel in cartwheel cells of the dorsal cochlear nucleus.
Mol Med Rep, 2015 Mar , 11 (1833-6).

12

Hoeijmakers JG et al. Painful peripheral neuropathy and sodium channel mutations.
Neurosci. Lett., 2015 Jun 2 , 596 (51-9).

13

Han C et al. The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy.
Neuromolecular Med., 2015 Jun , 17 (158-69).

14

Bao L Trafficking regulates the subcellular distribution of voltage-gated sodium channels in primary sensory neurons.
Mol Pain, 2015 , 11 (61).

15

Habib AM et al. Sodium channels and pain.
Handb Exp Pharmacol, 2015 , 227 (39-56).

16

Kharatmal SB et al. Voltage-Gated Sodium Channels as Therapeutic Targets for Treatment of Painful Diabetic Neuropathy.
Mini Rev Med Chem, 2015 , 15 (1134-47).

17

Leipold E et al. Cold-aggravated pain in humans caused by a hyperactive NaV1.9 channel mutant.
Nat Commun, 2015 , 6 (10049).

18

Dusmez D et al. Effect of verapamil and lidocaine on TRPM and NaV1.9 gene expressions in renal ischemia-reperfusion.
Transplant. Proc., 2014 Jan-Feb , 46 (33-9).

19

Hirofuji S et al. Role of sodium channels in recovery of sciatic nerve-stretch injury in rats.
Muscle Nerve, 2014 Sep , 50 (425-30).

20

Greaves E et al. Elevated peritoneal expression and estrogen regulation of nociceptive ion channels in endometriosis.
J. Clin. Endocrinol. Metab., 2014 Sep , 99 (E1738-43).

21

Hockley JR et al. Multiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli.
Pain, 2014 Oct , 155 (1962-75).

22

Waxman SG et al. Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use.
Lancet Neurol, 2014 Nov , 13 (1152-60).

23

Kiss T et al. Down regulation of sodium channels in the central nervous system of hibernating snails.
Physiol. Behav., 2014 May 28 , 131 (93-8).

24

Black JA et al. Nav1.9 expression in magnocellular neurosecretory cells of supraoptic nucleus.
Exp. Neurol., 2014 Mar , 253 (174-9).

25

Nutter TJ et al. Persistent modification of Nav1.9 following chronic exposure to insecticides and pyridostigmine bromide.
Toxicol. Appl. Pharmacol., 2014 Jun 15 , 277 (298-309).

26

Huang J et al. Gain-of-function mutations in sodium channel Na(v)1.9 in painful neuropathy.
Brain, 2014 Jun , 137 (1627-42).

27

Sidaway P Pain: Gain-of-function Nav1.9 mutations are associated with painful peripheral neuropathy.
Nat Rev Neurol, 2014 Jun , 10 (306).

28

Brouwer BA et al. Painful neuropathies: the emerging role of sodium channelopathies.
J. Peripher. Nerv. Syst., 2014 Jun , 19 (53-65).

29

Bennett DL et al. Painful and painless channelopathies.
Lancet Neurol, 2014 Jun , 13 (587-99).

30

Minett MS et al. Pain without nociceptors? Nav1.7-independent pain mechanisms.
Cell Rep, 2014 Jan 30 , 6 (301-12).

31

Muroi Y et al. Targeting voltage gated sodium channels NaV1.7, Na V1.8, and Na V1.9 for treatment of pathological cough.
Lung, 2014 Feb , 192 (15-20).

32

Xu L et al. [Expression of voltage gated sodium channel Nav1.9 in experimental pulpal lesions in the rats].
Zhonghua Kou Qiang Yi Xue Za Zhi, 2014 Feb , 49 (95-100).

33

Osorio N et al. Specialized functions of Nav1.5 and Nav1.9 channels in electrogenesis of myenteric neurons in intact mouse ganglia.
J. Neurosci., 2014 Apr 9 , 34 (5233-44).

34

Korogod SM et al. Dynamic excitation states and firing patterns are controlled by sodium channel kinetics in myenteric neurons: a simulation study.
Channels (Austin), 2014 , 8 (536-43).

35

Minett MS et al. Significant determinants of mouse pain behaviour.
PLoS ONE, 2014 , 9 (e104458).

36

Zimmer T et al. Voltage-gated sodium channels in the mammalian heart.
Glob Cardiol Sci Pract, 2014 , 2014 (449-63).

37

Luo J et al. Molecular surface of JZTX-V (β-Theraphotoxin-Cj2a) interacting with voltage-gated sodium channel subtype NaV1.4.
Toxins (Basel), 2014 , 6 (2177-93).

38

Leipold E et al. A de novo gain-of-function mutation in SCN11A causes loss of pain perception.
Nat. Genet., 2013 Sep 15 , ().

39

Black JA et al. Noncanonical roles of voltage-gated sodium channels.
Neuron, 2013 Oct 16 , 80 (280-91).

40

Zhang XY et al. Gain-of-function mutations in SCN11A cause familial episodic pain.
Am. J. Hum. Genet., 2013 Nov 7 , 93 (957-66).

41

Cox JJ et al. No pain, more gain.
Nat. Genet., 2013 Nov , 45 (1271-2).

42

Yu YQ et al. Activation of tetrodotoxin-resistant sodium channel NaV1.9 in rat primary sensory neurons contributes to melittin-induced pain behavior.
Neuromolecular Med., 2013 Mar , 15 (209-17).

43

Luo Y et al. [Inhibitory effect of NaV1.9 gene silencing on proliferation, phagocytosis and migration in RAW264.7 cells].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi, 2013 Mar , 29 (225-8).

44

Vanoye CG et al. Mechanism of sodium channel NaV1.9 potentiation by G-protein signaling.
J. Gen. Physiol., 2013 Feb , 141 (193-202).

45

Abbas N et al. The scorpion toxin Amm VIII induces pain hypersensitivity through gain-of-function of TTX-sensitive Na⁺ channels.
Pain, 2013 Aug , 154 (1204-15).

46

Liang J et al. Effect of amitriptyline on tetrodotoxin-resistant Nav1.9 currents in nociceptive trigeminal neurons.
Mol Pain, 2013 , 9 (31).

47

Zhang Y et al. Effects of (-)-gallocatechin-3-gallate on tetrodotoxin-resistant voltage-gated sodium channels in rat dorsal root ganglion neurons.
Int J Mol Sci, 2013 , 14 (9779-89).

48

Bird EV et al. Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas.
Mol Pain, 2013 , 9 (52).

49

Hodgdon KE et al. Dorsal root ganglia isolated from Nf1+/- mice exhibit increased levels of mRNA expression of voltage-dependent sodium channels.
Neuroscience, 2012 Mar 29 , 206 (237-44).

50

Qiu F et al. Increased expression of tetrodotoxin-resistant sodium channels Nav1.8 and Nav1.9 within dorsal root ganglia in a rat model of bone cancer pain.
Neurosci. Lett., 2012 Mar 23 , 512 (61-6).

51

Fukuoka T et al. Re-evaluation of the phenotypic changes in L4 dorsal root ganglion neurons after L5 spinal nerve ligation.
Pain, 2012 Jan , 153 (68-79).

52

Gaudioso C et al. Menthol pain relief through cumulative inactivation of voltage-gated sodium channels.
Pain, 2012 Feb , 153 (473-84).

53

Gilchrist J et al. Animal toxins can alter the function of Nav1.8 and Nav1.9.
Toxins (Basel), 2012 Aug , 4 (620-32).

54

Ding H et al. Alterations of gene expression of sodium channels in dorsal root ganglion neurons of estrogen receptor knockout (ERKO) mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
Endocrine, 2012 Aug , 42 (118-24).

55

Huang CY et al. Co-expression of high-voltage-activated ion channels Kv3.4 and Cav1.2 in pioneer axons during pathfinding in the developing rat forebrain.
, 2012 Apr 2 , ().

56

Hu F et al. 17β-Estradiol regulates the gene expression of voltage-gated sodium channels: role of estrogen receptor α and estrogen receptor β.
Endocrine, 2012 Apr , 41 (274-80).

57

Kao DJ et al. CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons.
J Neuroinflammation, 2012 , 9 (189).

58

Ito A et al. Anti-hyperalgesic effects of calcitonin on neuropathic pain interacting with its peripheral receptors.
Mol Pain, 2012 , 8 (42).

59

Due MR et al. Neuroexcitatory effects of morphine-3-glucuronide are dependent on Toll-like receptor 4 signaling.
J Neuroinflammation, 2012 , 9 (200).

60

Byers MR et al. Odontoblasts in developing, mature and ageing rat teeth have multiple phenotypes that variably express all nine voltage-gated sodium channels.
Arch. Oral Biol., 2011 Nov , 56 (1199-220).

61

Franck MC et al. Essential role of Ret for defining non-peptidergic nociceptor phenotypes and functions in the adult mouse.
, 2011 Mar 14 , ().

62

Shou WT et al. [Role of voltage-sodium channels in neuropathic pain].
Zhejiang Da Xue Xue Bao Yi Xue Ban, 2011 Mar , 40 (217-21).

63

Fukuoka T et al. Comparative study of voltage-gated sodium channel α-subunits in non-overlapping four neuronal populations in the rat dorsal root ganglion.
Neurosci. Res., 2011 Jun , 70 (164-71).

64

Bosmans F et al. Functional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensors.
J. Gen. Physiol., 2011 Jul , 138 (59-72).

65

Liu M et al. The roles of sodium channels in nociception: implications for mechanisms of neuropathic pain.
Pain Med, 2011 Jul , 12 Suppl 3 (S93-9).

66

Moraes ER et al. Differential effects of Tityus bahiensis scorpion venom on tetrodotoxin-sensitive and tetrodotoxin-resistant sodium currents.
Neurotox Res, 2011 Jan , 19 (102-14).

67

Ho C et al. Single-cell analysis of sodium channel expression in dorsal root ganglion neurons.
Mol. Cell. Neurosci., 2011 Jan , 46 (159-66).

68

Widmark J et al. Differential evolution of voltage-gated sodium channels in tetrapods and teleost fishes.
Mol. Biol. Evol., 2011 Jan , 28 (859-71).

69

Chen X et al. TNF-α enhances the currents of voltage gated sodium channels in uninjured dorsal root ganglion neurons following motor nerve injury.
Exp. Neurol., 2011 Feb , 227 (279-86).

70

Baroni D et al. Molecular differential expression of voltage-gated sodium channel α and β subunit mRNAs in five different mammalian cell lines.
J. Bioenerg. Biomembr., 2011 Dec , 43 (729-38).

71

Lolignier S et al. Nav1.9 channel contributes to mechanical and heat pain hypersensitivity induced by subacute and chronic inflammation.
PLoS ONE, 2011 , 6 (e23083).

72

von Schack D et al. Dynamic Changes in the MicroRNA Expression Profile Reveal Multiple Regulatory Mechanisms in the Spinal Nerve Ligation Model of Neuropathic Pain.
PLoS ONE, 2011 , 6 (e17670).

73

Fukuoka T et al. Laminae-specific distribution of alpha-subunits of voltage-gated sodium channels in the adult rat spinal cord.
Neuroscience, 2010 Sep 1 , 169 (994-1006).

74

Leo S et al. Exploring the role of nociceptor-specific sodium channels in pain transmission using Nav1.8 and Nav1.9 knockout mice.
Behav. Brain Res., 2010 Mar 17 , 208 (149-57).

75

Ohno K et al. Altered expression of sodium channel distribution in the dorsal root ganglion after gradual elongation of rat sciatic nerves.
J. Orthop. Res., 2010 Apr , 28 (481-6).

76

Persson AK et al. Sodium-calcium exchanger and multiple sodium channel isoforms in intra-epidermal nerve terminals.
Mol Pain, 2010 , 6 (84).

77

Herold KF et al. Isoflurane inhibits the tetrodotoxin-resistant voltage-gated sodium channel Nav1.8.
Anesthesiology, 2009 Sep , 111 (591-9).

78

Zhang L et al. [Nav1.8 and Nav1.9 mRNA expression in rat trigeminal ganglion at different interval after molar extraction].
Zhonghua Kou Qiang Yi Xue Za Zhi, 2009 May , 44 (301-3).

79

Ritter AM et al. The voltage-gated sodium channel Nav1.9 is required for inflammation-based urinary bladder dysfunction.
Neurosci. Lett., 2009 Mar 6 , 452 (28-32).

80

Tan J et al. Human and rat Nav1.3 voltage-gated sodium channels differ in inactivation properties and sensitivity to the pyrethroid insecticide tefluthrin.
Neurotoxicology, 2009 Jan , 30 (81-9).

81

Black JA et al. Sodium channel activity modulates multiple functions in microglia.
Glia, 2009 Aug 1 , 57 (1072-81).

82

Copel C et al. Activation of neurokinin 3 receptor increases Na(v)1.9 current in enteric neurons.
J. Physiol. (Lond.), 2009 Apr 1 , 587 (1461-79).

83

Desaphy JF et al. Involvement of voltage-gated sodium channels blockade in the analgesic effects of orphenadrine.
Pain, 2009 Apr , 142 (225-35).

84

Yen YT et al. Role of acid-sensing ion channel 3 in sub-acute-phase inflammation.
, 2009 , 5 (1).

85

Persson AK et al. Correlational analysis for identifying genes whose regulation contributes to chronic neuropathic pain.
, 2009 , 5 (7).

86

Thakor DK et al. Increased peripheral nerve excitability and local NaV1.8 mRNA up-regulation in painful neuropathy.
, 2009 , 5 (14).

87

Qiao GF et al. Characterization of persistent TTX-R Na+ currents in physiological concentration of sodium in rat visceral afferents.
Int. J. Biol. Sci., 2009 , 5 (293-7).

88

Maingret F et al. Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism.
J. Gen. Physiol., 2008 Mar , 131 (211-25).

89

Drenth JP et al. Primary erythermalgia as a sodium channelopathy: screening for SCN9A mutations: exclusion of a causal role of SCN10A and SCN11A.
Arch Dermatol, 2008 Mar , 144 (320-4).

90

Ragsdale DS How do mutant Nav1.1 sodium channels cause epilepsy?
, 2008 Jun , 58 (149-59).

91

Strickland IT et al. Changes in the expression of NaV1.7, NaV1.8 and NaV1.9 in a distinct population of dorsal root ganglia innervating the rat knee joint in a model of chronic inflammatory joint pain.
, 2008 Jul , 12 (564-72).

92

Waxman SG et al. Nav1.9, G-proteins, and nociceptors.
J. Physiol. (Lond.), 2008 Feb 15 , 586 (917-8).

93

Ostman JA et al. GTP up-regulated persistent Na+ current and enhanced nociceptor excitability require NaV1.9.
J. Physiol. (Lond.), 2008 Feb 15 , 586 (1077-87).

94

Wada A et al. Voltage-dependent Na(v)1.7 sodium channels: multiple roles in adrenal chromaffin cells and peripheral nervous system.
Acta Physiol (Oxf), 2008 Feb , 192 (221-31).

95

Black JA et al. Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas.
Ann. Neurol., 2008 Dec , 64 (644-53).

96

Keh SM et al. Increased nerve fiber expression of sensory sodium channels Nav1.7, Nav1.8, And Nav1.9 in rhinitis.
Laryngoscope, 2008 Apr , 118 (573-9).

97

Wells JE et al. Expression of Nav1.9 channels in human dental pulp and trigeminal ganglion.
, 2007 Oct , 33 (1172-6).

98

Padilla F et al. Expression and localization of the Nav1.9 sodium channel in enteric neurons and in trigeminal sensory endings: implication for intestinal reflex function and orofacial pain.
Mol. Cell. Neurosci., 2007 May , 35 (138-52).

99

Coste B et al. Pharmacological dissection and distribution of NaN/Nav1.9, T-type Ca2+ currents, and mechanically activated cation currents in different populations of DRG neurons.
J. Gen. Physiol., 2007 Jan , 129 (57-77).

100

Hillsley K et al. Dissecting the role of sodium currents in visceral sensory neurons in a model of chronic hyperexcitability using Nav1.8 and Nav1.9 null mice.
J. Physiol. (Lond.), 2006 Oct 1 , 576 (257-67).

101

Rogers M et al. The role of sodium channels in neuropathic pain.
Semin. Cell Dev. Biol., 2006 Oct , 17 (571-81).

102

Wang S et al. Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice.
Neurobiol. Aging, 2006 Jun , 27 (895-903).

103

Fang X et al. Intense isolectin-B4 binding in rat dorsal root ganglion neurons distinguishes C-fiber nociceptors with broad action potentials and high Nav1.9 expression.
J. Neurosci., 2006 Jul 5 , 26 (7281-92).

104

Amaya F et al. The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity.
J. Neurosci., 2006 Dec 13 , 26 (12852-60).

105

Fang X et al. trkA is expressed in nociceptive neurons and influences electrophysiological properties via Nav1.8 expression in rapidly conducting nociceptors.
J. Neurosci., 2005 May 11 , 25 (4868-78).

106

Priest BT et al. Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.
Proc. Natl. Acad. Sci. U.S.A., 2005 Jun 28 , 102 (9382-7).

107

Rush AM et al. Contactin regulates the current density and axonal expression of tetrodotoxin-resistant but not tetrodotoxin-sensitive sodium channels in DRG neurons.
Eur. J. Neurosci., 2005 Jul , 22 (39-49).

108

Raymond CK et al. Expression of alternatively spliced sodium channel alpha-subunit genes. Unique splicing patterns are observed in dorsal root ganglia.
J. Biol. Chem., 2004 Oct 29 , 279 (46234-41).

109

Rush AM et al. PGE2 increases the tetrodotoxin-resistant Nav1.9 sodium current in mouse DRG neurons via G-proteins.
Brain Res., 2004 Oct 15 , 1023 (264-71).

110

Wood JN et al. Voltage-gated sodium channels and pain pathways.
J. Neurobiol., 2004 Oct , 61 (55-71).

111

Beyak MJ et al. Two TTX-resistant Na+ currents in mouse colonic dorsal root ganglia neurons and their role in colitis-induced hyperexcitability.
Am. J. Physiol. Gastrointest. Liver Physiol., 2004 Oct , 287 (G845-55).

112

Schwab Y et al. Expression of tetrodotoxin-sensitive and resistant sodium channels by rat melanotrophs.
Neuroreport, 2004 May 19 , 15 (1219-23).

113

Coste B et al. Gating and modulation of presumptive NaV1.9 channels in enteric and spinal sensory neurons.
Mol. Cell. Neurosci., 2004 May , 26 (123-34).

114

Coggeshall RE et al. Differential expression of tetrodotoxin-resistant sodium channels Nav1.8 and Nav1.9 in normal and inflamed rats.
Neurosci. Lett., 2004 Jan 23 , 355 (45-8).

115

Wood JN et al. Ion channel activities implicated in pathological pain.
Novartis Found. Symp., 2004 , 261 (32-40; discussion 40-54).

116

Herzog RI et al. Calmodulin binds to the C terminus of sodium channels Nav1.4 and Nav1.6 and differentially modulates their functional properties.
J. Neurosci., 2003 Sep 10 , 23 (8261-70).

117

Klein JP et al. Patterned electrical activity modulates sodium channel expression in sensory neurons.
J. Neurosci. Res., 2003 Oct 15 , 74 (192-8).

118

Delmas P et al. Na+ channel Nav1.9: in search of a gating mechanism.
Trends Neurosci., 2003 Feb , 26 (55-7).

119

Baker MD et al. GTP-induced tetrodotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones.
J. Physiol. (Lond.), 2003 Apr 15 , 548 (373-82).

120

Rugiero F et al. Selective expression of a persistent tetrodotoxin-resistant Na+ current and NaV1.9 subunit in myenteric sensory neurons.
J. Neurosci., 2003 Apr 1 , 23 (2715-25).

121

Dib-Hajj SD et al. Structure of the sodium channel gene SCN11A: evidence for intron-to-exon conversion model and implications for gene evolution.
Mol. Neurobiol., 2002 Oct-Dec , 26 (235-50).

122

Dib-Hajj S et al. NaN/Nav1.9: a sodium channel with unique properties.
Trends Neurosci., 2002 May , 25 (253-9).

123

Ogata N et al. Molecular diversity of structure and function of the voltage-gated Na+ channels.
Jpn. J. Pharmacol., 2002 Apr , 88 (365-77).

124

Decosterd I et al. The pattern of expression of the voltage-gated sodium channels Na(v)1.8 and Na(v)1.9 does not change in uninjured primary sensory neurons in experimental neuropathic pain models.
Pain, 2002 Apr , 96 (269-77).

125

Liu Cj et al. Fibroblast growth factor homologous factor 1B binds to the C terminus of the tetrodotoxin-resistant sodium channel rNav1.9a (NaN).
J. Biol. Chem., 2001 Jun 1 , 276 (18925-33).

126

Tyrrell L et al. Glycosylation alters steady-state inactivation of sodium channel Nav1.9/NaN in dorsal root ganglion neurons and is developmentally regulated.
J. Neurosci., 2001 Dec 15 , 21 (9629-37).

127

Benn SC et al. Developmental expression of the TTX-resistant voltage-gated sodium channels Nav1.8 (SNS) and Nav1.9 (SNS2) in primary sensory neurons.
J. Neurosci., 2001 Aug 15 , 21 (6077-85).

128

Diss JK et al. Expression profiles of voltage-gated Na(+) channel alpha-subunit genes in rat and human prostate cancer cell lines.
Prostate, 2001 Aug 1 , 48 (165-78).

129

Ogata K et al. Cloning and expression study of the mouse tetrodotoxin-resistant voltage-gated sodium channel alpha subunit NaT/Scn11a.
Biochem. Biophys. Res. Commun., 2000 Jan 7 , 267 (271-7).

130

Jeong SY et al. Identification of a novel human voltage-gated sodium channel alpha subunit gene, SCN12A.
Biochem. Biophys. Res. Commun., 2000 Jan 7 , 267 (262-70).

131

Dib-Hajj SD et al. Coding sequence, genomic organization, and conserved chromosomal localization of the mouse gene Scn11a encoding the sodium channel NaN.
Genomics, 1999 Aug 1 , 59 (309-18).