Papers associated with scn8a

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	Solubility phase transition of maternal RNAs during vertebrate oocyte-to-embryo transition., Hwang H, Chen S, Ma M, Divyanshi, Fan HC, Borwick E, Böke E, Mei W, Yang J., Dev Cell. December 4, 2023; 58 (23): 2776-2788.e5.
	Α- and β-subunit composition of voltage-gated sodium channels investigated with μ-conotoxins and the recently discovered μO§-conotoxin GVIIJ., Wilson MJ, Zhang MM, Gajewiak J, Azam L, Rivier JE, Olivera BM, Yoshikami D., J Neurophysiol. April 1, 2015; 113 (7): 2289-301.
	Neurosteroids allopregnanolone sulfate and pregnanolone sulfate have diverse effect on the α subunit of the neuronal voltage-gated sodium channels Nav1.2, Nav1.6, Nav1.7, and Nav1.8 expressed in xenopus oocytes., Horishita T, Yanagihara N, Ueno S, Sudo Y, Uezono Y, Okura D, Minami T, Kawasaki T, Sata T., Anesthesiology. September 1, 2014; 121 (3): 620-31.
	The endocannabinoid anandamide inhibits voltage-gated sodium channels Nav1.2, Nav1.6, Nav1.7, and Nav1.8 in Xenopus oocytes., Okura D, Horishita T, Ueno S, Yanagihara N, Sudo Y, Uezono Y, Sata T., Anesth Analg. March 1, 2014; 118 (3): 554-62.
	Functional expression of Rat Nav1.6 voltage-gated sodium channels in HEK293 cells: modulation by the auxiliary β1 subunit., He B, Soderlund DM., PLoS One. January 1, 2014; 9 (1): e85188.
	Differential state-dependent modification of inactivation-deficient Nav1.6 sodium channels by the pyrethroid insecticides S-bioallethrin, tefluthrin and deltamethrin., McCavera SJ, Soderlund DM., Neurotoxicology. June 1, 2012; 33 (3): 384-90.
	Expression of the voltage- and Ca2+-dependent BK potassium channel subunits BKβ1 and BKβ4 in rodent astrocytes., Seidel KN, Derst C, Salzmann M, Höltje M, Priller J, Markgraf R, Heinemann SH, Heilmann H, Skatchkov SN, Eaton MJ, Veh RW, Prüss H., Glia. June 1, 2011; 59 (6): 893-902.
	Independent and joint modulation of rat Nav1.6 voltage-gated sodium channels by coexpression with the auxiliary β1 and β2 subunits., Tan J, Soderlund DM., Biochem Biophys Res Commun. April 22, 2011; 407 (4): 788-92.
	Localization of receptor site on insect sodium channel for depressant β-toxin BmK IT2., He H, Liu Z, Dong B, Zhang J, Shu X, Zhou J, Ji Y., PLoS One. January 7, 2011; 6 (1): e14510.
	Molecular determination of selectivity of the site 3 modulator (BmK I) to sodium channels in the CNS: a clue to the importance of Nav1.6 in BmK I-induced neuronal hyperexcitability., He H, Liu Z, Dong B, Zhou J, Zhu H, Ji Y., Biochem J. October 15, 2010; 431 (2): 289-98.
	Divergent actions of the pyrethroid insecticides S-bioallethrin, tefluthrin, and deltamethrin on rat Na(v)1.6 sodium channels., Tan J, Soderlund DM., Toxicol Appl Pharmacol. September 15, 2010; 247 (3): 229-37.
	Membrane trauma and Na+ leak from Nav1.6 channels., Wang JA, Lin W, Morris T, Banderali U, Juranka PF, Morris CE., Am J Physiol Cell Physiol. October 1, 2009; 297 (4): C823-34.
	Synthesis, solution structure, and phylum selectivity of a spider delta-toxin that slows inactivation of specific voltage-gated sodium channel subtypes., Yamaji N, Little MJ, Nishio H, Billen B, Villegas E, Nishiuchi Y, Tytgat J, Nicholson GM, Corzo G., J Biol Chem. September 4, 2009; 284 (36): 24568-82.
	Structure/function characterization of micro-conotoxin KIIIA, an analgesic, nearly irreversible blocker of mammalian neuronal sodium channels., Zhang MM, Green BR, Catlin P, Fiedler B, Azam L, Chadwick A, Terlau H, McArthur JR, French RJ, Gulyas J, Rivier JE, Smith BJ, Norton RS, Olivera BM, Yoshikami D, Bulaj G., J Biol Chem. October 19, 2007; 282 (42): 30699-706.
	Structure and sodium channel activity of an excitatory I1-superfamily conotoxin., Buczek O, Wei D, Babon JJ, Yang X, Fiedler B, Chen P, Yoshikami D, Olivera BM, Bulaj G, Norton RS., Biochemistry. September 4, 2007; 46 (35): 9929-40.
	Use-dependent potentiation of the Nav1.6 sodium channel., Zhou W, Goldin AL., Biophys J. December 1, 2004; 87 (6): 3862-72.
	The pentapeptide QYNAD does not block voltage-gated sodium channels., Cummins TR, Renganathan M, Stys PK, Herzog RI, Scarfo K, Horn R, Dib-Hajj SD, Waxman SG., Neurology. January 28, 2003; 60 (2): 224-9.
	Developmental expression of the novel voltage-gated sodium channel auxiliary subunit beta3, in rat CNS., Shah BS, Stevens EB, Pinnock RD, Dixon AK, Lee K., J Physiol. August 1, 2001; 534 (Pt 3): 763-76.
	Sodium channels and neurological disease: insights from Scn8a mutations in the mouse., Meisler MH, Kearney J, Escayg A, MacDonald BT, Sprunger LK., Neuroscientist. April 1, 2001; 7 (2): 136-45.
	The absence of resurgent sodium current in mouse spinal neurons., Pan F, Beam KG., Dev Biol. December 4, 1999; 849 (1-2): 162-8.
	A mutation that causes ataxia shifts the voltage-dependence of the Scn8a sodium channel., Smith MR, Goldin AL., Neuroreport. September 29, 1999; 10 (14): 3027-31.
	Functional analysis of the mouse Scn8a sodium channel., Smith MR, Smith RD, Plummer NW, Meisler MH, Goldin AL., J Neurosci. August 15, 1998; 18 (16): 6093-102.
	Functional analysis of a voltage-gated sodium channel and its splice variant from rat dorsal root ganglia., Dietrich PS, McGivern JG, Delgado SG, Koch BD, Eglen RM, Hunter JC, Sangameswaran L., J Neurochem. June 1, 1998; 70 (6): 2262-72.

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