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Items: 1 to 20 of 92

1.

Aberrant sodium channel activity in the complex seizure disorder of Celf4 mutant mice.

Sun W, Wagnon JL, Mahaffey CL, Briese M, Ule J, Frankel WN.

J Physiol. 2013 Jan 1;591(1):241-55. doi: 10.1113/jphysiol.2012.240168.

2.

Etiology of a genetically complex seizure disorder in Celf4 mutant mice.

Wagnon JL, Mahaffey CL, Sun W, Yang Y, Chao HT, Frankel WN.

Genes Brain Behav. 2011 Oct;10(7):765-77. doi: 10.1111/j.1601-183X.2011.00717.x.

3.

CELF4 regulates translation and local abundance of a vast set of mRNAs, including genes associated with regulation of synaptic function.

Wagnon JL, Briese M, Sun W, Mahaffey CL, Curk T, Rot G, Ule J, Frankel WN.

PLoS Genet. 2012;8(11):e1003067. doi: 10.1371/journal.pgen.1003067.

4.

Role of the hippocampus in Nav1.6 (Scn8a) mediated seizure resistance.

Makinson CD, Tanaka BS, Lamar T, Goldin AL, Escayg A.

Neurobiol Dis. 2014 Aug;68:16-25. doi: 10.1016/j.nbd.2014.03.014.

5.

The voltage-gated sodium channel Scn8a is a genetic modifier of severe myoclonic epilepsy of infancy.

Martin MS, Tang B, Papale LA, Yu FH, Catterall WA, Escayg A.

Hum Mol Genet. 2007 Dec 1;16(23):2892-9.

6.

FGF14 localization and organization of the axon initial segment.

Xiao M, Bosch MK, Nerbonne JM, Ornitz DM.

Mol Cell Neurosci. 2013 Sep;56:393-403. doi: 10.1016/j.mcn.2013.07.008.

7.

Physiological and genetic analysis of multiple sodium channel variants in a model of genetic absence epilepsy.

Oliva MK, McGarr TC, Beyer BJ, Gazina E, Kaplan DI, Cordeiro L, Thomas E, Dib-Hajj SD, Waxman SG, Frankel WN, Petrou S.

Neurobiol Dis. 2014 Jul;67:180-90. doi: 10.1016/j.nbd.2014.03.007.

8.

Reduced sodium channel Na(v)1.1 levels in BACE1-null mice.

Kim DY, Gersbacher MT, Inquimbert P, Kovacs DM.

J Biol Chem. 2011 Mar 11;286(10):8106-16. doi: 10.1074/jbc.M110.134692.

9.

An Scn1a epilepsy mutation in Scn8a alters seizure susceptibility and behavior.

Makinson CD, Dutt K, Lin F, Papale LA, Shankar A, Barela AJ, Liu R, Goldin AL, Escayg A.

Exp Neurol. 2016 Jan;275 Pt 1:46-58. doi: 10.1016/j.expneurol.2015.09.008.

PMID:
26410685
10.

Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons.

Royeck M, Horstmann MT, Remy S, Reitze M, Yaari Y, Beck H.

J Neurophysiol. 2008 Oct;100(4):2361-80. doi: 10.1152/jn.90332.2008.

11.

Cell-type-dependent molecular composition of the axon initial segment.

Lorincz A, Nusser Z.

J Neurosci. 2008 Dec 31;28(53):14329-40. doi: 10.1523/JNEUROSCI.4833-08.2008.

12.

Evidence for a role of Nav1.6 in facilitating increases in neuronal hyperexcitability during epileptogenesis.

Hargus NJ, Nigam A, Bertram EH 3rd, Patel MK.

J Neurophysiol. 2013 Sep;110(5):1144-57. doi: 10.1152/jn.00383.2013.

13.

Convulsive seizures and SUDEP in a mouse model of SCN8A epileptic encephalopathy.

Wagnon JL, Korn MJ, Parent R, Tarpey TA, Jones JM, Hammer MF, Murphy GG, Parent JM, Meisler MH.

Hum Mol Genet. 2015 Jan 15;24(2):506-15. doi: 10.1093/hmg/ddu470.

14.
15.

Neuronal voltage-gated ion channels are genetic modifiers of generalized epilepsy with febrile seizures plus.

Hawkins NA, Martin MS, Frankel WN, Kearney JA, Escayg A.

Neurobiol Dis. 2011 Mar;41(3):655-60. doi: 10.1016/j.nbd.2010.11.016.

16.

Neuronal signaling in central nervous system.

Shu Y.

Sheng Li Xue Bao. 2011 Feb 25;63(1):1-8. Review.

17.

Resurgent-like currents in mouse vas deferens myocytes are mediated by NaV1.6 voltage-gated sodium channels.

Teramoto N, Zhu HL, Yotsu-Yamashita M, Inai T, Cunnane TC.

Pflugers Arch. 2012 Nov;464(5):493-502. doi: 10.1007/s00424-012-1153-4.

PMID:
22986623
18.

Functional reciprocity between Na+ channel Nav1.6 and beta1 subunits in the coordinated regulation of excitability and neurite outgrowth.

Brackenbury WJ, Calhoun JD, Chen C, Miyazaki H, Nukina N, Oyama F, Ranscht B, Isom LL.

Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):2283-8. doi: 10.1073/pnas.0909434107.

19.
20.

Pumilio-2 regulates translation of Nav1.6 to mediate homeostasis of membrane excitability.

Driscoll HE, Muraro NI, He M, Baines RA.

J Neurosci. 2013 Jun 5;33(23):9644-54. doi: 10.1523/JNEUROSCI.0921-13.2013.

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