Papers associated with ganglion (and nav1)

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	GiTx1(β/κ-theraphotoxin-Gi1a), a novel toxin from the venom of Brazilian tarantula Grammostola iheringi (Mygalomorphae, Theraphosidae): Isolation, structural assessments and activity on voltage-gated ion channels., Montandon GG., Biochimie. September 1, 2020; 176 138-149.
	The mechanosensitive ion channel TRAAK is localized to the mammalian node of Ranvier., Brohawn SG., Elife. November 1, 2019; 8
	Prdm12 Directs Nociceptive Sensory Neuron Development by Regulating the Expression of the NGF Receptor TrkA., Desiderio S., Cell Rep. March 26, 2019; 26 (13): 3522-3536.e5.
	Antidepressants inhibit Nav1.3, Nav1.7, and Nav1.8 neuronal voltage-gated sodium channels more potently than Nav1.2 and Nav1.6 channels expressed in Xenopus oocytes., Horishita T., Naunyn Schmiedebergs Arch Pharmacol. December 1, 2017; 390 (12): 1255-1270.
	Heterologous expression of NaV1.9 chimeras in various cell systems., Goral RO., Pflugers Arch. December 1, 2015; 467 (12): 2423-35.
	Rational Engineering Defines a Molecular Switch That Is Essential for Activity of Spider-Venom Peptides against the Analgesics Target NaV1.7., Klint JK., Mol Pharmacol. December 1, 2015; 88 (6): 1002-10.
	Α- and β-subunit composition of voltage-gated sodium channels investigated with μ-conotoxins and the recently discovered μO§-conotoxin GVIIJ., Wilson MJ., J Neurophysiol. April 1, 2015; 113 (7): 2289-301.
	Isolation, synthesis and characterization of ω-TRTX-Cc1a, a novel tarantula venom peptide that selectively targets L-type Cav channels., Klint JK., Biochem Pharmacol. May 15, 2014; 89 (2): 276-86.
	Functional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensors., Bosmans F., J Gen Physiol. July 1, 2011; 138 (1): 59-72.
	μ-Conotoxins that differentially block sodium channels NaV1.1 through 1.8 identify those responsible for action potentials in sciatic nerve., Wilson MJ., Proc Natl Acad Sci U S A. June 21, 2011; 108 (25): 10302-7.
	Phyla- and Subtype-Selectivity of CgNa, a Na Channel Toxin from the Venom of the Giant Caribbean Sea Anemone Condylactis Gigantea., Billen B., Front Pharmacol. November 23, 2010; 1 133.
	Isolation and structure-activity of mu-conotoxin TIIIA, a potent inhibitor of tetrodotoxin-sensitive voltage-gated sodium channels., Lewis RJ., Mol Pharmacol. March 1, 2007; 71 (3): 676-85.
	RE-1 silencer of transcription/neural restrictive silencer factor modulates ectodermal patterning during Xenopus development., Olguín P., J Neurosci. March 8, 2006; 26 (10): 2820-9.
	State-dependent block of rat Nav1.4 sodium channels expressed in xenopus oocytes by pyrazoline-type insecticides., Silver K., Neurotoxicology. June 1, 2005; 26 (3): 397-406.
	Role of auxiliary beta1-, beta2-, and beta3-subunits and their interaction with Na(v)1.8 voltage-gated sodium channel., Vijayaragavan K., Biochem Biophys Res Commun. June 25, 2004; 319 (2): 531-40.
	Differential modulation of Nav1.7 and Nav1.8 peripheral nerve sodium channels by the local anesthetic lidocaine., Chevrier P., Br J Pharmacol. June 1, 2004; 142 (3): 576-84.
	Modulation of Nav1.7 and Nav1.8 peripheral nerve sodium channels by protein kinase A and protein kinase C., Vijayaragavan K., J Neurophysiol. April 1, 2004; 91 (4): 1556-69.
	Molecular cloning and functional expression of the human sodium channel beta1B subunit, a novel splicing variant of the beta1 subunit., Qin N., Eur J Biochem. December 1, 2003; 270 (23): 4762-70.
	Repressor element-1 silencing transcription/neuron-restrictive silencer factor is required for neural sodium channel expression during development of Xenopus., Armisén R., J Neurosci. October 1, 2002; 22 (19): 8347-51.
	Point mutations in homology domain II modify the sensitivity of rat Nav1.8 sodium channels to the pyrethroid insecticide cismethrin., Soderlun DM., Neurotoxicology. December 1, 2001; 22 (6): 755-65.
	Gating properties of Na(v)1.7 and Na(v)1.8 peripheral nerve sodium channels., Vijayaragavan K., J Neurosci. October 15, 2001; 21 (20): 7909-18.
	Nav1.3 sodium channels: rapid repriming and slow closed-state inactivation display quantitative differences after expression in a mammalian cell line and in spinal sensory neurons., Cummins TR., J Neurosci. August 15, 2001; 21 (16): 5952-61.

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