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Animal Toxins Can Alter the Function of Nav1.8 and Nav1.9
Department of Physiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
Solomon H. Snyder Department of Neuroscience, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
* Author to whom correspondence should be addressed.
Received: 4 July 2012; in revised form: 24 July 2012 / Accepted: 27 July 2012 / Published: 14 August 2012
Abstract: Human voltage-activated sodium (Nav) channels are adept at rapidly transmitting electrical signals across long distances in various excitable tissues. As such, they are amongst the most widely targeted ion channels by drugs and animal toxins. Of the nine isoforms, Nav1.8 and Nav1.9 are preferentially expressed in DRG neurons where they are thought to play an important role in pain signaling. Although the functional properties of Nav1.8 have been relatively well characterized, difficulties with expressing Nav1.9 in established heterologous systems limit our understanding of the gating properties and toxin pharmacology of this particular isoform. This review summarizes our current knowledge of the role of Nav1.8 and Nav1.9 in pain perception and elaborates on the approaches used to identify molecules capable of influencing their function.
Keywords: Nav1.8; Nav1.9; pain; animal toxins; voltage sensor; voltage-activated sodium channel
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MDPI and ACS Style
Gilchrist, J.; Bosmans, F. Animal Toxins Can Alter the Function of Nav1.8 and Nav1.9. Toxins 2012, 4, 620-632.
Gilchrist J, Bosmans F. Animal Toxins Can Alter the Function of Nav1.8 and Nav1.9. Toxins. 2012; 4(8):620-632.
Gilchrist, John; Bosmans, Frank. 2012. "Animal Toxins Can Alter the Function of Nav1.8 and Nav1.9." Toxins 4, no. 8: 620-632.