Relevant bibliographies by topics / Sodium channels

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Sodium channels'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Sodium channels"

1

Sula, Altin, and B. A. Wallace. "Interpreting the functional role of a novel interaction motif in prokaryotic sodium channels." Journal of General Physiology 149, no. 6 (May 18, 2017): 613–22. http://dx.doi.org/10.1085/jgp.201611740.

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Voltage-gated sodium channels enable the translocation of sodium ions across cell membranes and play crucial roles in electrical signaling by initiating the action potential. In humans, mutations in sodium channels give rise to several neurological and cardiovascular diseases, and hence they are targets for pharmaceutical drug developments. Prokaryotic sodium channel crystal structures have provided detailed views of sodium channels, which by homology have suggested potentially important functionally related structural features in human sodium channels. A new crystal structure of a full-length prokaryotic channel, NavMs, in a conformation we proposed to represent the open, activated state, has revealed a novel interaction motif associated with channel opening. This motif is associated with disease when mutated in human sodium channels and plays an important and dynamic role in our new model for channel activation.
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Warmke, Jeffrey W., Robert A. G. Reenan, Peiyi Wang, Su Qian, Joseph P. Arena, Jixin Wang, Denise Wunderler, et al. "Functional Expression of Drosophila para Sodium Channels." Journal of General Physiology 110, no. 2 (August 1, 1997): 119–33. http://dx.doi.org/10.1085/jgp.110.2.119.

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The Drosophila para sodium channel α subunit was expressed in Xenopus oocytes alone and in combination with tipE, a putative Drosophila sodium channel accessory subunit. Coexpression of tipE with para results in elevated levels of sodium currents and accelerated current decay. Para/TipE sodium channels have biophysical and pharmacological properties similar to those of native channels. However, the pharmacology of these channels differs from that of vertebrate sodium channels: (a) toxin II from Anemonia sulcata, which slows inactivation, binds to Para and some mammalian sodium channels with similar affinity (Kd ≅ 10 nM), but this toxin causes a 100-fold greater decrease in the rate of inactivation of Para/TipE than of mammalian channels; (b) Para sodium channels are >10-fold more sensitive to block by tetrodotoxin; and (c) modification by the pyrethroid insecticide permethrin is >100-fold more potent for Para than for rat brain type IIA sodium channels. Our results suggest that the selective toxicity of pyrethroid insecticides is due at least in part to the greater affinity of pyrethroids for insect sodium channels than for mammalian sodium channels.
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Barnes, S., and B. Hille. "Veratridine modifies open sodium channels." Journal of General Physiology 91, no. 3 (March 1, 1988): 421–43. http://dx.doi.org/10.1085/jgp.91.3.421.

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The state dependence of Na channel modification by the alkaloid neurotoxin veratridine was investigated with single-channel and whole-cell voltage-clamp recording in neuroblastoma cells. Several tests of whole-cell Na current behavior in the presence of veratridine supported the hypothesis that Na channels must be open in order to undergo modification by the neurotoxin. Modification was use dependent and required depolarizing pulses, the voltage dependence of production of modified channels was similar to that of normal current activation, and prepulses that caused inactivation of normal current had a parallel effect on the generation of modified current. This hypothesis was then examined directly at the single-channel level. Modified channel openings were easily distinguished from normal openings by their smaller current amplitude and longer burst times. The modification event was often seen as a sudden, dramatic reduction of current through an open Na channel and produced a somewhat flickery channel event having a mean lifetime of 1.6 s at an estimated absolute membrane potential of -45 mV (23 degrees C). The modified channel had a slope conductance of 4 pS, which was 20-25% the size of the slope conductance of normal channels with the 300 mM NaCl pipette solution used. Most modified channel openings were initiated by depolarizing pulses, began within the first 10 ms of the depolarizing step, and were closely associated with the prior opening of single normal Na channels, which supports the hypothesis that modification occurs from the normal open state.
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Duch, D. S., E. Recio-Pinto, C. Frenkel, S. R. Levinson, and B. W. Urban. "Veratridine modification of the purified sodium channel alpha-polypeptide from eel electroplax." Journal of General Physiology 94, no. 5 (November 1, 1989): 813–31. http://dx.doi.org/10.1085/jgp.94.5.813.

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In the interest of continuing structure-function studies, highly purified sodium channel preparations from the eel electroplax were incorporated into planar lipid bilayers in the presence of veratridine. This lipoglycoprotein originates from muscle-derived tissue and consists of a single polypeptide. In this study it is shown to have properties analogous to sodium channels from another muscle tissue (Garber, S. S., and C. Miller. 1987. Journal of General Physiology. 89:459-480), which have an additional protein subunit. However, significant qualitative and quantitative differences were noted. Comparison of veratridine-modified with batrachotoxin-modified eel sodium channels revealed common properties. Tetrodotoxin blocked the channels in a voltage-dependent manner indistinguishable from that found for batrachotoxin-modified channels. Veratridine-modified channels exhibited a range of single-channel conductance and subconductance states. The selectivity of the veratridine-modified sodium channels for sodium vs. potassium ranged from 6-8 in reversal potential measurements, while conductance ratios ranged from 12-15. This is similar to BTX-modified eel channels, though the latter show a predominant single-channel conductance twice as large. In contrast to batrachotoxin-modified channels, the fractional open times of these channels had a shallow voltage dependence which, however, was similar to that of the slow interaction between veratridine and sodium channels in voltage-clamped biological membranes. Implications for sodium channel structure are discussed.
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Scheuer, T., and W. A. Catterall. "Control of neuronal excitability by phosphorylation and dephosphorylation of sodium channels." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1299–302. http://dx.doi.org/10.1042/bst0341299.

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Currents through voltage-gated sodium channels drive action potential depolarization in neurons and other excitable cells. Smaller currents through these channels are key components of currents that control neuronal firing and signal integration. Changes in sodium current have profound effects on neuronal firing. Sodium channels are controlled by neuromodulators acting through phosphorylation of the channel by serine/threonine and tyrosine protein kinases. That phosphorylation requires specific molecular interaction of kinases and phosphatases with the channel molecule to form localized signalling complexes. Such localization is required for effective neurotransmitter-mediated regulation of sodium channels by protein kinase A. Analogous molecular complexes between sodium channels, kinases and other signalling molecules are expected to be necessary for specific and localized transmitter-mediated modulation of sodium channels by other protein kinases.
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Huguenard, John R. "Sodium Channels." Neuron 33, no. 4 (February 2002): 492–94. http://dx.doi.org/10.1016/s0896-6273(02)00592-5.

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Wood, John N., and Federico Iseppon. "Sodium channels." Brain and Neuroscience Advances 2 (January 2018): 239821281881068. http://dx.doi.org/10.1177/2398212818810684.

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In 2000, with the completion of the human genome project, nine related channels were found to comprise the complete voltage-gated sodium gene family and they were renamed NaV1.1–NaV1.9. This millennial event reflected the extraordinary impact of molecular genetics on our understanding of electrical signalling in the nervous system. In this review, studies of animal electricity from the time of Galvani to the present day are described. The seminal experiments and models of Hodgkin and Huxley coupled with the discovery of the structure of DNA, the genetic code and the application of molecular genetics have resulted in an appreciation of the extraordinary diversity of sodium channels and their surprisingly broad repertoire of functions. In the present era, unsuspected roles for sodium channels in a huge range of pathologies have become apparent.
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Yatani, A., D. L. Kunze, and A. M. Brown. "Effects of dihydropyridine calcium channel modulators on cardiac sodium channels." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 1 (January 1, 1988): H140—H147. http://dx.doi.org/10.1152/ajpheart.1988.254.1.h140.

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To investigate whether cardiac sodium channels have dihydropyridine (DHP) receptors we studied the effects of the optically pure (greater than 95%) enantiomers of the DHPs PN200–110 and BAY-K 8644 and the racemic DHP nitrendipine (NTD). Whole cell and single-channel sodium currents were recorded from cultured ventricular cells of neonatal rats using the patch-clamp method. NTD reduced cardiac sodium currents in a voltage-dependent manner. Inhibitory effects were due to an increase in traces without activity. The unit conductance remained unchanged. At negative holding potentials, NTD transiently increased the probability of channel opening. Both (+) and (-) PN 200–110 blocked sodium channels, although the (-) isomer was about one order of magnitude less effective. The blocking effects were voltage dependent. (+) BAY-K 8644 had similar blocking effects. (-) BAY-K 8644 produced an increase in sodium currents due to an increased frequency of channel openings and a marked prolongation of open time without any significant change in unit conductance. The DHPs have effects on cardiac sodium whole cell and single-channel currents that appear identical to and are as stereospecific as their effects on cardiac calcium currents, although the concentrations required are larger. In contrast the inwardly rectifying potassium channel (IK1) is unaffected by these DHPs. We conclude that functionally equivalent DHP receptors are present in cardiac sodium and calcium channels but not potassium channels and take this as evidence of the homology between sodium and calcium channels.
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Tomaselli, G. F., A. M. Feldman, G. Yellen, and E. Marban. "Human cardiac sodium channels expressed in Xenopus oocytes." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 3 (March 1, 1990): H903—H906. http://dx.doi.org/10.1152/ajpheart.1990.258.3.h903.

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We report the expression of voltage-dependent Na+ channels in Xenopus oocytes injected with total RNA isolated from explanted human hearts. The expressed channels demonstrate characteristic voltage-dependent gating, inhibition by tetrodotoxin, and selectivity for Na+. Oocytes injected with sterile water or intentionally degraded RNA had no similar channel activity. The antiarrhythmic agent lidocaine (20 microM) inhibits current flow through the channel in a voltage-dependent fashion. Na+ channels expressed by injection of human cardiac RNA into Xenopus oocytes qualitatively resemble channels in the native tissue.
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Hahin, R. "Removal of inactivation causes time-invariant sodium current decays." Journal of General Physiology 92, no. 3 (September 1, 1988): 331–50. http://dx.doi.org/10.1085/jgp.92.3.331.

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The kinetic properties of the closing of Na channels were studied in frog skeletal muscle to obtain information about the dependence of channel closing on the past history of the channel. Channel closing was studied in normal and modified channels. Chloramine-T was used to modify the channels so that inactivation was virtually removed. A series of depolarizing prepulse potentials was used to activate Na channels, and a -140-mV postpulse was used to monitor the closing of the channels. Unmodified channels decay via a biexponential process with time constants of 72 and 534 microseconds at 12 degrees C. The observed time constants do not depend upon the potential used to activate the channels. The contribution of the slow component to the total decay increases as the activating prepulse is lengthened. After inactivation is removed, the biexponential character of the decay is retained, with no change in the magnitude of the time constants. However, increases in the duration of the activating prepulse over the range where the current is maximal 1-75 ms) produce identical biexponential decays. The presence of biexponential decays suggests that either two subtypes of Na channels are found in muscle, or Na channels can exist in one of two equally conductive states. The time-invariant decays observed suggest that channel closure does not depend upon their past history.
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Dissertations / Theses on the topic "Sodium channels"

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Thompson, Andrew J. "Actions of pyrethroid on sodium channels." Thesis, University of Nottingham, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243690.

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Mahdavi, Somayeh. "Computational Study of Mammalian Sodium Channels." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13883.

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Mammalian sodium (NaV) channels are membrane proteins with potential therapeutic applications. Lack of crystal structures is the main bottleneck for studying these channels. Constructing a model of NaV channels using computational methods is an alternative way to study NaV channels and would be valuable in structure-based drug design. I constructed a homology model for NaV1.4 based on the crystal structure of bacterial counterparts. The extensive functional data for the binding of µ–conotoxin GIIIA to NaV1.4 were used to validate the model. The predictions of the binding were in good agreement with mutagenesis data. The standard binding free energy of GIIIA was also calculated from its potential of mean force (PMF) and was consistent with the experimental value. I then used the validated model to study binding of other µ-conotoxins, including KIIIA, PIIIA, and BuIIIB. The results indicated that there is a common motif for binding of µ–conotoxins to NaV1 which is useful in understanding experimental results and designing new analogues. The NaV1.4 model was also used to study the ion permeation. Linking of the residues at the selectivity filter (DEKA) with residues in the neighbouring domain was found to be important for keeping the permeation pathway open. The results revealed that there was a Na+ ion binding site inside the DEKA locus, and 1-2 Na+ ions could occupy the vestibule near the EEDD ring. These sites are separated by a low free energy barrier, suggesting inward conduction occurs when a Na+ ion in the vestibule goes over the free energy barrier and pushes the Na+ ion in the filter to the intracellular cavity, consistent with the classical knock-on mechanism. The model also provides a good description of the observed Na+/K+ selectivity. In summary, the validated model of NaV1.4 provides a reasonable platform for future studies of mammalian NaV channels and design selective analogues with therapeutic applications.
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McNair, William Parkhill. "Clinical and functional characterization of an SCN5A mutation associated with dilated cardiomyopathy /." Connect to abstract via ProQuest. Full text is not available online, 2008.

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Fjell, Hjelmström Jenny. "Tetrodotoxin-resistant sodium channels in neuropathic pain /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4181-5/.

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Small, T. K. "Drug action on voltage-gated sodium channels." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19492/.

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Voltage-gated sodium (Nav) channels are therapeutic targets for several disorders affecting humans, including epilepsy, neurodegeneration and neuropathic pain. Typically, drugs treating these conditions exert a use- and voltage-dependent inhibition of Na currents, an action attributed to the stabilisation of the slow inactivated state which is formed during prolonged depolarisation. The binding site has been suggested to reside in the channel pore at a site only accessible from the intracellular environment. What gives different chemicals having this action in common selectivity for certain disorders (e.g. neuroprotection versus epilepsy) remains a mystery. Several channel subtypes exist, with types Nav1.2 and Nav1.6 being major isoforms found in the brain, raising the possibility that different subtypes exhibit differential drug sensitivity. To investigate this issue and explore the site of drug action further, the action of several Nav channel modulators, including lidocaine (a local anaesthetic) and sipatrigine (a neuroprotective agent), were studied on Na currents generated by Nav1.2a and Nav1.6 channels stably expressed in cell lines, and by acutely dissociated native cells, using electrophysiological techniques. The findings indicated that different drugs have some selectivity for particular channel subtypes. In addition, to study the slow inactivated state more selectively, fast inactivation was inhibited chemically. Inhibition of this mechanism altered both normal channel function and drug action. Drug effect during external and internal application to cells was also compared. Seemingly contrary to the current hypothesis of an internal site of action, drugs were more potent following external application, suggesting that their site of action may be different from the putative intracellularly-accessible “local anaesthetic receptor”. These experimental results were tested using a mathematical simulation of drug diffusion during whole-cell voltage-clamped electrophysiological recordings, to determine whether variations in the physicochemical properties of these drugs could explain their different potencies on internal and external application.
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Browne, Liam Edward. "Drug binding sites on Nat1.8 sodium channels." Thesis, University of Leeds, 2008. http://etheses.whiterose.ac.uk/3258/.

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The voltage-gated sodium channel, Nav 1.8, is known to play an important role in pain signalling. In this thesis, the functional properties and drug binding sites of wild type and mutant Nav 1.8 sodium channel currents were studied in mammalian sensory neuron-derived ND7/23 cells using whole-cell patch clamp. While the voltage-dependence of activation was similar for wild type human and rat Nay 1.8 channels, the voltage-dependence of steady-state inactivation was more hyperpolarised for hNav 1.8 compared to rNav 1.8. Furthermore, as a consequence of the different time course for inactivation between human and rat channels, inhibition during frequent stimulation was less pronounced for hNav 1.8 than for rNav 1.8. Thus, this would imply that the human channel is more inactivated at normal resting potentials, and can support higher firing frequencies than the rat channel. The action of tetracaine, ralfmamide, 227c89, Vl02862, and Nav1. 8-selective compound A-803467 on wild type hNav 1.8 and rNav 1.8 channels was studied. All compounds showed preferential block of inactivated channels rather than resting channels. Compound A-803467 showed greater affinity for inactivated hNav 1.8 channels than for inactivated rNav 1.8 channels. Unexpectedly, an increase in current was observed for V102862 and A-803467 during recovery from inactivation, likely due to "disinhibition" of resting block. For A-803467, rather than usedependent inhibition, this disinhibition increased the current during frequent stimulation, while for VI 02862 it led to the absence of inhibition during low frequency stimulation. Thus while both V 102862 and A-803467 are potent inhibitors ofNav 1.8, V102862, rather than A-803467 might be a more useful blocker where physiological firing frequencies are higher. Alanine mutations at residues 1381, N390, L14l0, V14l4, Il706, F1710 and Y1717 were made in the pore-lining S6 segments of the hN av 1. 8 channel, and at the corresponding positions in the rNav 1.8 channel. Many of the mutations caused shifts in voltage-dependence of activation and inactivation, and gave a faster time course of inactivation, indicating that the native residues at these positions are important for both activation and inactivation in Nav 1.8 sodium channels. The affinity of tetracaine for the resting and inactivated channels was reduced by hNav1.8 mutations 138lA, F1710A and Y1717A (only inactivated state affinity was measured for the latter), and by mutation F17l0A for A-803467. For mutation L1410A both compounds caused complete resting block at very low concentrations; this block was removed by further stimulation. While tetracaine did not show disinhibition for wild type channels during recovery from inactivation, it was seen particularly for mutants L1410 and F1710A. All mutations increased the extent of disinhibition of A-803467. These results suggest that the Nav 1.8-selective compound A-803467 acts within the pore S6 segments with a differing but partially overlapping site to that of the local anaesthetic tetracaine.
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Lee, So Ra. "Pharmacological and biophysical characterization of a prokaryotic voltage-gated sodium channel." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1477.

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The pedigree of voltage-gated sodium channels spans the millennia from eukaryotic members that initiate the action potential firing in excitable tissues to primordial ancestors that act as enviro-protective complexes in bacterial extremophiles. Eukaryotic sodium channels (eNavs) are central to electrical signaling throughout the cardiovascular and nervous systems in animals and are established clinical targets for the therapeutic management of epilepsy, cardiac arrhythmia and painful syndromes as they are inhibited by local anesthetic compounds. Alternatively, bacterial voltage-gated sodium channels (bNavs) likely regulate the survival response against extreme pH conditions, electrophiles and hypo-osmotic shock and may represent a founder of the voltage-gated cation channel family. Despite apparent differences between eNav and bNav channel physiology, gating and gene structure, the discovery that bNavs are amenable to crystallographic study opens the door for the possibility of structure-guided rational design of the next generation of therapeutics that target eNavs. Here I summarize the gating behavior of a bacterial channel NaChBac and discuss mechanisms of local anesthetic inhibition in light of the growing number of bNav structures. Also, an interesting novel observation on cross-lineage modulation of NaChBac by eNav beta subunit is reported. This auxiliary subunit modulation is isoform specific and I show the discrete effects of each isoforms on NaChBac, with functional and biochemical analysis. I also report a novel mutation that alters inactivation kinetic drastically and a possible mechanism of NaChBac inactivation is discussed.
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Robins, Gerard George. "Second messenger regulation of human epithelial sodium channels." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402198.

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Baines, Deborah Louise. "Voltage dependent sodium channels of nerve and muscle." Thesis, University of Bristol, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335553.

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Ekberg, Jenny. "Novel peptide toxin and protein modulators of voltage-gated ion channels /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe20102.pdf.

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Books on the topic "Sodium channels"

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A, Allen T. Jeff, Noble D, and Reuter Harald, eds. Sodium-calcium exchange. Oxford: Oxford University Press, 1989.

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Ruben, Peter C., ed. Voltage Gated Sodium Channels. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3.

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Bock, Gregory, and Jamie A. Goode, eds. Sodium Channels and Neuronal Hyperexcitability. Chichester, UK: John Wiley & Sons, Ltd, 2001. http://dx.doi.org/10.1002/0470846682.

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Bock, Gregory, and Jamie A. Goode, eds. Sodium Channels and Neuronal Hyperexcitability. Chichester, UK: John Wiley & Sons, Ltd, 2001. http://dx.doi.org/10.1002/0470846682.

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Parnham, Michael J., Kevin Coward, and Mark D. Baker, eds. Sodium Channels, Pain, and Analgesia. Basel: Birkhäuser-Verlag, 2005. http://dx.doi.org/10.1007/3-7643-7411-x.

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Gregory, Bock, and Goode Jamie, eds. Sodium channels and neuronal hyperexcitability. Chichester, England: Wiley, 2002.

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A, Allen T. Jeff, Noble Denis, and Reuter Harald, eds. Sodium-calcium exchange. Oxford [England]: Oxford University Press, 1989.

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W, Hilgemann Donald, Philipson Kenneth D, Vassort Guy, New York Academy of Sciences., and International Conference on Sodium-Calcium Exchange (3rd : 1995 : Woods Hole, Mass.), eds. Sodium-calcium exchange: Proceedings of the Third International Conference. New York, N.Y: The New York Academy of Sciences, 1996.

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Y, Kao C., Levinson S. R, and New York Academy of Sciences., eds. Tetrodotoxin, saxitoxin, and the molecular biology of the sodium channel. New York, N.Y: New York Academy of Sciences, 1986.

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Chahine, Mohamed, ed. Voltage-gated Sodium Channels: Structure, Function and Channelopathies. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90284-5.

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Book chapters on the topic "Sodium channels"

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Engel, Dominique. "Sodium Channels." In Encyclopedia of Computational Neuroscience, 2729–33. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_134.

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Engel, Dominique. "Sodium Channels." In Encyclopedia of Computational Neuroscience, 1–5. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_134-1.

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Gupta, Rajesh. "Sodium Channels." In Pain Management, 31–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-55061-4_12.

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Pichon, Y., M. Pelhate, and U. Heilig. "Sodium Channels." In ACS Symposium Series, 212–25. Washington, DC: American Chemical Society, 1987. http://dx.doi.org/10.1021/bk-1987-0356.ch016.

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Scheuer, Todd. "Bacterial Sodium Channels: Models for Eukaryotic Sodium and Calcium Channels." In Voltage Gated Sodium Channels, 269–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_13.

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Peters, Colin H., and Peter C. Ruben. "Introduction to Sodium Channels." In Voltage Gated Sodium Channels, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_1.

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Gilchrist, John, Baldomero M. Olivera, and Frank Bosmans. "Animal Toxins Influence Voltage-Gated Sodium Channel Function." In Voltage Gated Sodium Channels, 203–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_10.

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Laedermann, Cédric J., Isabelle Decosterd, and Hugues Abriel. "Ubiquitylation of Voltage-Gated Sodium Channels." In Voltage Gated Sodium Channels, 231–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_11.

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Corry, Ben, Sora Lee, and Christopher A. Ahern. "Pharmacological Insights and Quirks of Bacterial Sodium Channels." In Voltage Gated Sodium Channels, 251–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_12.

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Groome, James R. "The Voltage Sensor Module in Sodium Channels." In Voltage Gated Sodium Channels, 7–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_2.

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Conference papers on the topic "Sodium channels"

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Oliveira, Eugenio Eduardo. "Pyrethroids and voltage sensors in sodium channels." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.91249.

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Hsieh, J. C., S. K. Lin, W. C. Tzeng, and S. M. Shieh. "Simulated blocking potassium channels medication on variant mutant SCN5A sodium channels." In Computers in Cardiology, 2005. IEEE, 2005. http://dx.doi.org/10.1109/cic.2005.1588247.

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Rahman, M. Mostafizur, Mufti Mahmud, and Stefano Vassanelli. "Self-gating of sodium channels at neuromuscular junction." In 5th International IEEE/EMBS Conference on Neural Engineering (NER 2011). IEEE, 2011. http://dx.doi.org/10.1109/ner.2011.5910524.

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Soares, Marília A. G., Frederico A. O. Cruz, and Dilson Silva. "Magnetic and electric fields across sodium and potassium channels." In INTERNATIONAL CONFERENCE OF COMPUTATIONAL METHODS IN SCIENCES AND ENGINEERING 2015 (ICCMSE 2015). AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4938910.

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Rahman, M. Mostafizur, Mufti Mahmud, and Stefano Vassanelli. "Sodium channels' kinetics under self-gating condition at neuromuscular junction." In 2011 4th International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2011. http://dx.doi.org/10.1109/bmei.2011.6098478.

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Ji, H., R. Zhao, D. Bhattarai, H. G. Nie, and G. Ali. "Plasmin Cleaves Human Epithelial Sodium Channels to Resolve Lung Edema." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1156.

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Milanese, D., L. N. Ng, A. Fu, E. R. M. Taylor, C. Contardi, and M. Ferraris. "UV Written Channels in Germano Borosilicate Glasses Doped with Sodium." In Bragg Gratings, Photosensitivity, and Poling in Glass Waveguides. Washington, D.C.: OSA, 1999. http://dx.doi.org/10.1364/bgpp.1999.cb4.

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Lam, Yee Cheong, Gongyue Tang, and Deguang Yan. "Geometry Effect on the Electrokinetic Instability of the Electroosmotic Flow in Microfluidic Channels." In ASME 2008 First International Conference on Micro/Nanoscale Heat Transfer. ASMEDC, 2008. http://dx.doi.org/10.1115/mnht2008-52070.

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To study the effect of geometry on electroosmotic flow in micro channels, we fabricated PDMS-glass microchannels of different designs, which have patterned channels with abrupt contraction of different sizes. Using fluorescent imaging technology, we demonstrated the effect of geometry on the instability of DC driven electroosmotic flow in microfluidic channels. For certain geometry and conductivity of the electrolyte solution (Sodium Bicarbonate), there is a threshold voltage for electroosmotic instability, exhibiting itself as “ripple”. Generally, the factors which affect the threshold voltage include channel width, channel geometry, and electrolyte conductivity. Narrower channel resulted in higher onset voltage. As conductivity of the electrolyte increases, the threshold voltage tends to increase. Early transition to unstable electroosmotic flow in microfluidic channels was observed under relatively low Re.
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Luo, Gang, Peiwei Sun, Xi Bai, Huasong Cao, Kai Wang, and Huanjun Zhu. "Modeling and Sensitivity Analysis of the Sodium-Water Reaction Accident in Parallel Channels." In 2021 28th International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/icone28-64490.

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Abstract A pressure wave propagation across the second loop of a sodium-cooled fast reactor may lead to severe damage to the pipes and the equipment due to a large leakage sodium-water reaction accident. Therefore, the pressure source and the pressure wave propagation calculation and analysis can be significant for a sodium-cooled fast reactor’s design and operation. A mathematical model with code was built to calculate and predict both the pressure source and the pressure wave propagation after the large leak sodium-water reaction accident occurred in an SFR steam generator. In the pressure source model, the sodium-water reaction produces hydrogen and squeezes sodium nearby. It is assumed that the sodium-water reaction carries out instantaneously, and a spherical-to-column bubble is assumed to grow up at the reaction zone. Under such assumptions, the pressure source model can obtain the hydrogen bubble’s volume and pressure in the steam generator. In the pressure wave propagation model, flow is assumed to be one-dimensional. With the basic theory of mass conservation, momentum conservation, and the Isentropic relation of the working fluid, the numerical solution is calculated by a grid divided by the method of characteristics, considering both precision and efficiency. However, plenty of parameters, both of the pressure source and the parallel channels, can affect the accident in different ways and scales. Considering that to practice a large leakage sodium-water reaction experiment can be somewhat difficult because of its danger, inconvenience, and high cost, it is quite essential to conduct a sensitivity analysis through the program for the purpose of facilitating the design of an SFR. Since most sodium-cooled fast reactor designs are multimodules, a parallel channel structure with multiple pressure boundaries is modeled for sensitivity analysis. Sensitivity analysis was performed on multiple sets of important parameters, including different hydrogen bubble properties, different pressure boundaries, and different equipment types. Following the sensitivity study, the code can be used for the accident analysis in a future commercial demonstration fast reactor by indicating various parameter guidance for the design and construction.
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Guzmán-Ramírez, Gregorio, Agustín Segovia-Ríos, Jorge Sierra-Arellano, Juvencio Robles, Enrique Díaz-Herrera, and Eusebio Juaristi. "Ionized Sodium Clusters Fragmentation Channels: A New Extended Hardness Definition Approach." In 2007. AIP, 2008. http://dx.doi.org/10.1063/1.2901843.

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Reports on the topic "Sodium channels"

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Tortella, Frank. Neuronal Sodium Channels in Neurodegeneration and Neuroprotection. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395689.

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Tortella, Frank C. Neuronal Sodium Channels in Neurodegeneration and Neuroprotection. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada406069.

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Gordon, Dalia, Ke Dong, and Michael Gurevitz. Unexpected Specificity of a Sea Anemone Small Toxin for Insect Na-channels and its Synergic Effects with Various Insecticidal Ligands: A New Model to Mimic. United States Department of Agriculture, November 2010. http://dx.doi.org/10.32747/2010.7697114.bard.

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Motivated by the high risks to the environment and human health imposed by the current overuse of chemical insecticides we offer an alternative approach for the design of highly active insect-selective compounds that will be based on the ability of natural toxins to differentiate between insect and mammalian targets. We wish to unravel the interacting surfaces of insect selective toxins with their receptor sites on voltage-gated sodium channels. In this proposal we put forward two recent observations that may expedite the development of a new generation of insect killers that mimic the highly selective insecticidal toxins: (i) A small (27aa) highly insecticidal sea anemone toxin, Av3, whose toxicity to mammals is negligible; (ii) The prominent positive cooperativity between distinct channel ligands, such as the strong enhancement of pyrethroids effects by anti-insect selective scorpion depressant toxins. We possess a repertoire of insecticidal toxins and sodium channel subtypes all available in recombinant form for mutagenesis followed by analysis of various pharmacological, electrophysiological, and structural methods. Our recent success to express Av3 provides for the first time a selective toxin for receptor site-3 on insect sodium channels. In parallel, our recent success to determine the structures and bioactive surfaces of insecticidal site-3 and site-4 toxins establishes a suitable system for elucidation of toxin-receptor interacting faces. This is corroborated by our recent identification of channel residues involved with these two receptor sites. Our specific aims in this proposal are to (i) Determine the bioactive surface of Av3 toward insect Na-channels; (ii) Identify channel residues involved in binding or activity of the insecticidal toxins Av3 and LqhaIT, which differ substantially in their potency on mammals; (iii) Illuminate channel residues involved in recognition by the anti-insect depressant toxins; (iv) Determine the face of interaction of both site-3 (Av3) and site-4 (LqhIT2) toxins with insect sodium channels using thermodynamic mutant cycle analysis; and, (v) Examine whether Av3, LqhIT2, pyrethroids, and indoxacarb (belongs to a new generation of insecticides), enhance allosterically the action of one another on the fruit fly and cockroach paraNa-channels and on their kdr and super-kdr mutants. This research establishes the grounds for rational design of novel anti-insect peptidomimetics with minimal impact on human health, and offers a new approach in insect pest control, whereby a combination of allosterically interacting compounds increases insecticidal action and reduces risks of resistance buildup.
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Gurevitz, Michael, Michael Adams, and Eliahu Zlotkin. Insect Specific Alpha Neurotoxins from Scorpion Venoms: Mode of Action and Structure-Function Relationships. United States Department of Agriculture, June 1996. http://dx.doi.org/10.32747/1996.7613029.bard.

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This study was motivated by the need to develop new means and approaches to the design of future, environmentally-safe, insecticides. Utilization of anti-insect selective toxins from scorpion venoms and clarification of the molecular basis for their specificity, are a major focus in this project and may have an applicative value. Our study concentrated on the highly insecticidal toxin, LqhaIT, and was devoted to: (I) Characterization of the neuropharmacological and electrophysiological features of this toxin. (II) Establishment of a genetic system for studying structure/activity relationships of the toxin. (III) Analysis of the insecticidal efficacy of an entomopathogenic baculovirus engineered and expressing LqhaIT. The results obtained in this project suggest that: 1) The receptor binding site of LqhaIT on insect sodium channels differs most likely from its analogous receptor site 3 on vertebrate sodium channels. 2) The effects of LqhaIT are presynaptic. Hyperexcitation at the neuromuscular results from dramatic slowing of sodium channel inactivation and enhanced peak sodium currents causes by LqhaIT. 3) The putative toxic surface of LqhaIT involves aromatic and charged amino acid residues located around the C-terminal region and five-residue-turn of the toxin (unpublished). 4) The anti-insect/anti-mammalian toxicity ratio can be altered by site-directed mutagenesis (publication 8). This effect was partly shown at the level of sodium channel function. 5) The insecticidal efficacy of AcNPV baculovirus increased to a great extent when infection was accompanied by expression of LqhaIT (publication 5).
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Catterall, William A. Prevention of Paralytic Neurotoxin Action on Voltage-Sensitive Sodium Channels. Fort Belvoir, VA: Defense Technical Information Center, February 1992. http://dx.doi.org/10.21236/ada257915.

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Catterall, William A. Molecular Basis of Paralytic Neurotoxin Action on Voltage-Sensitive Sodium Channels. Fort Belvoir, VA: Defense Technical Information Center, October 1986. http://dx.doi.org/10.21236/ada179898.

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Gurevitz, Michael, Michael E. Adams, Boaz Shaanan, Oren Froy, Dalia Gordon, Daewoo Lee, and Yong Zhao. Interacting Domains of Anti-Insect Scorpion Toxins and their Sodium Channel Binding Sites: Structure, Cooperative Interactions with Agrochemicals, and Application. United States Department of Agriculture, December 2001. http://dx.doi.org/10.32747/2001.7585190.bard.

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Integrated pest management in modern crop protection may combine chemical and biological insecticides, particularly due to the risks to the environment and livestock arising from the massive use of non-selective chemicals. Thus, there is a need for safer alternatives, which target insects more specifically. Scorpions produce anti-insect selective polypeptide toxins that are biodegradable and non-toxic to warm-blooded animals. Therefore, integration of these substances into insect pest control strategies is of major importance. Moreover, clarification of the molecular basis of this selectivity may provide valuable information pertinent to their receptor sites and to the future design of peptidomimetic anti-insect specific substances. These toxins may also be important for reducing the current overuse of chemical insecticides if they produce a synergistic effect with conventional pesticides. Based on these considerations, our major objectives were: 1) To elucidate the three-dimensional structure and toxic-site of scorpion excitatory, "depressant, and anti-insect alpha toxins. 2) To obtain an initial view to the sodium channel recognition sites of the above toxins by generating peptide decoys through a phage display system. 3) To investigate the synergism between toxins and chemical insecticides. Our approach was to develop a suitable expression system for toxin production in a recombinant form and for elucidation of toxin bioactive sites via mutagenesis. In parallel, the mode of action and synergistic effects of scorpion insecticidal toxins with pyrethroids were studied at the sodium channel level using electrophysiological methods. Objective 1 was achieved for the alpha toxin, LqhaIT Zilberberg et al., 1996, 1997; Tugarinov et al., 1997; Froy et al., 2002), and the excitatory toxin, Bj-xtrIT (Oren et al., 1998; Froy et al., 1999; unpublished data). The bioactive surface of the depressant toxin, LqhIT2, has been clarified and a crystal of the toxin is now being analyzed (unpublished). Objective 2 was not successful thus far as no phages that recognize the toxins were obtained. We therefore initiated recently an alternative approach, which is introduction of mutations into recombinant channels and creation of channel chimeras. Objective 3 was undertaken at Riverside and the results demonstrated synergism between LqhaIT or AaIT and pyrethroids (Lee et al., 2002). Furthermore, negative cross-resistance between pyrethroids and scorpion toxins (LqhaIT and AaIT) was demonstrated at the molecular level. Although our study did not yield a product, it paves the way for future design of selective pesticides by capitalizing on the natural competence of scorpion toxins to distinguish between sodium channels of insects and vertebrates. We also show that future application of anti-insect toxins may enable to decrease the amounts of chemical pesticides due to their synergism.
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Gurevitz, Michael, William A. Catterall, and Dalia Gordon. face of interaction of anti-insect selective toxins with receptor site-3 on voltage-gated sodium channels as a platform for design of novel selective insecticides. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7699857.bard.

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Voltage-gated sodium channels (Navs) play a pivotal role in excitability and are a prime target of insecticides like pyrethroids. Yet, these insecticides are non-specific due to conservation of Navs in animals, raising risks to the environment and humans. Moreover, insecticide overuse leads to resistance buildup among insect pests, which increases misuse and risks. This sad reality demands novel, more selective, insect killers whose alternative use would avoid or reduce this pressure. As highly selective insect toxins exist in venomous animals, why not exploit this gift of nature and harness them in insect pest control? Many of these peptide toxins target Navs, and since their direct use via transformed crop plants or mediator microorganisms is problematic in public opinion, we focus on the elucidation of their receptor binding sites with the incentive of raising knowledge for design of toxin peptide mimetics. This approach is preferred nowadays by agro-industries in terms of future production expenses and public concern. However, characterization of a non-continuous epitope, that is the channel receptor binding site for such toxins, requires a suitable experimental system. We have established such a system within more than a decade and reached the stage where we employ a number of different insect-selective toxins for the identification of their receptor sites on Navs. Among these toxins we wish to focus on those that bind at receptor site-3 and inhibit Nav inactivation because: (1) We established efficient experimental systems for production and manipulation of site-3 toxins from scorpions and sea anemones. These peptides vary in size and structure but compete for site-3 on insect Navs. Moreover, these toxins exhibit synergism with pyrethroids and with other channel ligands; (2) We determined their bioactive surfaces towards insect and mammalian receptors (see list of publications); (3) We found that despite the similar mode of action on channel inactivation, the preference of the toxins for insect and mammalian channel subtypes varies greatly, which can direct us to structural features in the basis of selectivity; (4) We have identified by channel loop swapping and point mutagenesis extracellular segments of the Navinvolved with receptor site-3. On this basis and using channel scanning mutagenesis, neurotoxin binding, electrophysiological analyses, and structural data we offer: (i) To identify the residues that form receptor site-3 at insect and mammalian Navs; (ii) To identify by comparative analysis differences at site-3 that dictate selectivity toward various Navs; (iii) To exploit the known toxin structures and bioactive surfaces for modeling their docking at the insect and mammalian channel receptors. The results of this study will enable rational design of novel anti-insect peptide mimetics with minimized risks to human health and to the environment. We anticipate that the release of receptor site-3 molecular details would initiate a worldwide effort to design peptide mimetics for that site. This will establish new strategies in insect pest control using alternative insecticides and the combined use of compounds that interact allosterically leading to increased efficiency and reduced risks to humans or resistance buildup among insect pests.
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Gurevitz, Michael, William A. Catterall, and Dalia Gordon. Learning from Nature How to Design Anti-insect Selective Pesticides - Clarification of the Interacting Face between Insecticidal Toxins and their Na-channel Receptors. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7697101.bard.

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Structural details on the interacting faces of toxins and sodium channels (Navs), and particularly identification of elements that confer specificity for insects, are difficult to approach and require suitable experimental systems. Therefore, natural toxins capable of differential recognition of insect and mammalian Navs are valuable leads for design of selective compounds in insect control. We have characterized several scorpion toxins that vary in preference for insect and mammalian Navs, and identified residues important for their action. However, despite many efforts worldwide, only little is known about the receptor sites of these toxins, and particularly on differences between these sites on insect and mammalian Navs. Another problem arises from the massive overuse of chemical insecticides, which increases resistance buildup among various insect pests. A possible solution to this problem is to combine different insecticidal compounds, especially those that provide synergic effects. Our recent finding that combinations of insecticidal receptor site-3 toxins (sea anemone and scorpion alpha) with scorpion beta toxins or their truncated derivatives are synergic in toxicity to insects is therefore timely and strongly supports this approach. Our ability to produce toxins and various Navs in recombinant forms, enable thorough analysis and structural manipulations of both toxins and receptors. On this basis we propose to (1) restrict by mutagenesis the activity of insecticidal scorpion -toxins and sea anemone toxins to insects, and clarify the molecular basis of their synergic toxicity with antiinsect selective -toxins; (2) identify Nav elements that interact with scorpion alpha and sea anemone toxins and those that determine toxin selectivity to insects; (3) determine toxin-channel pairwise side-chain interactions by thermodynamic mutant cycle analysis using our large collection of mutant -toxins and Nav mutants identified in aim 2; (4) clarify the mode of interaction of truncated -toxins with insect Navs, and elucidate how they enhance the activity of insecticidal site-3 toxins. This research may lead to rational design of novel anti-insect peptidomimetics with minimal impact on human health and the environment, and will establish the grounds for a new strategy in insect pest control, whereby a combination of allosterically interacting compounds increase insecticidal action and reduce risks of resistance buildup.
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Chejanovsky, Nor, and Bruce D. Hammock. Enhancement of Baculoviruses' Insecticidal Potency by Expression of Synergistic Anti-Insect Scorpion Toxins. United States Department of Agriculture, January 1996. http://dx.doi.org/10.32747/1996.7573070.bard.

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The extensive use or non-specific, hazardous, chemical insecticides demands the development of "healthier" alternative means for pest control. Insect-specific, baculoviruses expressing anti-insect toxin genes (from mites or scorpions) demonstrated in laboratory assays and field trials enhanced insecticidal activity and provided some protection from lepidopterous larvae to agricultural plantations. To utilize recombinant baculoviruses as commercial biopesticides in row crop agriculture, further increase in their speed of kill should be achieved and the reduction in crop damage should be comparable to the levels obtained with organic insecticides (the problem). In this project we developed strategies to improve further the efficacy of recombinant baculoviruses which included: I) Synergism among baculoviruses expressing different anti-insect toxins: a) Synergism among two complementary anti-insect scorpion neurotoxins each expressed by a separate recombinant baculovirus, both regulated by the same or a different viral promoter. b) Synergism among two complementary anti-insect scorpion neurotoxins expressed by the same recombinant virus, both regulated by the same or a different viral promoter respectively. The above included two classes of pharmacologically complementary toxins: i) toxins with strictly anti-insect selectivity (excitatory and depressant); ii) toxins with preferential anti-insect activity (anti-insect alpha toxins). c) Synergism among wild type viruses, recombinant baculoviruses and chemicals (insecticides and phytochemicals) II) Identification of more potent toxins against lepidopterous pests for their expression by baculoviruses. Our approach was based on the synergistic effect displayed by the combined application of pairs of anti-insect toxins to blowfly and lepidopterous larvae that resulted in 5 fold increase in their insecticidal activity without apparent increase in their anti-mammal toxicity (toxins LqhIT2 and LqhaIT, LqhIT2 and AaIT, and LqhaIT and AaIT (1). Thus, we developed new concepts and produced a "second generation" of recombinant baculoviruses with enhanced potencies and speeds of kill comparable to classical insecticides. These achievements contribute to make these biopesticides a viable alternative to minimize the use of hazardous chemicals in pest control. Also, our project contributed new tools and model systems to advance the study of insect sodium channels.
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