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Letteratura scientifica selezionata sul tema "Sodium channels"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

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Articoli di riviste sul tema "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 (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

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2

Warmke, Jeffrey W., Robert A. G. Reenan, Peiyi Wang, et al. "Functional Expression of Drosophila para Sodium Channels." Journal of General Physiology 110, no. 2 (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 si

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3

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 (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.

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4

Scheuer, T., and W. A. Catterall. "Control of neuronal excitability by phosphorylation and dephosphorylation of sodium channels." Biochemical Society Transactions 34, no. 6 (2006): 1299–302. http://dx.doi.org/10.1042/bst0341299.

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Abstract (sommario):

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 signal

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5

Barnes, S., and B. Hille. "Veratridine modifies open sodium channels." Journal of General Physiology 91, no. 3 (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 curre

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6

Huguenard, John R. "Sodium Channels." Neuron 33, no. 4 (2002): 492–94. http://dx.doi.org/10.1016/s0896-6273(02)00592-5.

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7

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 ge

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8

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 (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 transient

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9

Segal, Michael M., and Andrea F. Douglas. "Late Sodium Channel Openings Underlying Epileptiform Activity Are Preferentially Diminished by the Anticonvulsant Phenytoin." Journal of Neurophysiology 77, no. 6 (1997): 3021–34. http://dx.doi.org/10.1152/jn.1997.77.6.3021.

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Segal, Michael M. and Andrea F. Douglas. Late sodium channel openings underlying epileptiform activity are preferentially diminished by the anticonvulsant phenytoin. J. Neurophysiol. 77: 3021–3034, 1997. Late openings of sodium channels were observed in outside-out patch recordings from hippocampal neurons in culture. In previous studies of such neurons, a persistent sodium current appeared to underlie the ictal epileptiform activity. All the channel currents were blocked by tetrodotoxin. In addition to the transient openings of sodium channels making up the peak sodium current, there were two

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10

Terlau, H., M. Stocker, K. J. Shon, J. M. McIntosh, and B. M. Olivera. "MicroO-conotoxin MrVIA inhibits mammalian sodium channels, but not through site I." Journal of Neurophysiology 76, no. 3 (1996): 1423–29. http://dx.doi.org/10.1152/jn.1996.76.3.1423.

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Abstract (sommario):

1. A 31-amino-acid peptide from the venom of the snail-hunting species Conus marmoreus, microO-conotoxin MrVIA, inhibits mammalian voltage-gated sodium channels through a novel mechanism distinct from saxitoxin, tetrodotoxin, or mu-conotoxin. 2. MicroO-Conotoxin MrVIA blocks rat brain type II sodium channels expressed in Xenopus oocytes (IC50 approximately 200 nM, Hill coefficient approximately 1.6 +/- 0.2, mean +/- SE). Channel activation/inactivation kinetics and current-voltage relationships were unperturbed. 3. MicroO-Conotoxin MrVIA does not cause phasic or use-dependent inhibition of sod

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Più fonti

Tesi sul tema "Sodium channels"

1

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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2

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 agreemen

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3

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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4

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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5

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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Abstract (sommario):

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 di

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6

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 b

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7

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 ch

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8

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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9

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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10

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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Libri sul tema "Sodium channels"

1

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

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2

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

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3

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

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4

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

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5

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

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6

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

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7

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

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8

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. The New York Academy of Sciences, 1996.

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9

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 Academy of Sciences, 1986.

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10

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

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Capitoli di libri sul tema "Sodium channels"

1

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

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2

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

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3

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

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4

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

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5

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

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6

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

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7

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

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8

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

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9

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

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10

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

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Atti di convegni sul tema "Sodium channels"

1

Bavarian, Behzad, Koushik Kosanam, Lisa Reiner, and Pranav Meddhali. "Inhibition of Microbial Induced Corrosion of Concrete Using Admixture and Surface Applied Corrosion Inhibitors." In CONFERENCE 2023. AMPP, 2023. https://doi.org/10.5006/c2023-18768.

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Abstract Microbiologically Induced Corrosion (MIC) is a complex problem facing global concrete sewer structures. Despite the substantial efforts made, MIC of concrete sewers remains a significant challenge. Concrete is susceptible to corrosion induced by microbial species which convert the main binding agent Ca(OH)2 to CaSO4, leading to the disintegration of concrete, loss of strength and structure failure short of its predicted life. Concrete specimens were prepared with corrosion inhibitors and immersed in sodium sulfide and sulfuric acid solutions for more than 400 days. The concrete sample

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2

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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3

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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4

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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5

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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6

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 voltag

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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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8

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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9

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. OSA, 1999. http://dx.doi.org/10.1364/bgpp.1999.cb4.

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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 s

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Rapporti di organizzazioni sul tema "Sodium channels"

1

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

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

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3

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, 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

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4

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, 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

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5

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

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Gurevitz, Michael, Michael E. Adams, Boaz Shaanan, et al. 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, 2001. http://dx.doi.org/10.32747/2001.7585190.bard.

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Abstract (sommario):

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

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8

Mobberley, Jennifer, Jiyoung Son, and Kristin Engbrecht. Chemical imaging for in situ detection and discrimination of aquatic toxins targeting voltage gated sodium channels. Office of Scientific and Technical Information (OSTI), 2024. http://dx.doi.org/10.2172/2476537.

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Mangas, Iris, Antonio F. Hernandez, Kevin Crofton, et al. Adverse Outcome Pathway on Binding to voltage gate sodium channels during development leading to cognitive impairment. Organisation for Economic Co-Operation and Development (OECD), 2025. https://doi.org/10.1787/3acd09e8-en.

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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, 2013. http://dx.doi.org/10.32747/2013.7699857.bard.

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Abstract (sommario):

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 t

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