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Tesi sul tema "Sodium channels"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

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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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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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11

Nilsson, Johanna. "Molecular mechanisms of local anaesthetic action on voltage-gated ion channels /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-748-7/.

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12

Dautova, Yana. "Atrial arrhythmias in murine hearts modelling sodium channelopathies." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609529.

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13

DeGraff, David J. "Implications for the androgenic regulation of IGFBP-2 in the development of metastatic and androgen independent prostate cancer." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 160 p, 2008. http://proquest.umi.com/pqdweb?did=1459919011&sid=13&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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14

Radford, Matthew. "Purification structure and stability of voltage-gated sodium channels." Thesis, Birkbeck (University of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535845.

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Abstract (sommario):

Voltage gated sodium channels (VGSC) are integral membrane proteins that selectively transport sodium ions across cellular membranes in response to changes in membrane potential. In vertebrates sodium channels are composed of a pore forming alpha subunit and one or more auxiliary beta subunit. There are a total of nine different alpha subunit isoforms and four known beta subunits. In higher eukaryotes VGSCs are responsible for fast electrical signalling through the propagation of action potentials in excitable cells such as neurons and muscle. Voltage gated sodium channels due to their physiol

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15

Meng, Guangsi. "Computational Design of Selective Toxin Blockers of Sodium Channels." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/27255.

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Developments in heterologous expression of ion channels and determination of toxin-channel complex structures have prompted searches for peptide drugs to treat diseases caused by dysfunctional channels. In this project, we build computational models of voltage-gated sodium (NaV) channels using the latest experimental results for the human NaV1.2 channel and analyze the binding modes, which are then applied to the NaV1.7 channel with the aim of developing selective channel blockers. Our main focus is NaV1.2 in the central nervous system and NaV1.7 in the peripheral nervous system. NaV1.7 is

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16

Rahman, Mohammed Mostafizur. "Bistability and Hysteresis of Sodium Channels at Neuromuscular Junction." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422123.

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All voluntary movements in mammals are accomplished by muscles which are controlled by the brain through a specialized synapse called neuromuscular junction (NMJ). To have full control over the movement disorders caused due to dysfunctions of neuromuscular junction (e.g., Myasthenia Gravis, Lambert-Eaton Myasthenic Syndrome) and for the engineering of rehabilitation neuroprosthetic devices, a clear knowledge about the neuromuscular junction transmission mechanism during the communication between the neuron and the muscle is essential. The NMJ is the place where the axon terminal of a motor ne

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17

Zhang, Hongling. "Sigma Receptors Modulation of Voltage-gated Ion Channels in Rat Autonomic Neurons." [Tampa, Fla.] : University of South Florida, 2005. http://purl.fcla.edu/fcla/etd/SFE0001183.

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18

Spafford, John David. "The evolution of voltage-gated sodium channels as interpreted from a study of sodium currents and channels from the hydrozoan jellyfish, Polyorchis penicillatus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ34840.pdf.

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19

Konstas, Angelos Aristeidis. "The regulation and functional interaction of the epilethial sodium channel (ENaC) and renal potassium channels." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249463.

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20

Chang, Chi-Chun, and n/a. "Interaction between delta epithelial sodium channel ([delta]ENaC) and COMMD1." University of Otago. Department of Physiology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080512.123318.

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Abstract (sommario):

The epithelial sodium channel (ENaC) is a key regulator of salt homeostasis. The classic ENaC consists of three subunits: α, β and γ, which are highly expressed in the kidney and colon where they mediate electrogenic Na⁺ influx into cells under the tight hormonal regulation of aldosterone. A fourth ENaC subunit named [delta]ENaC also generates Na⁺ influx with the β- and γENaC subunits in Xenopus oocytes. However [delta]ENaC differs to the other subunits in its channel properties and tissue distribution, suggesting that [delta]ENaC may possess a physiological role other than salt regulation.

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21

Tibbs, Victoria Celestine. "Characterization of A-kinase anchoring proteins associated with the type IIA sodium channel /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/6303.

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22

Hui, Kwokyin. "Molecular determinants of mu-conotoxin block of single sodium channels." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ54789.pdf.

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23

Malek, Julie Anne. "Voltage-gated sodium channels and nerve regeneration in the leech." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410686.

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24

Hynes, Judith Audrey. "Trafficking of voltage-gated sodium channels involved in pain perception." Thesis, University of Leeds, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590477.

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Abstract (sommario):

Chronic pain is a highly unmet clinical need; often treatment is only partially effective, and is frequently accompanied by unpleasant side effects. The voltage-gated sodium channel Nav1. 7 has emerged as an attractive target in the treatment of pain. Expressed preferentially in nociceptive DRG neurons, Nav1.7 functions at the plasma membrane to transmit peripherally generated pain signals towards the central nervous system. Manipulating Nav1.7 trafficking mechanisms to reduce the cell surface density of the channel is thus a promising approach to reduce the sensation of pain, yet there are no

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25

FERREIRA, ANDREA DE LIMA. "STUDY OF SODIUM AND POTASSIUM ION CHANNELS VIA STOCHASTIC DYNAMIC." PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 2011. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=18111@1.

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COORDENAÇÃO DE APERFEIÇOAMENTO DO PESSOAL DE ENSINO SUPERIOR<br>PROGRAMA DE SUPORTE À PÓS-GRADUAÇÃO DE INSTS. DE ENSINO<br>O presente trabalho apresenta uma revisão sobre os Canais Iônicos de Sódio e de Potássio fazendo uma relacão com os aspectos biofísicos, computacionais e matemáticos. Estudamos os canais iônicos, sob o ponto de vista da Mecânica Estatìstica, mais precisamente, considerando os canais iônicos como um processo markoviano. O objetivo principal deste trabalho é representar a dinâmica dos canais iônicos utilizando a caminhada aleatória e elaborar programas computacionais que sim

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26

Ji, Hong-Long. "Fibrinolytic regulation of pulmonary epithelial sodium channels : a critical review." Thesis, University of Kent, 2015. https://kar.kent.ac.uk/57157/.

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Luminal fluid homeostasis in the respiratory system is crucial to maintain the gas- blood exchange in normal lungs and mucociliary clearance in the airways. Epithelial sodium channels (ENaC) govern ~70% of alveolar fluid clearance. Four ENaC subunits have been cloned, namely, α, β, γ, and δ ENaC subunits in mammalian cells. This critical review focuses on the expression and function of ENaC in human and murine lungs, and the post-translational regulation by fibrinolysins. Nebulized urokinase was intratracheally delivered for clinical models of lung injury with unknown mechanisms. The central h

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27

Lam, Tai-chung. "Genetic and environmental factors of hypertension." Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31980946.

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28

Allen, Samantha M. "Characterization of beta subunits of voltage sensitive sodium channels in the LNCaP progression model and in the normal mouse prostate." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 114 p, 2007. http://proquest.umi.com/pqdweb?did=1253509351&sid=1&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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29

Lam, Tai-chung, and 林泰忠. "Genetic and environmental factors of hypertension." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31980946.

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30

Lopreato, Gregory Francis. "A PCR-based census of sodium channel genes in the genome of the weakly electric teleost, Sternopygus macrurus : evolutionary implications /." Full text (PDF) from UMI/Dissertation Abstracts International, 2000. http://wwwlib.umi.com/cr/utexas/fullcit?p3004322.

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31

Gawenis, Lara Renee. "Calcium and sodium absorption across the small intestine of cystic fibrosis mice /." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012969.

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32

Wiemuth, Dominik, and n/a. "Regulation of the epithelial sodium channel (ENac) by ubiquitination." University of Otago. Department of Physiology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20061127.162243.

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Abstract (sommario):

The epithelial sodium channel (ENaC) is the central component of the sodium absorption pathway in epithelia. It is critical for sodium homeostasis and blood pressure control, which is demonstrated by rare genetic disorders such as Liddle�s syndrome and pseudohypoaldosteronism type I, that are associated with hyper- and hypotension, respectively. ENaC is mainly regulated by mechanisms that control the expression of active channels at the cell surface. Ubiquitin ligases of the Nedd4-like family, such as Nedd4 and Nedd4-2 decrease epithelial sodium absorption by binding to and targeting ENaC fo

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33

Miyamoto, Kazuhide. "Studies on Solution Structures for Inactivation Gate Peptides of Sodium Channels." 京都大学 (Kyoto University), 2001. http://hdl.handle.net/2433/150908.

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34

Tan, Chong Da. "Metabolic regulation of epithelial sodium channels in human airway epithelial cells." Thesis, St George's, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546781.

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35

Whitaker, William Richard James. "The distribution of voltage-gated sodium channels in the human brain." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621736.

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36

Chernoff, Daniel Michael. "Kinetics of local anesthetic binding to sodium channels : role of pKaÌ³." Thesis, Massachusetts Institute of Technology, 1988. http://hdl.handle.net/1721.1/29203.

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Thesis (Ph. D.)--Harvard University--Massachusetts Institute of Technology Division of Health Sciences and Technology, Program in Medical Engineering and Medical Physics, 1989.<br>On t.p. "a" is subscript.<br>Includes bibliographical references (leaves 165-175).<br>by Daniel Michael Chernoff.<br>Ph.D.

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37

Cusdin, Fiona Susan. "Mutational studies on the β3 subunit of voltage-gated sodium channels". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611610.

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38

Glenn, L. Lee, and Jeff Knisley. "Transients in Branching Multipolar Neurons With Tapering Dendrites and Sodium Channels." Digital Commons @ East Tennessee State University, 2005. https://dc.etsu.edu/etsu-works/7523.

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Book Summary: Computational models of neural networks have proven insufficient to accurately model brain function, mainly as a result of simplifications that ignore the physical reality of neuronal structure in favor of mathematically tractable algorithms and rules. Even the more biologically based "integrate and fire" and "compartmental" styles of modeling suffer from oversimplification in the former case and excessive discretization in the second. This book introduces an integrative approach to modeling neurons and neuronal circuits that retains the integrity of the biological units at all h

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39

Richardson, Jessica Lindsay. "The structure of function of voltage-dependant potassium and sodium channels." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1693029641&sid=8&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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40

Baquero, Gonzalez Arian F. "The Regulation of Epithelial Sodium Channels in Mammalian Taste Receptor Cells." DigitalCommons@USU, 2009. https://digitalcommons.usu.edu/etd/418.

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Nutrient recognition is one of the main physiological roles of the gustatory system. In mammals, it is well established that the taste of sodium salts is primarily mediated by sodium influx through the epithelial sodium channel. The epithelial sodium channel is a sodium-specific ion channel that is expressed across a wide range of transporting epithelia such as colon, kidney, and taste. In addition to its role as a salt taste receptor, sodium influx through the epithelial sodium channel is important systemically for maintaining sodium balance and blood pressure. Following our earlier work on

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41

Molinarolo, Steven. "Biochemical techniques for the study of voltage-gated sodium channel auxiliary subunits." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6217.

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Voltage-gated sodium channels auxiliary subunits evolutionary emerged nearly 500 million years ago during the Cambrian explosion. These subunits alter one the most important ion channels to electrical signaling, the voltage-gated sodium channels support the propagation of electric impulses in animals. The mechanism for the auxiliary subunits effects on the channels is poorly understand, as is the stoichiometry between the auxiliary subunit and the channel. The focus of my thesis is to generate assays and to use these approaches to understand the interactions different types of voltage-gated ch

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42

Zhang, Ao. "Role of the Neurofascins in targeting voltage-gated sodium channels in myelinated nerves." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8821.

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The nodes of Ranvier are short, periodical interruptions in the myelin sheath of myelinated axons, at which voltage-gated sodium channels are highly concentrated. The correct targeting of sodium channels to the nodes of Ranvier permits rapid propagation of action potentials in myelinated axons. The nodes of Ranvier contain a unique set of ion channels, cell-adhesion molecules, and cytoplasmic adaptor proteins. Neurofascins are cell adhesion molecules of the immunoglobulin superfamily and previous work has shown they are involved in the assembly of the node of Ranvier. The Neurofascin (Nfasc) g

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43

Tatulian, Lucine. "Sodium and potassium ion channels as targets for the control of epilepsy." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252275.

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44

Alves, Simoes Marta. "Targeting SNARE proteins and the trafficking of sodium channels in inflammatory pain." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/20767/.

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45

Glenn, L. Lee, and Jeffrey R. Knisley. "Voltage Transients in Branching Multipolar Neurons With Tapering Dendrites and Sodium Channels." Digital Commons @ East Tennessee State University, 2005. https://dc.etsu.edu/etsu-works/7537.

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Book Summary: With contributions from more than 40 renowned experts, Modeling in the Neurosciences: From Ionic Channels to Neural Networks is essential for those interested in neuronal modeling and quantitative neiroscience. Focusing on new mathematical and computer models, techniques and methods, this monograph represents a cohesive and comprehensive treatment of various aspects of the neurosciences from the biophysical, cellular and netwrok levels. Many state-of-the-art examples are presented as to how mathematical and computer modeling can contribute to the understanding of mechanisms and s

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46

Petitprez, Séverine. "Cardiac and muscle channelopathies : roles and regulation of voltage-gated sodium channels." Paris 7, 2009. http://www.theses.fr/2009PA077257.

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La contraction des cellules musculaires est due à la propagation d'un stimulus électrique appelé potentiel d'action (PA). Il est produit par l'ouverture séquentielle de plusieurs canaux ioniques générant des courants à travers les membranes cellulaires. Les canaux sodiques dépendant du voltage (Nav) déclenchent la première phase du PA. Les variants Nav1. 4 et Nav1. 5 sont exprimés respectivement dans le muscle et le coeur. Des mutations de leurs gènes (SCN4A et SCN5A) provoquent respectivement des pathologies neuromusculaires et des arythmies cardiaques. Mon travail de thèse a consisté à étudi

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47

Stocker, Patrick J. "Sialic Acid Modulation of Cardiac Voltage-Gated Sodium Channel Gating Throughout the Developing Myocardium." [Tampa, Fla] : University of South Florida, 2005. http://purl.fcla.edu/usf/dc/et/SFE0001304.

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48

Farrag, Khalid Gamal. "A study of the physiology and pharmacology of voltage-gated sodium channels in normal and modified channel states." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399295.

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49

Jarecki, Brian W. "GATING OF THE SENSORY NEURONAL VOLTAGE-GATED SODIUM CHANNEL NAv1.7: ANALYSIS OF THE ROLE OF D3 AND D4 / S4-S5 LINKERS IN TRANSITION TO AN INACTIVATED STATE." Thesis, Connect to resource online, 2010. http://hdl.handle.net/1805/2119.

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Thesis (Ph.D.)--Indiana University, 2010.<br>Title from screen (viewed on April 1, 2010). Department of Pharmacology and Toxicology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Theodore R. Cummins, Grant D. Nicol, Gerry S. Oxford, Andy Hudmon, John H. Schild. Includes vitae. Includes bibliographical references (leaves 232-266).

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50

Lucas, Brooke. "The Role of the Defective Nav1.4 Channels in the Mechanism of Hyperkalemic Periodic Paralysis." Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/20550.

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Hyperkalemic periodic paralysis (HyperKPP) is an autosomal dominant human skeletal muscle channelopathy that causes periods of myotonic discharge and periodic paralysis due to defective Nav1.4 sodium channels. Patients are asymptomatic at birth, attacks become short and frequent during childhood, and more severe during adolescence. Since the Nav1.4 content in the cell membrane is relatively constant during childhood, it was hypothesized that some symptoms start with the defective Nav1.4 channels, while other symptoms start after some changes occur in gene expression affecting other membrane ch

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