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Bibliographies thématiques / Chloride channels / Livres

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Livres sur le sujet « Chloride channels »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 25 juillet 2025

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1

Roland, Kozlowski, ed. Chloride channels. Isis Medical Media, 1999.

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2

Mary, Fuller Catherine, ed. Calcium-activated chloride channels. Academic Press, 2002.

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3

J, Alvarez-Leefmans F., Russell John M. 1942-, and International Brain Research Organization. Congress, eds. Chloride channels and carriers in nerve, muscle, and glial cells. Plenum Press, 1990.

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4

Giovanni, Biggio, Costa Erminio, and Capo Boi Conference on Neuroscience (5th : 1987 : Villasimius, Italy), eds. Chloride channels and their modulation by neurotransmitters and drugs. Raven Press, 1988.

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5

W, Olsen Richard, and Venter J. Craig, eds. Benzodiazepine/GABA receptors and chloride channels: Structural and functional properties. A.R. Liss, 1986.

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6

H, Durham John, Hardy Marcos A, and New York Academy of Sciences., eds. Bicarbonate, chloride, and proton transport systems. New York Academy of Sciences, 1989.

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7

Michael, Pusch, ed. Chloride movements across cellular membranes. Boston, 2007.

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8

Alvarez-Leefmans, Francisco J., and John M. Russell, eds. Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9685-8.

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9

Tung, Jennifer Jean. Evaluation of Chloride Intracellular Channels 4 and 1 Functions in Developmental and Pathological Angiogenesis. [publisher not identified], 2012.

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10

Kirk, Kevin L. The cystic fibrosis transmembrane conductance regulator. Landes Bioscience / Eurekah.com, 2003.

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11

Kirk, Kevin L. The cystic fibrosis transmembrane conductance regulator. Landes Bioscience : Eurekah.com, 2004.

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12

Jilishitz, Irina. Chloride Intracellular Channels 1 and 4 function in distinct branches of S1P signaling to regulate endothelial cell behavior and vascular development. [publisher not identified], 2016.

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13

Wong, Simeon. Regulation of Clc-2 chloride channel by protein kinase C phosphorylation. National Library of Canada, 2000.

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14

Ahmed, Najma Nusarat. Proteins which interact with and regulate the chloride channel, CIC-2. National Library of Canada, 2001.

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15

Mao, De Yu. Chloride Intracellular Channel (CLIC) proteins function to modulate Rac1 and RhoA downstream of endothelial G-protein coupled receptors signaling. [publisher not identified], 2019.

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16

Kleinzeller, Arnost, Douglas M. Fambrough, and William B. Guggino. Chloride Channels. Elsevier Science & Technology Books, 1994.

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17

Kozlowski, Ronald. Chloride Channels. Informa Healthcare, 2000.

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18

(Editor), William B. Guggino, Arnost Kleinzeller (Series Editor), and Douglas M. Fambrough (Series Editor), eds. Chloride Channels, Volume 42 (Current Topics in Membranes). Academic Press, 1994.

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19

Fuller, Catherine Mary. Calcium-Activated Chloride Channels. Elsevier Science & Technology Books, 2002.

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20

Alvarez-Leefmans, F. J., and Russell John M. Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells. Springer London, Limited, 2013.

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21

Physiology And Pathology Of Chloride Transporters And Channels In The Nervous System From Molecules To Diseases. Academic Press, 2009.

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22

Alvarez-Leefmans, F. J. "Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells". Springer, 2013.

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23

Pusch, Michael. Chloride Movements Across Cellular Membranes. Elsevier Science & Technology Books, 2011.

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24

Physiology and Pathology of Chloride Transporters and Channels in the Nervous System. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374373-2.x0001-5.

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25

Ischemic preconditioning of the myocardium: Role of chloride and inward-rectifier potassium channels. National Library of Canada, 2001.

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26

Chang, Martin Chung-San. On the regulation and function of potassium and chloride channels in human T lymphocytes. 1999.

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27

Fuller, Catherine Mary. Calcium-Activated Chloride Channels (Current Topics in Membranes, Volume 53) (Current Topics in Membranes). Academic Press, 2002.

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28

Pahapill, Peter Ain. Regulation of potassium and chloride channels in normal human T lymphocytes: a patch-clamp study. 1990.

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29

(Editor), Kevin L. Kirk, and David C. Dawson (Editor), eds. The Cystic Fibrosis Transmembrane Conductance Regulator (Molecular Biology Intelligence Unit). Springer, 2003.

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30

Olsen, Richard W. Benzodiazepine/Gaba Receptors and Chloride Channels: Structural and Functional Properties (Receptor Biochemistry and Methodology, Vol 5). Wiley-Liss, 1986.

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31

Delpire, Eric, and F. Javier Alvarez-Leefmans. Physiology and Pathology of Chloride Transporters and Channels in the Nervous System: From Molecules to Diseases. Elsevier Science & Technology Books, 2009.

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32

Wei, Lin. Electrophysiological Studies of Cftr Function: Effects of Cftr Mutations and Interactions With Other Chloride Channels (Acta Biomedica Lovaniensia, 236). Leuven Univ Pr, 2001.

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33

Mason, Peggy. The Neuron at Rest. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0009.

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Neuronal membrane potential depends on the distribution of ions across the plasma membrane and the permeability of the membrane to those ions afforded by transmembrane proteins. Ions cannot pass through a lipid bilayer but enter or exit neurons through ion channels. When activated by voltage or a ligand, ion channels open to form a pore through which selective ions can pass. The ion channels that support a resting membrane potential are critical to setting a cell’s excitability. From the distribution of an ionic species, the Nernst potential can be used to predict the steady-state potential fo

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34

Shaibani, Aziz. Myotonia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0021.

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Myotonia is a slow relaxation phase of a muscle after normal contraction. Patients report myotonia as muscle stiffness and sometimes pain. They usually adapt to it well. Falls due to myotonia may lead to accidents. Checking for percussion and action myotonia should be part of neuromuscular examination. Electrically silent myotonia is a sign of Brody’s syndrome. Myotonia may be incidentally discovered during EMG. The most important task is to differentiate between myotonia and paramyotonia clinically and electromyographically. Most myotonic disorders are caused by mutations of sodium, and chlor

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35

Adragna, Norma, and Peter Lauf. Cell Volume and Signaling. Springer, 2014.

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36

Cell Volume and Signaling (Advances in Experimental Medicine and Biology). Springer, 2005.

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37

O’Riordan, Stephen MP, and Antoinette Moran. Cystic fibrosis-related diabetes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0008.

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This chapter on CFRD reviews the ever-evolving topic and provides up-to-date information on how to diagnose and manage cystic fibrosis-related diabetes CFRD in the acute and chronic setting. The treatments necessary to treat and prolong life in CF, including their unique dietary requirements, must always be followed as a first priority, with diabetes care adjusted accordingly. Early intervention with insulin has been shown to reverse clinical deterioration, even in those with mild diabetes. Newly emerging treatments for CF which have the potential to restore defective chloride channels may hav

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38

Pitt, Matthew. Investigation of channelopathies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754596.003.0008.

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The chapter begins with a general description of the clinical findings in conditions where hyperexcitability occurs. These are divided into the dystrophic conditions, such as myotonia dystrophy, and the non-dystrophic conditions, which include myotonia congenita, paramyotonia congenita, and potassium-aggravated myotonia. Conditions where hypoexcitability occurs such as periodic paralysis are next discussed. The associated disorders of sodium, calcium, chloride, and potassium channels are described. Next, the protocols for the neurophysiological tests that are used in myotonia, and the short ex

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39

Andrews, Leslie K. Nucleotide interaction regulates the chloride channel, ClC-4. 2004.

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40

Hoffmann, Robert Daniel. Functional and Biochemical Characterization of Gmclc1, a Vacuolar Chloride Channel from Soybean. GRIN Verlag GmbH, 2013.

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41

Dhani, Sonja Urmilla. An investigation of the endosomal trafficking of the ClC-2 chloride channel. 2006.

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42

Cheung, Min Rex. A view of the cystic fibrosis transmembrane conductance regulator chloride channel from the sixth transmembrane domain. 1997.

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43

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Cystic fibrosis-associated liver disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0022.

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Pathophysiology 162Clinical features 162Diagnosis 163Management 164Cystic fibrosis (CF) is an autosomal recessive disease resulting from mutations in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) (see Chapter 21). CFTR functions as a transmembrane chloride channel in the apical membrane of most secretory epithelia and the disease thus affects lungs, pancreas, exocrine glands, gut, and liver. In CF-associated liver disease the biliary tract is most commonly involved in a spectrum from asymptomatic to biliary cirrhosis. The liver disease runs from mild and su

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44

Ducharme, Guillaume. The small conductance swelling-activated chloride channel in primary rat microglia: Biophysical characterization and its contribution to volume regulation and phagocytosis. 2007.

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45

Kriemler, Susi. Exercise, physical activity, and cystic fibrosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0033.

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Cystic fibrosis (CF) is the most common genetic autosomal recessive disease of the Caucasian race, generally leading to death in early adulthood.1 The frequency of the gene carrier (heterozygote) is 1:20–25 in Caucasian populations, 1:2000 in African-Americans, and practically non-existent in Asian populations. The disease occurs in about 1 in every 2500 life births of the white population. Mean survival has risen from 8.4 years in 1969 to 32 years in 2000 due to improvements in treatment. The genetic defect causes a pathological electrolyte transport through the cell membranes by a defective

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