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Relevant bibliographies by topics / Calcium channels

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Academic literature on the topic 'Calcium channels'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 June 2025

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Journal articles on the topic "Calcium channels"

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Triggle, David J. "Calcium, calcium channels, and calcium channel antagonists." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1474–81. http://dx.doi.org/10.1139/y90-224.

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Voltage-dependent Ca2+ channels are an important pathway for Ca2+ influx in excitable cells. They also represent an important site of action for a therapeutic group of agents, the Ca2+ channel antagonists. These drugs enjoy considerable use in the cardiovascular area including angina, some arrhythmias, hypertension, and peripheral vascular disorders. The voltage-dependent Ca2+ channels exist in a number of subclasses characterized by electrophysiologic, permeation, and pharmacologic criteria. The Ca2+ channel antagonists, including verapamil, nifedipine, and diltiazem, serve to characterize the L channel class. This channel class has been characterized as a pharmacologic receptor, since it possesses specific drug-binding sites for both antagonists and activators and it is regulated by homologous and heterologous influences. The Ca2+ channels of both voltage- and ligand-regulated classes are likely to continue to be major research targets for new drug design and action.Key words: calcium, calcium channels, calcium antagonists, 1,4-dihydropyridines, channel regulation, receptor regulation.

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Greenberg, David A. "Calcium channels and calcium channel antagonists." Annals of Neurology 21, no. 4 (April 1987): 317–30. http://dx.doi.org/10.1002/ana.410210402.

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Collier, M. L., G. Ji, Y. X. Wang, and M. I. Kotlikoff. "Calcium-Induced Calcium Release in Smooth Muscle." Journal of General Physiology 115, no. 5 (May 1, 2000): 653–62. http://dx.doi.org/10.1085/jgp.115.5.653.

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Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca2+ channels. In heart cells, a tight coupling between the gating of single L-type Ca2+ channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca2+ channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca2+ sparks and propagated Ca2+ waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca2+ channels. L-type Ca2+ channels can open without triggering Ca2+ sparks and triggered Ca2+ sparks are often observed after channel closure. CICR is a function of the net flux of Ca2+ ions into the cytosol, rather than the single channel amplitude of L-type Ca2+ channels. Moreover, unlike CICR in striated muscle, calcium release is completely eliminated by cytosolic calcium buffering. Thus, L-type Ca2+ channels are loosely coupled to RYR through an increase in global [Ca2+] due to an increase in the effective distance between L-type Ca2+ channels and RYR, resulting in an uncoupling of the obligate relationship that exists in striated muscle between the action potential and calcium release.

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Mochida, Sumiko. "Presynaptic Calcium Channels." International Journal of Molecular Sciences 20, no. 9 (May 6, 2019): 2217. http://dx.doi.org/10.3390/ijms20092217.

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Presynaptic Ca2+ entry occurs through voltage-gated Ca2+ (CaV) channels which are activated by membrane depolarization. Depolarization accompanies neuronal firing and elevation of Ca2+ triggers neurotransmitter release from synaptic vesicles. For synchronization of efficient neurotransmitter release, synaptic vesicles are targeted by presynaptic Ca2+ channels forming a large signaling complex in the active zone. The presynaptic CaV2 channel gene family (comprising CaV2.1, CaV2.2, and CaV2.3 isoforms) encode the pore-forming α1 subunit. The cytoplasmic regions are responsible for channel modulation by interacting with regulatory proteins. This article overviews modulation of the activity of CaV2.1 and CaV2.2 channels in the control of synaptic strength and presynaptic plasticity.

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Friedman, P. A., and F. A. Gesek. "Hormone-responsive Ca2+ entry in distal convoluted tubules." Journal of the American Society of Nephrology 4, no. 7 (January 1994): 1396–404. http://dx.doi.org/10.1681/asn.v471396.

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This editorial review focuses on recent observations regarding the mechanism and regulation of calcium transport in hormone-sensitive distal convoluted tubules. Parathyroid hormone (PTH) and calcitonin increase active calcium absorption by distal convoluted tubules. Occupancy of these peptide hormone receptors results in the activation of both protein kinase A and protein kinase C. The inhibition of either kinase blocks calcium transport. The time course of stimulation of calcium entry in distal convoluted tubules by PTH is slow compared with that by calcitonin. The latency associated with PTH action may be due to the induction of protein synthesis. PTH and calcitonin hyperpolarize membrane voltage, which in turn increases calcium entry. Calcium entry is mediated by calcium channels. These channels exhibit a low, single-channel conductance and are sensitive to dihydropyridine-type calcium channel blockers. Unlike L-type calcium channels, the channel open probability of distal convoluted tubule calcium entry channels is increased upon hyperpolarization. This novel combination of properties suggests that the underlying structure of these calcium entry channels may be unique.

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Gollasch, M., J. Hescheler, J. M. Quayle, J. B. Patlak, and M. T. Nelson. "Single calcium channel currents of arterial smooth muscle at physiological calcium concentrations." American Journal of Physiology-Cell Physiology 263, no. 5 (November 1, 1992): C948—C952. http://dx.doi.org/10.1152/ajpcell.1992.263.5.c948.

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Entry of Ca through voltage-dependent Ca channels is an important regulator of the function of smooth muscle, cardiac muscle, and neurons. Although Ca channels have been extensively studied since the first descriptions of Ca action potentials (P. Fatt and B. Katz. J. Physiol. Lond. 120: 171-204, 1953), the permeation rate of Ca through single Ca channels has not been measured directly under physiological conditions. Instead, single Ca channels have typically been examined using high concentrations (80-110 mM) of another divalent charge carrier, Ba, so as to maximize the amplitude of the single-channel currents. Calculations of unitary currents at 2 mM Ca indicated that the single-channel currents would be immeasurably small (i.e., < 0.1 pA). We provide here the first direct measurements of single Ca channel currents at a physiological Ca concentration. Contrary to earlier estimates, we have found that currents through single Ca channels in arterial smooth muscle are 0.1-0.3 pA at 2 mM Ca and physiological membrane potentials. These relatively large unitary currents permit direct measurement of Ca channel properties under conditions that do not distort their function. Our data also indicate that Ca permeates these channels at relatively high rates in physiological Ca concentrations and membrane potentials.

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Reuter, H., S. Kokubun, and B. Prod'hom. "Properties and modulation of cardiac calcium channels." Journal of Experimental Biology 124, no. 1 (September 1, 1986): 191–201. http://dx.doi.org/10.1242/jeb.124.1.191.

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Voltage-dependent calcium channels are widely distributed in excitable membranes and are involved in the regulation of many cellular functions. These channels can be modulated by neurotransmitters and drugs. There is one particular type of calcium channel in cardiac cells (L-type) whose gating is affected in different ways by beta-adrenoceptor and 1,4-dihydropyridine agonists. We have analysed single calcium channel currents (i) in myocytes from rat hearts in the absence and presence of isoproterenol or 8-bromo-cAMP. We have found that both compounds have similar effects on calcium channel properties. They increase the overall open state probability (po) of individual calcium channels while i remains unaffected. Analysis of the gating kinetics of calcium channels showed: a slight increase in the mean open times of calcium channels, a reduction in time intervals between bursts of channel openings, an increase in burst length and a prominent reduction in failures of calcium channels to open upon depolarization. These kinetic changes caused by isoproterenol and 8-bromo-cAMP can account for the increase in po. Since the macroscopic calcium current, ICa, can be described by ICa = N X po X i, the increase in po accounts for the well-known increase in ICa by beta-adrenergic catecholamines. Cyclic AMP-dependent phosphorylation of calcium channels is a likely metabolic step involved in this modulation. Another class of drug that modulates calcium channel gating is the 1,4-dihydropyridines which can either enhance or reduce ICa, either by prolonging the open state of the channels or by facilitating the inactivated state. Both effects depend strongly on membrane potential and are independent of cyclic AMP-dependent phosphorylation reactions.

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Shuttleworth, T. J., and O. Mignen. "Calcium entry and the control of calcium oscillations." Biochemical Society Transactions 31, no. 5 (October 1, 2003): 916–19. http://dx.doi.org/10.1042/bst0310916.

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During oscillatory Ca2+ signals, the agonist-induced enhanced entry of extracellular Ca2+ plays a critical role in modulating the frequency of the oscillations. Although it was originally assumed that the entry of Ca2+ under these conditions occurred via the well-known, and apparently ubiquitous, store-operated mechanism, subsequent studies suggested that this was unlikely. It is now known that, in many cell types, a novel non-capacitative Ca2+-selective pathway whose activation is dependent on arachidonic acid is responsible, and the channels involved [ARC channels (arachidonate-regulated Ca2+ channels)] have been characterized. These ARC channels co-exist with the store-operated CRAC channels (Ca2+-release-activated Ca2+ channel) in cells, but each plays a unique and non-overlapping role in Ca2+ signalling. In particular, it is the ARC channels that are specifically activated at the low agonist concentrations that give rise to oscillatory Ca2+ signals and provide the predominant mode of Ca2+ entry under these conditions. The indications are that Ca2+ entry through the ARC channels increases the likelihood that low concentrations of Ins(1,4,5)P3 will trigger repetitive Ca2+ release. At higher agonist concentrations, store-depletion is more complete and sustained resulting in the activation of CRAC channels. At the same time the ARC channels are turned off, resulting in what we have described as a reciprocal regulation of these two distinct Ca2+ entry pathways.

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Triggle, C. R., and M. Wolowyk. "Calcium Channels Symposium." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1472–73. http://dx.doi.org/10.1139/y90-223.

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Calcium is an essential element for just about all cellular processes, and yet abnormally high levels of cellular calcium can cause cell death. The processes that control cellular levels of this metal ion are thus of critical importance to both normal and pathophysiological conditions. Essential in the regulation of intracellular calcium levels are the calcium channels associated with cell membranes, for instance, with the plasma and sarcoplasmic reticulum membranes of muscle cells. In recent years, there has been a tremendous increase in our knowledge of the structure and function of these channels. However, we also now realize that the term "calcium channels" is used to refer to a rather heterogeneous population of entities. In some instances, notably receptor-operated calcium channels, we have only indirect evidence for their existence, whereas with the voltage-dependent channels, considerable information is now available on their comparative physiology, pharmacology, and biochemistry. The main objective of the Symposium presented in Calgary during the 1989 CFBS meeting was to bring together experts in the area of the calcium channels associated with both smooth and striated muscle function so that they could present the current state of knowledge in this area.Dr. David Triggle, from the State University of New York in Buffalo, reviewed the importance of calcium and calcium channels in cellular function and highlighted the pharmacology of calcium channel antagonists particularly with respect to their effects on the L-type calcium channels associated with smooth muscle. Dr. Sidney Fleischer from Vanderbilt University, Nashville, Tennessee, focused on his work associated with the isolation and characterization of the calcium release channel – ryanodine receptor of the sarcoplasmic reticulum from striated muscle. Dr. Fleischer has referred interested readers to his recent review in the 1989 issue of the Annual Reviews of Biophysics and Biophysical Chemistry (18: 333–364). Dr. Balwant Tuana from the University of Ottawa presented an update complemented by original data from his laboratory in the Department of Pharmacology on the current state of knowledge of the structure of the L-type calcium channel associated with both skeletal and cardiac muscle. The last two speakers, Dr. Wayne Giles and Dr. Hamid Akbarali, both from the Department of Medical Physiology at the University of Calgary, completed the program by presenting a review of data concerning the electrical physiological properties of calcium-activated channels in cardiac and smooth muscle. Their manuscript highlights their recent studies, with co-workers in Calgary, of the properties of calcium-activated potassium currents from the human cystic artery.The organizers of this symposium, hosted by the Pharmacological Society of Canada, gratefully acknowledge the financial support of the Alberta Heart and Stroke Foundation, Alberta Heritage Foundation for Medical Research, Canadian Heart and Stroke Foundation, Canadian Federation of Biological Societies, Charles River Laboratories (Canada Ltd.), SynPhar Laboratories Inc., Fisher Scientific Ltd., Novopharm Ltd., and Mandel Scientific Co. Ltd. The artistic contribution from Sylvia Ficken of Medical Audiovisual Services in the Faculty of Medicine at Memorial University of Newfoundland, who drew the symposium logo reproduced on the title page, is also gratefully acknowledged.

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Kolesnikov, D. O., E. R. Grigorieva, M. A. Nomerovskaya, D. S. Reshetin, A. V. Shalygin, and E. V. Kaznacheyeva. "The Effect of Calcium Ions on the Electrophysiological Properties of Single ANO6 Channels." Acta Naturae 16, no. 1 (May 10, 2024): 40–47. http://dx.doi.org/10.32607/actanaturae.27338.

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Proteins belonging to the anoctamin (ANO) family form calcium-activated chloride channels (CaCCs). The most unusual member of this family, ANO6 (TMEM16F), simultaneously exhibits the functions of calcium-dependent scramblase and the ion channel. ANO6 affects the plasma membrane dynamics and phosphatidylserine transport; it is also involved in programmed cell death. The properties of ANO6 channels remain the subject of debate. In this study, we investigated the effect of variations in the intracellular and extracellular concentrations of calcium ions on the electrophysiological properties of endogenous ANO6 channels by recording single ANO6 channels. It has been demonstrated that (1) a high calcium concentration in an extracellular solution increases the activity of endogenous ANO6 channels, (2) the permeability of endogenous ANO6 channels for chloride ions is independent of the extracellular concentration of calcium ions, (3) that an increase in the intracellular calcium concentration leads to the activation of endogenous ANO6 channels with double amplitude, and (4) that the kinetics of the channel depend on the plasma membrane potential rather than the intracellular concentration of calcium ions. Our findings give grounds for proposing new mechanisms for the regulation of the ANO6 channel activity by calcium ions both at the inner and outer sides of the membrane.

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Dissertations / Theses on the topic "Calcium channels"

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Roberts, Dewi. "Calcium-dependent inactivation of Cav1.3 calcium channels." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446186.

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Peterson, Blaise. "Molecular determinants of dihydropyridine binding on L-type calcium channels /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6269.

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Farrington, Jasmine. "Calcium release activated calcium channels in human lung mast cells." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6609/.

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Nakayama, Shinsuke. "Calcium channels in detrusor smooth muscle." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334328.

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Xie, Mian. "Calcium Channel Beta Subunits and SCA6-Type Calcium Channel Alpha Subunits C-Termini Regulate Targeting and Function of Presynaptic Calcium Channels in Hippocampal Neurons." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1188326628.

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Yasuda, Takahiro. "Modulation of calcium channel function and toxin sensitivity by auxiliary subunits /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18052.pdf.

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Doughty, Stephen William. "Molecular modelling of voltage-gated calcium channels." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362014.

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Warburton, Steven Peter Marc. "Calcium ion channels in insect skeletal muscle." Thesis, University of Nottingham, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363592.

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Richardson, C. Mark. "Presynaptic calcium channels in skate electric organ." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319614.

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Pearson, Hugh Anthony. "Physiology and pharmacology of insect calcium channels." Thesis, University College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308295.

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Books on the topic "Calcium channels"

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1921-, Hurwitz Leon, Partridge L. Donald, and Leach John K, eds. Calcium channels: Their properties, functions, regulation, and clinical relevance. Boca Raton, Fla: CRC Press, 1991.

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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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Weiss, Norbert, and Alexandra Koschak, eds. Pathologies of Calcium Channels. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40282-1.

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Zamponi, Gerald Werner, and Norbert Weiss, eds. Voltage-Gated Calcium Channels. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08881-0.

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Zamponi, Gerald W. Voltage-gated calcium channels. New York: Springer, 2011.

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Mary, Fuller Catherine, ed. Calcium-activated chloride channels. San Diego, Calif: Academic Press, 2002.

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1936-, Grinnell Alan D., Armstrong David 1951-, Jackson Meyer B, and Eckert Roger, eds. Calcium and ionchannel modulation. New York: Plenum, 1988.

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W, Putney James, ed. Calcium signaling. Boca Raton, Fla: CRC Press, 2000.

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Alan, Grinnell, Armstrong David 1951-, Jackson Meyer B, and Eckert Roger, eds. Calcium and ion channel modulation. New York: Plenum Press, 1988.

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Stephens, Gary, and Sumiko Mochida, eds. Modulation of Presynaptic Calcium Channels. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6334-0.

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Book chapters on the topic "Calcium channels"

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Ertel, Eric, and Théophile Godfraind. "Calcium channel blockers and calcium channels." In Calcium Channel Blockers, 11–80. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7859-3_2.

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Ducsay, Charles A. "Calcium Channels." In Uterine Function, 169–94. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0575-0_6.

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Nelson, Mark T. "Calcium Channels." In Ion Channel Reconstitution, 507–22. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-1361-9_20.

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Leslie, Steven W. "Calcium Channels." In Recent Developments in Alcoholism, 289–302. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-1684-6_10.

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Reynolds, Ian J., and Solomon H. Snyder. "Calcium Antagonist Receptors." In Ion Channels, 213–49. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-7302-9_6.

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Turner, Ray W. "Cav3 Calcium Channel Interactions with Potassium Channels." In Voltage-Gated Calcium Channels, 237–52. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08881-0_10.

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Bangalore, R., J. Ferrante, M. Hawthorn, W. Zheng, A. Rutledge, M. Gopalakrishnan, and D. J. Triggle. "The Regulation of Neuronal Calcium Channels." In Calcium Antagonists, 221–29. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1725-8_31.

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Beech, D. J., and T. B. Bolton. "Calcium Channels in Intestinal Smooth Muscle." In Calcium Antagonists, 285–90. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1725-8_39.

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Pietrobon, Daniela. "Cav2.1 Channels and Migraine." In Pathologies of Calcium Channels, 3–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_1.

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Wissenbach, Ulrich. "Pharmacology of TRPV Channels." In Pathologies of Calcium Channels, 549–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_27.

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Conference papers on the topic "Calcium channels"

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Busch, N. A., S. R. Reiken, Mehmet Toner, and M. L. Yarmush. "Intracellular Calcium Dynamics During Photolysis." In ASME 1997 International Mechanical Engineering Congress and Exposition, 25–31. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-1308.

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Abstract The objective of this investigation was to gain a deeper understanding of the intracellular events which precede photolysis of cells. A model system, consisting of malignant melanoma cells pre-treated with the calcium sensitive fluorescent dye, Fluo-3, was used to examine the intracellular calcium dynamics in single-cell photolysis experiments. Exposure of the cells to 632nm laser light in the presence of photosensitizer, tin chlorin e6, resulted in a rise in intracellular calcium. The increase in intracellular calcium was blocked using a variety of calcium channel blocking agents, including verapamil, nifedipine and nickel. Treatment with the channel blockers was also effective in either decreasing or eliminating cell death despite the presence of lethal doses of photosensitizer and irradiation. These results show that intracellular calcium rises prior to plasma membrane lysis, and that this early rise in intracellular calcium is necessary for membrane rupture.

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Sun, Y., Z. Zhang, L. Guo, S. Wang, Y. Yang, and Y. Gong. "Terahertz enhances the current of Mammalian Voltage-Gated Calcium Channel." In 2024 IEEE International Conference on Plasma Science (ICOPS), 1. IEEE, 2024. http://dx.doi.org/10.1109/icops58192.2024.10625927.

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Lewandowski, Zbigniew, Paul Stoodley, and Frank Roe. "Internal Mass Transport in Heterogeneous Biofilms Recent Advances." In CORROSION 1995, 1–17. NACE International, 1995. https://doi.org/10.5006/c1995-95222.

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Abstract Aerobic biofilms were found to have a complex structure consisting of microbial cell clusters (discrete aggregates of densely packed cells) and interstitial voids. We used the Confocal Scanning Laser Microscope (CSLM) in conjunction with dissolved oxygen microelectrodes to examine the structural and chemical heterogeneity of fully hydrated, living biofilms in real time under flow conditions. The oxygen distribution within the biofilm was strongly correlated with these structures. The voids facilitated oxygen transport from the bulk liquid through the biofilm. Water could freely move through the channels within the biofilm inducing convective mass transfer of dissolved and particulate substrates. Nuclear Magnetic Resonance Imaging (NMRI), in which the phase of the nuclear spin depends on the spin velocity, was used to show how fluid velocity varied in a conduit colonized with biofilm. Spin-lattice relaxation time was used at the same time to obtain images of biofilm density. The combined profiles revealed that the fluid velocity does not reach zero at the biofilm surface. This implied the existence of convective mixing inside the biofilm - a process which may have profound consequences for mass transport in biofilm systems. Particle tracking confirmed this hypothesis and provided detailed images of flow within the interstitial voids of the biofilm. Structural and chemical heterogeneity may contribute to initiation of corrosion (induce microbially influenced corrosion (MIC)) on metal surfaces where biofilms have accumulated. The Scanning Vibrating Electrode (SVE) has been used to spatially and temporally map ion currents in solution above MIC anodic and cathodic sites. Chemically active surfaces often create surpluses of charged species which locally disturb the electroneutrality of the surrounding solution. As these ions diffuse into the bulk water they create concentration gradients which can be measured using the SVE. We have used the SVE to map the course of corrosion under calcium alginate, a biopolymer, which we deposit under controlled conditions to simulate the presence of a biofilm.

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Jenson, Lacey J. "Voltage- and calcium-activated chloride channels in insect physiological systems." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93221.

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Pe�aranda, Angelina, Blas Echebarria, Enrique Alvarez-Lacalle, and Inmaculada R. Cantalapiedra. "Effects of Small Conductance Calcium Activated Potassium Channels in Cardiac Myocytes." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.308-050.

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Kaufman, I., R. Tindjong, D. G. Luchinsky, P. V. E. McClintock, and R. S. Eisenberg. "Resonant multi-ion conduction in a simple model of calcium channels." In 2013 International Conference on Noise and Fluctuations (ICNF). IEEE, 2013. http://dx.doi.org/10.1109/icnf.2013.6578926.

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Yu-Hong, Zhang, Zhan Yong, Zhao Tong-Jun, Han Ying-Rong, and Liu Hui. "Mechanism of Permeation in Calcium Channels Activation by Applied Magnetic Fields." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352558.

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Cheng, Pan, Wanyi Tang, and Hao He. "Two-photon activation of endogenous store-operated calcium channels without optogenetics." In Multiphoton Microscopy in the Biomedical Sciences XVIII, edited by Ammasi Periasamy, Peter T. So, Xiaoliang S. Xie, and Karsten König. SPIE, 2018. http://dx.doi.org/10.1117/12.2286586.

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Neamtu, Bogdan Mihai, Alexandru Farcuta, Beatrice Mihaela Radu, Andrei Dragomir, Ionela Maniu, and Daniel Dumitru Banciu. "Low Level Laser Modulation of Calcium Channels Leads to Neuronal Extensions Growth." In 2019 E-Health and Bioengineering Conference (EHB). IEEE, 2019. http://dx.doi.org/10.1109/ehb47216.2019.8969900.

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Dias, Thales Augusto Oliveira, and Silvia Graciela Ruginsk Leitão. "Participation of calcium channels in the action of angiotensin II in astrocytes." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.299.

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Background: The renin-angiotensin-aldosterone system is the main regulator of blood pressure and blood volume, with most effects being mediated by angiotensin II (Ang-II) - responsible, in the central nervous system, for actions such as thirst and sodium appetite. Astrocytes are believed to mediate such a response, as they express receptors for Ang-II and respond directly to dehydration with impacting morphological changes in the synaptic microenvironment. Many of its functions involve L-type calcium channels (LTCCs). Objectives: Evaluate the participation of LTCCs in the effects induced by AngII in cultured hypothalamic astrocytes. Methods: The effect of incubation with verapamil on the morphological responses induced by Ang-II was evaluated in hypothalamic astrocyte culture, by analyzing the expression of the cytoskeletal protein GFAP and the cell viability by the MTT assay, by immunofluorescence. Results: Incubation with Ang-II reduced the cell area considerably due to GFAP expression in relation to the control group (DMEM p<0.001), indicating that the results observed on GFAP expression did not result from cell death. Conclusion: Incubation with Ang-II alters the astrocyte morphology, reducing its area, effect at least in part, blocked by the action of Verapamil, indicating the participation of LTCCs in the mediation of this process.

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Reports on the topic "Calcium channels"

1

Sze, Heven. Identifying Calcium Channels and Porters in Plant Membranes. Office of Scientific and Technical Information (OSTI), April 1998. http://dx.doi.org/10.2172/7215.

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2

Schroeder, Julian I. Physiology and Regulation of Calcium Channels in Stomatal Guard Cells. Office of Scientific and Technical Information (OSTI), May 2007. http://dx.doi.org/10.2172/887459.

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3

Philosoph-Hadas, Sonia, Richard Crain, Shimon Meir, Nehemia Aharoni, and Susan Lurie. Calcium-Mediated Signal Transduction during Leaf Senescence. United States Department of Agriculture, November 1995. http://dx.doi.org/10.32747/1995.7604925.bard.

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We have examined the possibility that modulation of [Ca2+]cyt may represent a signal which induces senescence processes in leaves, through triggering of lipid hydrolysis leading to the cascade of detriorative events. Characterization of the signal transduction components operating during leaf senescence was gained by studying various Ca2+-dependent activities of parsley and chrysanthemum leaves, in relation to several senescence functions, and in response to senescence-modulating hormones (ethylene,ABA, BA and IAA). Some innovative findings regarding the control of senescence processes by [Ca2+]cyt were established: Several Ca2+-or CaM-related compounds were shown to modulate [Ca2+]cyt and action, thereby affecting whole leaf senescence. The involvement of [Ca2+]cyt in mediating the effects of senescence-modulating hormones has been demonstrated. Loss of energized Ca2+-transport capability of PM was found to an early event in leaf senescence, which occurs before changes in senescence parameters are observed, and while other PM ATPase enzymes still retain about 50% of their activities. A general pattern of increased phosphorylation of PM proteins with advanced senescence, which could be modified by plant hormones applied in vivo (BA) or in vitro (ABA), sa found. Taken together, all this indirect evidence indicate that [Ca2+]cyt is elevated due to the senescence-induced decrease in the ability to extrude Ca2+, which results particularly from reduced PM Ca2++-transport capability rather than increased operation of Ca2+ channels or elevated Ins(1,4,5)P3 levels. The direct proof for such a senescence-related elevation in [Ca2+]cyt was provided for the first time by the Ca2+ imaging measures with fura-2, showing a rise in [Ca2+]cyt of mesophyll cells upon senescence induction, which preceeded changes in typical senescence characteristics. This research provides strong evidence for regarding the rise in [Ca2+]cyt as a primary event in induction of the senescence syndrome in detached leaves. The findings have also broad implications for postharvest handling of leafy crops and ornamentals, and open new avenues for employing Ca2+-related inhibitors to delay leaf senescence.

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Freeman, Michael R. The Calcium Channel CaT1 in Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada443349.

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Owen, Laura. Modulation of the Cardiac Calcium Release Channel by Homocysteine Thiolactone. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2070.

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6

Karen S. Schumaker. Molecular Characterization of the Role of a Calcium Channel in Plant Development. Office of Scientific and Technical Information (OSTI), December 2004. http://dx.doi.org/10.2172/835288.

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7

Dornan, Thomas. Calcium Transport Inhibition, Stimulation, and Light Dependent Modulation of the Skeletal Calcium Release Channel (RyR1) by the Prototropic Forms of Pelargonidin. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1930.

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Slack, William, Anthony Bednar, and K. Killgore. Development of a trace element signature library across a large watershed for assessing large-scale fish movement patterns : supplemental data. Engineer Research and Development Center (U.S.), June 2025. https://doi.org/10.21079/11681/49787.

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Utilizing trace element or stable isotope analysis has proven to be an effective means to characterize early life history and large-scale movement patterns in fishes. Target species are assessed for analyte concentrations occurring in calcified hard structures and compared to signatures noted from associated watersheds. Our objective was to establish a trace element signature profile for major tributaries occurring within the Mississippi River Valley (MRV). Unfiltered water samples were obtained from 49 stations from Dubuque, IA downstream to Gramercy, LA (1387 river miles) from July through December 2023 during seasonally normal water conditions with three water samples (left descending bank, mid-channel, right descending bank) obtained from each sample station. Whole water samples were evaluated for the presence and relative concentration of Barium, Strontium, Calcium, Iron and Lithium, and were acidified with ultrapure nitric acid (Fisher Optima grade) prior to determination of total metal concentrations using ICP-AES and ICP-MS following modifications of USEPA methods 6010 and 6020, respectively. A Perkin Elmer Optima 8300DV ICP-AES was used to quantify Calcium, Iron, and Lithium whereas a Perkin Elmer NexION 350D ICP-MS was used for Barium and Strontium. Analytes were assessed for total concentrations and expressed as mg/L. In addition, Barium and Strontium concentrations were also normalized to Calcium as a pseudo-internal standard and reported as element/Ca ratios (mmol/mol).

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Fürtig, Marc-Alexander, Yana Kovalenko, Reinhold Kreutz, and Thomas G. Riemer. Psychiatric adverse events of calcium channel blockers – protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2024. http://dx.doi.org/10.37766/inplasy2024.8.0075.

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Yalovsky, Shaul, and Julian Schroeder. The function of protein farnesylation in early events of ABA signal transduction in stomatal guard cells of Arabidopsis. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7695873.bard.

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Loss of function mutations in the farnesyltransferase β subunit gene ERA1 (enhanced response to abscisic acid), cause abscisic acid hypersensitivity in seedlings and in guard cells. This results in slowed water loss of plants in response to drought. Farnesyltransferase (PFT) catalyses the attachment of the 15-carbon isoprenoid farnesyl to conserved cysteine residues located in a conserved C-terminal domain designated CaaX box. PFT is a heterodimeric protein comprised of an a and b sununits. The a subunit is shared between PFT and geranylgeranyltransferase-I (PGGTI) which catalyses the attachemt of the 20-carbon isoprenoid geranylgeranyl to CaaX box proteins in which the last amino acid is almost always leucine and in addition have a polybasic domain proximal to the CaaL box. Preliminary data presented in the proposal showed that increased cytoplasmic Ca2+ concentration in stomal guard cells in response to non-inductive ABA treatements. The goals set in the proposal were to characterize better how PFT (ERA1) affects ABA induced Ca2+ concentrations in guard cells and to identify putative CaaX box proteins which function as negative regulators of ABA signaling and which function is compromised in era1 mutant plants. To achieve these goals we proposed to use camelion Ca2+ sensor protein, high throughput genomic to identify the guard cell transcriptome and test prenylation of candidate proteins. We also proposed to focus our efforts of RAC small GTPases which are prenylated proteins which function in signaling. Our results show that farnesyltransferaseprenylates protein/s that act between the points of ABA perception and the activation of plasma membrane calcium influx channels. A RAC protein designated AtRAC8/AtRop10 also acts in negative regulation of ABA signaling. However, we discovered that this protein is palmitoylated and not prenylated although it contains a C-terminal CXXX motif. We further discovered a unique C-terminal sequence motif required for membrane targeting of palmitoylatedRACs and showed that their function is prenylation independent. A GC/MS based method for expression in plants, purification and analysis of prenyl group was developed. This method would allow highly reliable identification of prenylated protein. Mutants in the shared α subunit of PFT and PGGT-I was identified and characterized and was shown to be ABA hypersensitive but less than era1. This suggested that PFT and PGGT-I have opposing functions in ABA signaling. Our results enhanced the understanding of the role of protein prenylation in ABA signaling and drought resistance in plants with the implications of developing drought resistant plants. The results of our studies were published 4 papers which acknowledge support from BARD.

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