Relevant bibliographies by topics / Chloride channels

Contents

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

Academic literature on the topic 'Chloride channels'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Chloride channels"

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Lísal, Jiří, and Merritt Maduke. "Proton-coupled gating in chloride channels." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1514 (October 28, 2008): 181–87. http://dx.doi.org/10.1098/rstb.2008.0123.

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The physiologically indispensable chloride channel (CLC) family is split into two classes of membrane proteins: chloride channels and chloride/proton antiporters. In this article we focus on the relationship between these two groups and specifically review the role of protons in chloride-channel gating. Moreover, we discuss the evidence for proton transport through the chloride channels and explore the possible pathways that the protons could take through the chloride channels. We present results of a mutagenesis study, suggesting the feasibility of one of the pathways, which is closely related to the proton pathway proposed previously for the chloride/proton antiporters. We conclude that the two groups of CLC proteins, although in principle very different, employ similar mechanisms and pathways for ion transport.
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Jentsch, Thomas J. "Chloride channels." Current Opinion in Neurobiology 3, no. 3 (June 1993): 316–21. http://dx.doi.org/10.1016/0959-4388(93)90123-g.

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Kicińska, A., G. D bska, W. Kunz, and A. Szewczyk. "Mitochondrial potassium and chloride channels." Acta Biochimica Polonica 47, no. 3 (September 30, 2000): 541–51. http://dx.doi.org/10.18388/abp.2000_3977.

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Channels selective for potassium or chloride ions are present in inner mitochondrial membranes. They probably play an important role in mitochondrial events such as the formation of delta pH and regulation of mitochondrial volume changes. Mitochondrial potassium and chloride channels could also be the targets for pharmacologically active compounds such as potassium channel openers and antidiabetic sulfonylureas. This review describes the properties, pharmacology, and current observations concerning the functional role of mitochondrial potassium and chloride channels.
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Kim, Hyeong Jae, Peter Chang-Whan Lee, and Jeong Hee Hong. "Chloride Channels and Transporters: Roles beyond Classical Cellular Homeostatic pH or Ion Balance in Cancers." Cancers 14, no. 4 (February 9, 2022): 856. http://dx.doi.org/10.3390/cancers14040856.

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The canonical roles of chloride channels and chloride-associated transporters have been physiologically determined; these roles include the maintenance of membrane potential, pH balance, and volume regulation and subsequent cellular functions such as autophagy and cellular proliferative processes. However, chloride channels/transporters also play other roles, beyond these classical function, in cancerous tissues and under specific conditions. Here, we focused on the chloride channel-associated cancers and present recent advances in understanding the environments of various types of cancer caused by the participation of many chloride channel or transporters families and discuss the challenges and potential targets for cancer treatment. The modulation of chloride channels/transporters might promote new aspect of cancer treatment strategies.
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Duszyk, Marek, Andrew S. French, and S. F. Paul Man. "Cystic fibrosis affects chloride and sodium channels in human airway epithelia." Canadian Journal of Physiology and Pharmacology 67, no. 10 (October 1, 1989): 1362–65. http://dx.doi.org/10.1139/y89-217.

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Abnormalities of epithelial function in cystic fibrosis (CF) have been linked to defects in cell membrane permeability to chloride or sodium ions. Recently, a class of chloride channels in airway epithelial cells have been reported to lack their usual sensitivity to phosphorylation via cAMP-dependent protein kinase, suggesting that CF could be due to a single genetic defect in these channels. We have examined single chloride and sodium channels in control and CF human nasal epithelia using the patch-clamp technique. The most common chloride channel was not the one previously associated with CF, but it was also abnormal in CF cells. In addition, the number of sodium channels was unusually high in CF. These findings suggest a wider disturbance of ion channel properties in CF than would be produced by a defect in a single type of channel.Key words: ion channels, cystic fibrosis, airway, epithelium.
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Uchida, Shinichi. "In vivo role of CLC chloride channels in the kidney." American Journal of Physiology-Renal Physiology 279, no. 5 (November 1, 2000): F802—F808. http://dx.doi.org/10.1152/ajprenal.2000.279.5.f802.

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Chloride channels in the kidney are involved in important physiological functions such as cell volume regulation, acidification of intracellular vesicles, and transepithelial chloride transport. Among eight mammalian CLC chloride channels expressed in the kidney, three (CLC-K1, CLC-K2, and CLC-5) were identified to be related to kidney diseases in humans or mice. CLC-K1 mediates a transepithelial chloride transport in the thin ascending limb of Henle's loop and is essential for urinary concentrating mechanisms. CLC-K2 is a basolateral chloride channel in distal nephron segments and is necessary for chloride reabsorption. CLC-5 is a chloride channel in intracellular vesicles of proximal tubules and is involved in endocytosis. This review will cover the recent advances in research on the CLC chloride channels of the kidney with a special focus on the issues most necessary to understand their physiological roles in vivo, i.e., their intrarenal and cellular localization and their phenotypes of humans and mice that have their loss-of-function mutations.
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Wilczyński, Bartosz, Alicja Dąbrowska, Jolanta Saczko, and Julita Kulbacka. "The Role of Chloride Channels in the Multidrug Resistance." Membranes 12, no. 1 (December 28, 2021): 38. http://dx.doi.org/10.3390/membranes12010038.

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Nowadays, one of medicine’s main and most challenging aims is finding effective ways to treat cancer. Unfortunately, although there are numerous anti-cancerous drugs, such as cisplatin, more and more cancerous cells create drug resistance. Thus, it is equally important to find new medicines and research the drug resistance phenomenon and possibilities to avoid this mechanism. Ion channels, including chloride channels, play an important role in the drug resistance phenomenon. Our article focuses on the chloride channels, especially the volume-regulated channels (VRAC) and CLC chloride channels family. VRAC induces multidrug resistance (MDR) by causing apoptosis connected with apoptotic volume decrease (AVD) and VRAC are responsible for the transport of anti-cancerous drugs such as cisplatin. VRACs are a group of heterogenic complexes made from leucine-rich repetition with 8A (LRRC8A) and a subunit LRRC8B-E responsible for the properties. There are probably other subunits, which can create those channels, for example, TTYH1 and TTYH2. It is also known that the ClC family is involved in creating MDR in mainly two mechanisms—by changing the cell metabolism or acidification of the cell. The most researched chloride channel from this family is the CLC-3 channel. However, other channels are playing an important role in inducing MDR as well. In this paper, we review the role of chloride channels in MDR and establish the role of the channels in the MDR phenomenon.
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Zhao, Piao, Cheng Tang, Yuqin Yang, Zhen Xiao, Samantha Perez-Miller, Heng Zhang, Guoqing Luo, et al. "A new polymodal gating model of the proton-activated chloride channel." PLOS Biology 21, no. 9 (September 15, 2023): e3002309. http://dx.doi.org/10.1371/journal.pbio.3002309.

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The proton–activated chloride (PAC) channel plays critical roles in ischemic neuron death, but its activation mechanisms remain elusive. Here, we investigated the gating of PAC channels using its novel bifunctional modulator C77304. C77304 acted as a weak activator of the PAC channel, causing moderate activation by acting on its proton gating. However, at higher concentrations, C77304 acted as a weak inhibitor, suppressing channel activity. This dual function was achieved by interacting with 2 modulatory sites of the channel, each with different affinities and dependencies on the channel’s state. Moreover, we discovered a protonation–independent voltage activation of the PAC channel that appears to operate through an ion–flux gating mechanism. Through scanning–mutagenesis and molecular dynamics simulation, we confirmed that E181, E257, and E261 in the human PAC channel serve as primary proton sensors, as their alanine mutations eliminated the channel’s proton gating while sparing the voltage–dependent gating. This proton–sensing mechanism was conserved among orthologous PAC channels from different species. Collectively, our data unveils the polymodal gating and proton–sensing mechanisms in the PAC channel that may inspire potential drug development.
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Fahlke, Christoph, Timothy Knittle, Christina A. Gurnett, Kevin P. Campbell, and Alfred L. George. "Subunit Stoichiometry of Human Muscle Chloride Channels." Journal of General Physiology 109, no. 1 (January 1, 1997): 93–104. http://dx.doi.org/10.1085/jgp.109.1.93.

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Voltage-gated Cl− channels belonging to the ClC family appear to function as homomultimers, but the number of subunits needed to form a functional channel is controversial. To determine subunit stoichiometry, we constructed dimeric human skeletal muscle Cl− channels in which one subunit was tagged by a mutation (D136G) that causes profound changes in voltage-dependent gating. Sucrose-density gradient centrifugation experiments indicate that both monomeric and dimeric hClC-1 channels in their native configurations exhibit similar sedimentation properties consistent with a multimeric complex having a molecular mass of a dimer. Expression of the heterodimeric channel in a mammalian cell line results in a homogenous population of Cl− channels exhibiting novel gating properties that are best explained by the formation of heteromultimeric channels with an even number of subunits. Heteromultimeric channels were not evident in cells cotransfected with homodimeric WT-WT and D136G-D136G constructs excluding the possibility that functional hClC-1 channels are assembled from more than two subunits. These results demonstrate that the functional hClC-1 unit consists of two subunits.
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Higgins, Chris. "Chloride channels revisited." Nature 358, no. 6387 (August 1992): 536. http://dx.doi.org/10.1038/358536a0.

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Dissertations / Theses on the topic "Chloride channels"

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Low, Wendy. "Chloride channels in epithelia." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=68206.

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The outwardly rectifying chloride channel is found in most vertebrate cells however its physiological role is uncertain. Patch clamp, short-circuit current, and electronic cell sizing techniques were used to investigate the role of the outward rectifier in transepithelial chloride secretion and cell volume regulation, the two main functions that have been proposed for this channel in epithelia. Patch clamp studies of the human cell lines PANC-1 and T$ sb{84}$ showed that the chloride channel blockers IAA-94 and NPPB decrease the open probability of the outward rectifier, with half-maximal inhibition at 15 $ mu$M and 23 $ mu$M, respectively. At these concentrations the blockers did not affect cAMP-induced short-circuit current. They did inhibit the regulatory volume decrease (RVD) which occurs after hypotonic cell swelling, but only at much higher concentrations. Moreover, the commonly-used inhibitor DIDS, which blocks the outward rectifier in the 10-20 $ mu$M range, had no effect on the RVD when tested at 100 $ mu$M. The results indicate that the outwardly rectifying Cl channel does not mediate a significant fraction of transepithelial Cl secretion across T$ sb{84}$ cells. Although the data do not exclude a role for the outward rectifier in cell volume regulation, the selectivity and pharmacological properties of the swelling-induced anion conductance in T$ sb{84}$ cells is more similar to the ClC-2 channel than to the outward rectifier.
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Thompson, Christopher Hal. "Identification and characterization of a peptide toxin inhibitor of ClC-2 chloride channels." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/26604.

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Thesis (Ph.D)--Biology, Georgia Institute of Technology, 2009.
Committee Chair: McCarty, Nael; Committee Co-Chair: Harvey, Stephen; Committee Member: Hartzell, Criss; Committee Member: Kubanek, Julia; Committee Member: Lee, Robert. Part of the SMARTech Electronic Thesis and Dissertation Collection.
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Sabanov, Victor. "Chloride Channels and Brown Fat Cells." Doctoral thesis, Stockholm : Department of Physiology, Wenner-Gren Institute, Arrhenius Laboratories, Stockholm University, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-474.

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Bhandal, Narotam Singh. "Arthropod chloride channels as targets for pesticides." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335651.

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Pifferi, Simone. "Calcium Activated Chloride Channels In Olfactory Transduction." Doctoral thesis, SISSA, 2008. http://hdl.handle.net/20.500.11767/4668.

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Ca2+-activated Cl ̄ channels are an important component of olfactory transduction. Odorant binding to odorant receptors in the cilia of olfactory sensory neurons (OSNs) leads to an increase of intraciliary Ca2+ concentration by Ca2+ entry through cyclic nucleotide-gated channels. Ca2+ activates a Cl ̄ channel that leads to an efflux of Cl ̄ from the cilia, contributing to the amplification of the OSN depolarization. The molecular identity of this Cl ̄ channel remains elusive. Recent evidences have indicated that bestrophins are able to form Ca2+-activated Cl ̄ channels channels in heterologous systems. Immunohistochemistry revealed that mBest2 was expressed on the cilia of OSNs, the site of olfactory transduction, and co-localized with the main subunit of cyclic nucleotide-gated channels, CNGA2. We performed a functional comparison of the properties of Ca2+-activated Cl ̄ channels from native channels expressed in dendritic knob/cilia of mouse OSNs with those induced by heterologous expression of mBest2 in HEK-293 cells. Even if the two channels did not display identical characteristics, they have many similar features such as the same anion permeability, the Ca2+ sensitivity in micromolar range and the same side-specific blockage of the two Cl ̄ channel blockers commonly used to inhibit the odorant-induced Ca2+-activated Cl ̄ channels in OSNs, niflumic acid and 4-acetamido-4’-isothiocyanato-stilben-2,2’-disulfonate (SITS). However electroolfactogram recording from mBest2 null mice showed a normal sensitivity to odorant stimulation. Therefore mBest2 is a good candidate for being a molecular component of the olfactory Ca2+-activated Cl ̄ channels but its precise role in olfactory transduction remains to be clarified.
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Joo, Nam Soo. "Regulation of duodenal ion transport by uroguanylin and cloning of murine intestinal CIC-2 chloride channel." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9924893.

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Sin, Sai-lung Steven, and 冼世隆. "Chloride channel in glioma cell invasion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41508555.

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Sin, Sai-lung Steven. "Chloride channel in glioma cell invasion." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41508555.

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Halstead, Meredith. "Putative glutamate-gated chloride channels from Onchocerca volvulus." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=29439.

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Onchocerca volvulus, a filarial nematode, is the causative agent of onchocerciasis.
O. volvulus is a human parasite with no animal model host and is endemic in the tropics. O. volvulus material is scarce and must be conserved as part of the Onchocerciasis Control Program. A genomic library was constructed to provide a substantial source of renewable genetic material, in place of original parasite DNA.
Currently there is only one glutamate-gated chloride channel that has been sequenced from O. volvulus, but this has not yet been characterized. This GluClx partial cDNA sequence isolated by Cully et al., 1997, may be found in GenBank, accession number U59745. Specific primers were designed to amplify this gene from the genomic library. A fragment of this gene was isolated but the primers were non-specific, amplifying genes in addition to GluClx.
A motif is a short recognition sequence within a protein that may allow the modification of the protein. The cysteine loop in the N-terminal of all the ligand-gated ion channels is interesting because it contains the neurotransmitter-gated ion channel signature sequence. (Abstract shortened by UMI.)
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Starc, Tanja. "Structure function analysis of glutamate gated chloride channels." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79135.

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Glutamate-gated chloride channels (GluCl) belong to then icotinic ligand-gated ion channel family and are thus assumed to be heteropentamers. Each subunit contains a large extracellular N-terminal domain, four transmembrane domains (TM1--TM4), and an extracellular C terminal. Caenorhabditis elegans expresses various GluCl channels formed by alpha1, alpha2, alpha3, alpha4 and beta subunits. The best understood GluCl channel is expressed in pharyngeal muscle cells where it mediates response to the M3 motor neuron. alpha2 forms this channel, probably in association with beta. The alpha2 mutant lacks M3 neurotransmission which can be rescued by pharynx-specific alpha2 expression. My results show that alpha1 and alpha3 subunits cannot substitute for alpha2. Formation of chimeric constructs of alpha1, alpha2 and alpha3 pinpoints the M1--M3 transmembrane region of alpha2 as the minimal rescuing domain. This region may therefore be important for localization or, in association with another subunit, in the formation of the active channel.
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Books on the topic "Chloride channels"

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

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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. New York: Plenum Press, 1990.

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

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

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

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

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

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

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

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

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Book chapters on the topic "Chloride channels"

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Prescott, Steven A. "Chloride Channels." In Encyclopedia of Computational Neuroscience, 601–5. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_226.

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Prescott, Steven A. "Chloride Channels." In Encyclopedia of Computational Neuroscience, 1–4. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_226-1.

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Greger, R., and K. Kunzelmann. "Epithelial Chloride Channels." In Epithelial Secretion of Water and Electrolytes, 3–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75033-5_1.

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Hume, Joseph R., Paul C. Levesque, Pádraig Hart, Mei Lin Collier, John D. Warth, Yvonne Geary, Todd Chapman, and Burton Horowitz. "Chloride channels in heart." In Developments in Cardiovascular Medicine, 187–96. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-3990-8_16.

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Cuppoletti, John, Danuta H. Malinowska, and Ryuji Ueno. "ClC-2 Chloride Channels." In Ion Channels and Transporters of Epithelia in Health and Disease, 491–518. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-3366-2_15.

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Gallos, George, and Charles W. Emala. "Calcium-Activated Chloride Channels." In Calcium Signaling In Airway Smooth Muscle Cells, 85–106. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01312-1_5.

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Gerencser, G. A. "Chloride Channels in Molluscs." In Advances in Comparative and Environmental Physiology, 133–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78261-9_8.

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Cuppoletti, John, Danuta H. Malinowska, and Ryuji Ueno. "ClC-2 Chloride Channels." In Studies of Epithelial Transporters and Ion Channels, 495–522. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-55454-5_13.

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Liedtke, Carole M. "Chloride Channels in Cystic Fibrosis." In Ion Channels and Ion Pumps, 500–525. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2596-6_23.

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Koster, Anna K., and Merritt Maduke. "CLC Chloride Channels and Transporters." In Textbook of Ion Channels Volume II, 193–208. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003096276-13.

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Conference papers on the topic "Chloride channels"

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Shenoy, Ambika, Sascha Kopic, Michael Murek, Christina Caputo, John Geibel, and Marie Egan. "Cystic Fibrosis Transmembrane Conductance Regulator Protein And Calcium Activated Chloride Channels Mediate Chloride Efflux In Murine Macrophages." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6575.

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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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Chang, Chen-Ling, John Guofeng Bai, Kyong-Hoon Lee, Jae-Hyun Chung, Yaling Liu, and Wing Kam Liu. "Ion Diffusion Upon Concentrations in Open Nanofluidic Channels." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42362.

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The ion flow in nanochannels is investigated by using nanochannels in an open configuration that allows the direct observation of fluid diffusion through an optical microscope. An “open nanochannel” is a channel with the top open to air such that fluidics can be introduced from both the entrance and the top of the channels. The experimental results showed that the diffusion length of the potassium chloride and phosphate buffer decreased with their concentration. The observed behaviors were analyzed by the contact angle variation due to the electrowetting phenomena involving the interaction between electrical double layer and counter-ions in the solution.
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Gallos, George, Peter Yim, Yi Zhang, James M. Cook, Sundari Rallapalli, and Charles W. Emala. "Gabaa Channels Containing The Alpha5 Subunit Directly Relax Airway Smooth Muscle And Increase Chloride Channel Flux." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6034.

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Yim, Peter, George Gallos, Yi Zhang, and Charles W. Emala. "Concomitant Blockade Of Calcium-Activated Chloride Channels (CACC) And Sodium Potassium Chloride Cotransporter (NKCC) Attenuates Acetylcholine Contractions In Human Airway Smooth Muscle." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6033.

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Ozoe, Yoshihisa. "Molecular and functional characterization of histamine-gated chloride channels from the house fly, Musca domestica." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93015.

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Vemulakonda, Srilakshmi, Demosthenes G. Papamatheakis, A. Forrest, N. Leblanc, J. Angermann, L. D. Longo, and Sean M. Wilson. "INFLUENCE OF POSTNATAL MATURITY AND CHRONIC HYPOXIA ON CALCIUM ACTIVATED CHLORIDE CHANNELS IN PULMONARY ARTERIAL VASOCONSTRICTION." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6278.

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Brett, T., M. Sala-Rabanal, K. Berry, D. F. Steinberg, and C. G. Nichols. "Modulation of TMEM16B Channel Activity by the Calcium-Activated Chloride Channel Regulator 4 Suggests a Common Function for CLCA Proteins in Modifying TMEM16 Channels." 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.a2127.

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Vemulakonda, S., DG Papamatheakis, J. Angermann, D. Nguyen, WJ Pearce, LD Longo, and SM Wilson. "The Role of Calcium Activated Chloride Channels in Pulmonary Arterial Vasoconstriction Is Influenced by Long-Term Hypoxic Stress." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6245.

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Della Sala, A., A. Murabito, M. Mergiotti, C. S. Butnarasu, V. Sala, V. Capurro, L. Terranova, et al. "Rescue of Mutant CFTR Chloride Channels by a Mimetic Peptide Targeting the A-Kinase Anchoring Function of PI3Kγ." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5659.

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Reports on the topic "Chloride channels"

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Akanji, Bukunmi Abongwa. Functional expression of a glutamate-gated chloride channel (GLC-3) from adult Brugia malayi. Ames (Iowa): Iowa State University, January 2018. http://dx.doi.org/10.31274/cc-20240624-771.

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Lavoie, D., V. Tremblay, and C. Rivard. Sandstone composition and diagenesis of the Paskapoo Formation and their significance for shallow groundwater aquifer in the Fox Creek area, west-central Alberta. Natural Resources Canada/CMSS/Information Management, 2023. http://dx.doi.org/10.4095/331923.

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Abstract:
The shallow aquifer in the Fox Creek area is hosted by the Paleocene Paskapoo Formation. The formation consists of fluvial deposits with channel-filled high-energy sandstone cutting through fine-grained, low energy overbank sediments. Three internal members are recognized, these members define three hydrostratigraphic units (two aquifers versus one aquitard). In fall 2022, three boreholes were drilled and cored. The succession is slightly dominated by sandstone with subordinate fine-grained sediments and thin coal intervals. The calcareous to non-calcareous sandstone is either tight and well compacted or porous, friable to unconsolidated. The litharenite is composed of quartz, various types of rock fragments, chert, and feldspars. Detrital carbonates can be abundant. The post-sedimentation history of the sandstone recorded cementation and dissolution events from near surface, through shallow burial and late tectonic exhumation. The events include early clay coatings on grains, dissolution of metastable minerals, cementation from calcite, kaolinite and minor chlorite and late near surface fault-controlled freshwater circulation and dissolution. The late event resulted in friable to unconsolidated sandstone intervals.
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