Relevant bibliographies by topics / Calcium activated chlorine channels

Academic literature on the topic 'Calcium activated chlorine channels'

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Published: 14 March 2023

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Journal articles on the topic "Calcium activated chlorine channels"

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Hartzell, Criss, Ilva Putzier, and Jorge Arreola. "CALCIUM-ACTIVATED CHLORIDE CHANNELS." Annual Review of Physiology 67, no. 1 (March 17, 2005): 719–58. http://dx.doi.org/10.1146/annurev.physiol.67.032003.154341.

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Hao, Feng, Zhong Hai Yuan, Zhi Xin Wang, Hui Jing Xu, Fang Fang, Xin Gang Guan, Jiang Yong, and Li Yan. "Plasmid Construction of TMEM16A-pcDNA3.1 and its Application to Transient and Stable Transfection of FRT Cells." Advanced Materials Research 554-556 (July 2012): 1734–37. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1734.

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Calcium-activated chloride channels (CaCCs) play pivotal roles in many physiological Activities, including transepithelial fluid secretion, smooth muscle contraction and sensory transduction. TMEM16A is a bona fide calcium-activated chloride channel，which was discovered by three independent labs in 2008 after Calcium-activated chloride channel current was recorded about thirty years ago. In this study, DNA fragments encoding mouse TMEM16A with green fluorescence protein (GFP) fusion protein were subcloned into pcDNA3.1/Zeo. Transient transfection condition was optimized and Fischer Thyroid epithelial cells (FRT) expressing TMEM16A were got by stable transfection. The classical calcium-activated chloride channels current was recorded in FRT cells stably expressing TMEM16A by whole cell patch clamp technique. These results were beneficial for the delving into the effects of other bivalent cations on TMEM16A-CaCCs and the role of TMEM16A-CaCCs in cell proliferation and migration.
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Hussy, N. "Calcium-activated chloride channels in cultured embryonic Xenopus spinal neurons." Journal of Neurophysiology 68, no. 6 (December 1, 1992): 2042–50. http://dx.doi.org/10.1152/jn.1992.68.6.2042.

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1. Single-channel currents were recorded from Xenopus spinal neurons developing in vitro using the patch-clamp technique, to identify the channels underlying the large and small macroscopic Ca(2+)-activated Cl- currents (ICl(Ca)) present in these cells. 2. Channels of large (maxi-channels; 310 pS) and smaller conductance (mini-channels; 50-60 pS) are activated by elevation of cytoplasmic Ca2+ concentration. Channel activity is not altered by subsequent removal of Ca2+ from the bath, arguing against a direct ligand-type Ca2+ dependence. The much higher incidence of channel activation in cell-attached patches from cells permeabilized with the Ca2+ ionophore A23187 than in excised patches also suggests the involvement of some unidentified intracellular factor. 3. The reversal potential of maxi-Cl- channels is not altered by changes in Na+ concentration, but is shifted in the negative direction by the substitution of Cl- by methanesulfonate on the intracellular side of the patch, indicating their anionic selectivity. 4. Maxi-Cl- channels exhibited the presence of multiple probable subconductance states and showed marked voltage-dependent inactivation above and below +/- 20 mV. 5. Examination of maxi-Cl- channels at early times in culture (6-9 h) and 24 h later did not reveal any developmental change in the characteristics described above. However, the mean open duration of the channel was found to increase twofold during this period of time. 6. The simultaneous presence of maxi- and mini-Cl- channels prevented detailed characterization of the latter. The anionic selectivity of mini-Cl- channels is suggested by their reversal potential that lies close to the Cl- equilibrium potential.(ABSTRACT TRUNCATED AT 250 WORDS)
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Thomas, Miracle, Mark Simms, and Prosper N’Gouemo. "Activation of Calcium-Activated Chloride Channels Suppresses Inherited Seizure Susceptibility in Genetically Epilepsy-Prone Rats." Biomedicines 10, no. 2 (February 15, 2022): 449. http://dx.doi.org/10.3390/biomedicines10020449.

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Inherited seizure susceptibility in genetically epilepsy-prone rats (GEPR-3s) is associated with increased voltage-gated calcium channel currents suggesting a massive calcium influx resulting in increased levels of intraneuronal calcium. Cytosolic calcium, in turn, activates many processes, including chloride channels, to restore normal membrane excitability and limit repetitive firing of the neurons. Here we used EACT and T16Ainh-A01, potent activator and inhibitor of calcium-activated channels transmembrane protein 16A (TMEM16A), respectively, to probe the role of these channels in the pathophysiology of acoustically evoked seizures in the GEPR-3s. We used adult male and female GEPR-3s. Acoustically evoked seizures consisted of wild running seizures (WRSs) that evolved into generalized tonic-clonic seizures (GTCSs) and eventually culminated into forelimb extension (partial tonic seizures). We found that acute EACT treatment at relatively higher tested doses significantly reduced the incidences of WRSs and GTCSs, and the seizure severity in male GEPR-3s. Furthermore, these antiseizure effects were associated with delayed seizure onset and reduced seizure duration. Interestingly, the inhibition of TMEM16A channels reversed EACT’s antiseizure effects on seizure latency and seizure duration. No notable antiseizure effects were observed in female GEPR-3s. Together, these findings suggest that activation of TMEM16A channels may represent a putative novel cellular mechanism for suppressing GTCSs.
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Yamamura, Hisao. "TMEM16 as calcium-activated chloride channels." Folia Pharmacologica Japonica 142, no. 3 (2013): 144. http://dx.doi.org/10.1254/fpj.142.144.

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Li, Weiyan, Christopher Thaler, and Paul Brehm. "Calcium Channels in Xenopus Spinal Neurons Differ in Somas and Presynaptic Terminals." Journal of Neurophysiology 86, no. 1 (July 1, 2001): 269–79. http://dx.doi.org/10.1152/jn.2001.86.1.269.

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Calcium channels play dual roles in cell signaling by promoting membrane depolarization and allowing entry of calcium ions. Patch-clamp recordings of calcium and calcium-dependent currents from the soma of Xenopus spinal neurons indicate key functional differences from those of presynaptic terminals. Both terminals and somas exhibit prominent high-voltage-activated (HVA) calcium current, but only the soma expresses additional low-voltage-activated (LVA) T-type current. Further differences are reflected in the HVA current; N- and R-type channels are predominant in the soma while the terminal calcium current is composed principally of N type with smaller contribution by L- and R-type channels. Potential physiological significance for these different distributions of channel types may lie in the differential channel kinetics. Activation of somatic HVA calcium current occurs more slowly than HVA currents in terminals. Additionally, somatic LVA calcium current activates and deactivates much more slowly than any HVA calcium current. Fast-activating and -deactivating calcium current may be critical to processing the rapid exocytotic response in terminals, whereas slow LVA and HVA calcium currents may play a central role in shaping the somatic firing pattern. In support of different kinetic behavior between these two compartments, we find that somatic calcium current activates a prominent slow chloride current not observed in terminal recordings. This current activates in response to calcium entering through either LVA or HVA channels and likely functions as a modulator of excitability or synaptic input. The restriction of this channel type to the soma lends further support to the idea that differential expression of fast and slow channel types in these neurons is dictated by differences in signaling requirements for somatic and terminal compartments.
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Dibattista, Michele, Asma Amjad, Devendra Kumar Maurya, Claudia Sagheddu, Giorgia Montani, Roberto Tirindelli, and Anna Menini. "Calcium-activated chloride channels in the apical region of mouse vomeronasal sensory neurons." Journal of General Physiology 140, no. 1 (June 25, 2012): 3–15. http://dx.doi.org/10.1085/jgp.201210780.

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The rodent vomeronasal organ plays a crucial role in several social behaviors. Detection of pheromones or other emitted signaling molecules occurs in the dendritic microvilli of vomeronasal sensory neurons, where the binding of molecules to vomeronasal receptors leads to the influx of sodium and calcium ions mainly through the transient receptor potential canonical 2 (TRPC2) channel. To investigate the physiological role played by the increase in intracellular calcium concentration in the apical region of these neurons, we produced localized, rapid, and reproducible increases in calcium concentration with flash photolysis of caged calcium and measured calcium-activated currents with the whole cell voltage-clamp technique. On average, a large inward calcium-activated current of −261 pA was measured at −50 mV, rising with a time constant of 13 ms. Ion substitution experiments showed that this current is anion selective. Moreover, the chloride channel blockers niflumic acid and 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid partially inhibited the calcium-activated current. These results directly demonstrate that a large chloride current can be activated by calcium in the apical region of mouse vomeronasal sensory neurons. Furthermore, we showed by immunohistochemistry that the calcium-activated chloride channels TMEM16A/anoctamin1 and TMEM16B/anoctamin2 are present in the apical layer of the vomeronasal epithelium, where they largely colocalize with the TRPC2 transduction channel. Immunocytochemistry on isolated vomeronasal sensory neurons showed that TMEM16A and TMEM16B coexpress in the neuronal microvilli. Therefore, we conclude that microvilli of mouse vomeronasal sensory neurons have a high density of calcium-activated chloride channels that may play an important role in vomeronasal transduction.
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Pozdnyakov, Ilya, Olga Matantseva, and Sergei Skarlato. "Consensus channelome of dinoflagellates revealed by transcriptomic analysis sheds light on their physiology." Algae 36, no. 4 (December 15, 2021): 315–26. http://dx.doi.org/10.4490/algae.2021.36.12.2.

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Ion channels are membrane protein complexes mediating passive ion flux across the cell membranes. Every organism has a certain set of ion channels that define its physiology. Dinoflagellates are ecologically important microorganisms characterized by effective physiological adaptability, which backs up their massive proliferations that often result in harmful blooms (red tides). In this study, we used a bioinformatics approach to identify homologs of known ion channels that belong to 36 ion channel families. We demonstrated that the versatility of the dinoflagellate physiology is underpinned by a high diversity of ion channels including homologs of animal and plant proteins, as well as channels unique to protists. The analysis of 27 transcriptomes allowed reconstructing a consensus ion channel repertoire (channelome) of dinoflagellates including the members of 31 ion channel families: inwardly-rectifying potassium channels, two-pore domain potassium channels, voltage-gated potassium channels (Kv), tandem Kv, cyclic nucleotide-binding domain-containing channels (CNBD), tandem CNBD, eukaryotic ionotropic glutamate receptors, large-conductance calcium-activated potassium channels, intermediate/small-conductance calcium-activated potassium channels, eukaryotic single-domain voltage-gated cation channels, transient receptor potential channels, two-pore domain calcium channels, four-domain voltage-gated cation channels, cation and anion Cys-loop receptors, small-conductivity mechanosensitive channels, large-conductivity mechanosensitive channels, voltage-gated proton channels, inositole-1,4,5- trisphosphate receptors, slow anion channels, aluminum-activated malate transporters and quick anion channels, mitochondrial calcium uniporters, voltage-dependent anion channels, vesicular chloride channels, ionotropic purinergic receptors, animal volage-insensitive cation channels, channelrhodopsins, bestrophins, voltage-gated chloride channels H+/Cl- exchangers, plant calcium-permeable mechanosensitive channels, and trimeric intracellular cation channels. Overall, dinoflagellates represent cells able to respond to physical and chemical stimuli utilizing a wide range of Gprotein coupled receptors- and Ca2+-dependent signaling pathways. The applied approach not only shed light on the ion channel set in dinoflagellates, but also provided the information on possible molecular mechanisms underlying vital cellular processes dependent on the ion transport.
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Kaneko, Hiroshi, Frank Möhrlen, and Stephan Frings. "Calmodulin Contributes to Gating Control in Olfactory Calcium-activated Chloride Channels." Journal of General Physiology 127, no. 6 (May 30, 2006): 737–48. http://dx.doi.org/10.1085/jgp.200609497.

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In sensory neurons of the peripheral nervous system, receptor potentials can be amplified by depolarizing Cl currents. In mammalian olfactory sensory neurons (OSNs), this anion-based signal amplification results from the sequential activation of two distinct types of transduction channels: cAMP-gated Ca channels and Ca-activated Cl channels. The Cl current increases the initial receptor current about 10-fold and leads to the excitation of the neuron. Here we examine the activation mechanism of the Ca-dependent Cl channel. We focus on calmodulin, which is known to mediate Ca effects on various ion channels. We show that the cell line Odora, which is derived from OSN precursor cells in the rat olfactory epithelium, expresses Ca-activated Cl channels. Single-channel conductance, ion selectivity, voltage dependence, sensitivity to niflumic acid, and Ca sensitivity match between Odora channels and OSN channels. Transfection of Odora cells with CaM mutants reduces the Ca sensitivity of the Cl channels. This result points to the participation of calmodulin in the gating process of Ca-ativated Cl channels, and helps to understand how signal amplification works in the olfactory sensory cilia. Calmodulin was previously shown to mediate feedback inhibition of cAMP-synthesis and of the cAMP-gated Ca channels in OSNs. Our results suggest that calmodulin may also be instrumental in the generation of the excitatory Cl current. It appears to play a pivotal role in the peripheral signal processing of olfactory sensory information. Moreover, recent results from other peripheral neurons, as well as from smooth muscle cells, indicate that the calmodulin-controlled, anion-based signal amplification operates in various cell types where it converts Ca signals into membrane depolarization.
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Lalonde, Melanie, Melanie Kelly, and Steven Barnes. "Calcium-activated chloride channels in the retina." Channels 2, no. 4 (July 4, 2008): 252–60. http://dx.doi.org/10.4161/chan.2.4.6704.

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Dissertations / Theses on the topic "Calcium activated chlorine channels"

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Adair, Jeanette. "Alternate channel therapy for the pancreatic disease of Cystic Fibrosis." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251005.

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Sharma, Aarushi. "HUMAN CLCA2 MODULATES THE CONDUCTANCE OF CALCIUM-ACTIVATED CHLORIDE CHANNELS BY REGULATION OF INTRACELLULAR CALCIUM." OpenSIUC, 2016. https://opensiuc.lib.siu.edu/dissertations/1252.

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Chloride channels play an essential role in the physiology of the respiratory system, the gastrointestinal tract, and secretory glands. Their dysregulation underlies debilitating pathologies such as cystic fibrosis, asthma, and certain cancers. The CLCA (Chloride Channel Accessory) gene family is thought to determine severity of these diseases by modulating an unidentified Calcium-activated Chloride Channel (CaCC). Recent evidence indicates Ano1 to be the mediator of strong quintessential calcium-activated chloride current in several cell types. Ano1 is highly expressed in airway epithelium and downregulated in cystic fibrosis patients. Human CLCA2 is also expressed in epithelium of airways and mammary glands, and there it promotes calcium-activated chloride current. Hence, we hypothesized that CLCA2 modulates the conductance of Ano1. We tested this by introducing Ano1 and CLCA2 together or separately into HEK293 cells, which express endogenous Ano1 at a low level. Using whole-cell voltage clamp, we found that CLCA2 enhanced the conductance of the endogenous CaCC. This current was inhibited by a specific inhibitor of Ano1, tannic acid. CLCA2 also increased both the amplitude and the onset rate of the Ano1-mediated current. To determine the mechanism by which CLCA2 amplifies Ano1 mediated current, we used co-immunoprecipitation with or without a protein cross-linking agent and to test whether the interaction if any, was stable or transient, respectively. Neither any interaction, nor any change in Ano1 multimerization was found. We next tested whether CLCA2 enhanced Ano1 conductance by increasing its stability or surface localization. Surface-labelling the cells expressing Ano1 alone or both proteins with biotin, no difference in Ano1 level or surface expression was detected. Ano1 has recently been shown to be activated by intracellular calcium released from endoplasmic reticulum (ER) stores and by subsequent store-operated calcium entry (SOCE). Therefore, we investigated whether CLCA2 could increase intracellular calcium levels. With Fluo-4 dye calcium imaging, we found that CLCA2 expression enhanced both ER calcium stores and SOCE upon exhaustion of intracellular stores, and the SOCE response could be abolished by a specific inhibitor of SOCE, BTP-2. This inhibitor also abolished CLCA2-induced chloride current, establishing that CLCA2 enhances CaCC via SOCE. Moreover, knockdown of CLCA2 in MCF10A cells, that naturally express both proteins, reduced both ER calcium stores and SOCE. Mutations that abolished the metalloprotease activity of CLCA2 or deleted the cytoplasmic tail had little effect on its enhancement of chloride current or intracellular calcium, suggesting that the uncleaved ectodomain was responsible for both effects of CLCA2. Since, the ectodomain is the most conserved region of the protein, we found that another member of the CLCA family, CLCA1, was also effective in enhancing intracellular calcium storage and SOCE. Co-immunoprecipitation studies further revealed that CLCA2 interacts in a ternary complex with mediators of SOCE, STIM1 and ORAI1. These results explain the CaCC-enhancing effects of CLCA family members and suggest a broader role in other calcium-dependent processes. Understanding the modulatory relationship between these molecules may lead to better therapies for airway diseases and Ano1-dependent cancers. Furthermore, the discovery that CLCA2 regulates intracellular calcium levels may explain its effects on cellular differentiation, stress response, and cell death.
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Brookfield, Rebecca. "The pharmacology and cardiovascular function of TMEM16A channels." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/the-pharmacology-and-cardiovascular-function-of-tmem16a-channels(bdc16466-cecd-4343-9d40-b20bc647d70f).html.

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Calcium-activated chloride channels (CaCCs) are ubiquitously expressed in a plethora of cell types and, consequently, are involved in numerous cellular processes as diverse as epithelial secretion, regulation of cardiac excitability and smooth muscle contraction. Current pharmacology of CaCCs is limited to compounds with low potency and poor selectivity. The lack of knowledge surrounding the molecular identity of the CaCC has greatly hindered the development of more specific drugs and has impaired our understanding of the channel physiology and biophysics. The recent discovery that the TMEM16A gene codes for CaCCs has offered hope for new developments in these areas. CaCCs have been suggested as possible targets to treat a variety of conditions including asthma as well as pulmonary and systemic hypertension. Due to the ubiquitous expression of CaCCs and the ability of the channel to interact with a number of pharmacological compounds with diverse chemical structures however, it was hypothesised that TMEM16A could be a possible source for off-target drug effects and may represent a concern for safety pharmacology. The principal aim of this thesis was to assess the functional significance of TMEM16A in the cardiovascular system, as this is one of the major systems of concern for safety pharmacology and accounts for the largest number of post-market drug withdrawals. The main findings of this study can be summarised as follows: 1) RT-PCR analysis revealed a ubiquitous expression of TMEM16A in tissues of the rat and human cardiovascular systems, including systemic and pulmonary arteries as well as cardiac tissue. Analysis also revealed the presence of multiple TMEM16A splice variants in all rat tissues examined, in addition to a number of other TMEM16x family members. 2) Myography experiments using the “classical” CaCC blocker niflumic acid and newly identified TMEM16A blockers confirmed a functional role for TMEM16A in phenylephrine-induced vascular smooth muscle contraction. 3) The suitability of currently available Cl- channel blockers for use as pharmacological tools for TMEM16A research was assessed using conventional whole-cell patch clamp and high-throughput electrophysiology techniques to respectively compare their potencies and selectivity over other cardiovascular ion channels. Of the compounds tested, DIDS and T16Ainh-A01 appeared the most suitable blockers; however all compounds had a degree of non-selectivity, raising concerns for their use in functional studies. In conclusion, these findings provide evidence for the ubiquitous expression and functional significance of TMEM16A within the cardiovascular system and support the hypothesis that TMEM16A is a concern for safety pharmacology and should be included into future pre-clinical safety assays. The inadequacy of current inhibitors however highlights the urgency for the development of novel potent and selective channel modulators for future TMEM16A research.
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Georgiou, Panayiotis Paulou. "Calcium-activated potassium-channels in mammalian eggs." Thesis, University of Edinburgh, 1985. http://hdl.handle.net/1842/29774.

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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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Conrad, Rachel [Verfasser]. "Trafficking of voltage-activated calcium channels / Rachel Conrad." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1136717919/34.

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Millership, Joanne Ella. "Regulation and function of calcium-activated potassium channels." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503016.

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Marsey, Laura Louise. "Molecular and functional investigations of the calcium activated chloride channel in cystic fibrosis pancreatic duct cells." Thesis, University of East Anglia, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445193.

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Hagen, Brian M. "Regulation of calcium-activated potassium channels by localized calcium transients in murine colon." abstract and full text PDF (free order & download UNR users only), 2005. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3209955.

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D'hoedt, Dieter. "Structure-function analyses of small-conductance, calcium-activated potassium channels." Diss., [S.l.] : [s.n.], 2005. http://edoc.ub.uni-muenchen.de/archive/00006036.

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Books on the topic "Calcium activated chlorine channels"

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W, Tsien R., Clozel Jean-Paul, and Nargeot Joël, eds. Low-voltage-activated T-type calcium channels: Proceedings from the International Electrophysiology Meeting, Montpellier, 21-22 October 1996. Chester, England: Adis International, 1998.

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

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Calcium-activated chloride channels. San Diego, Calif: Academic Press, 2002.

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

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Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.

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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.
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Book chapters on the topic "Calcium activated chlorine channels"

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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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Forrest, Abigail S., Jeff E. Angermann, Rajesh Raghunathan, Catherine Lachendro, Iain A. Greenwood, and Normand Leblanc. "Intricate Interaction Between Store-Operated Calcium Entry and Calcium-Activated Chloride Channels in Pulmonary Artery Smooth Muscle Cells." In Advances in Experimental Medicine and Biology, 31–55. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-500-2_3.

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Engbers, Jordan, and Ray W. Turner. "Low-Voltage-Activated Calcium Channels." In Encyclopedia of Computational Neuroscience, 1640–43. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_130.

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Solinas, Sergio, Stefano Masoli, and Sathyaa Subramaniyam. "High-Voltage-Activated Calcium Channels." In Encyclopedia of Computational Neuroscience, 1319–24. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_230.

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Engbers, Jordan. "Low-Voltage-Activated Calcium Channels." In Encyclopedia of Computational Neuroscience, 1–5. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_130-2.

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Solinas, Sergio, Stefano Masoli, and Sathyaa Subramaniyam. "High-Voltage-Activated Calcium Channels." In Encyclopedia of Computational Neuroscience, 1–7. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_230-1.

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Lingle, Christopher J., Christopher R. Solaro, Murali Prakriya, and Jiu Ping Ding. "Calcium-Activated Potassium Channels in Adrenal Chromaffin Cells." In Ion Channels, 261–301. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-1775-1_7.

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Kume, Hiroaki. "Large-Conductance Calcium-Activated Potassium Channels." In Calcium Signaling In Airway Smooth Muscle Cells, 49–83. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01312-1_4.

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Kaczorowski, Gregory J., and Thomas R. Jones. "High Conductance Calcium-Activated Potassium Channels." In Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction, 169–98. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7362-8_8.

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De Waard, Michel, Christina A. Gurnett, and Kevin P. Campbell. "Structural and Functional Diversity of Voltage-Activated Calcium Channels." In Ion Channels, 41–87. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-1775-1_2.

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Conference papers on the topic "Calcium activated chlorine channels"

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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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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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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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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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Remy, Kenneth E., Ding Bang Xu, Herng-Yu S. Chang, Peter Yim, and Charles W. Emala. "Novel Expression Of The TMEM16 Family Of Calcium Activated Chloride Channels In Human Airway Epithelium And Smooth Muscle Cells." 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.a6035.

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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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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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Fang, Shijing, Anne L. Crews, Joungjoa Park, and Kenneth B. Adler. "Interactions Between A Calcium-Activated Chloride Channel And Marcks In Airway Mucin Secretion." 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.a4239.

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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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Shiwarski, Daniel, Carol Bertrand, Ann Marie Egloff, Xin Huang, Raja Seethala, Jennifer Grandis, Susanne Gollin, and Umamaheswar Duvvuri. "Abstract LB-220: TMEM16A, a novel calcium-activated chloride channel, modulates tumor proliferation via MAPK and Cyclin-D1 signaling." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-220.

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