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Academic literature on the topic 'Potassium channel'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Potassium channel"

1

Hopkins, W. F., J. L. Miller, and G. P. Miljanich. "Voltage-gated Potassium Channel Inhibitors." Current Pharmaceutical Design 2, no. 4 (August 1996): 389–96. http://dx.doi.org/10.2174/1381612802666220925203618.

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Forty years have transpired since tetraethylammonium was first used to selectively inhibit the potassiuin conductance in squid axons. Since then, a large body of work has emerged describing inhibitors of voltage-gated potassium currents in a variety of cells. The advent of molecular cloning techniques and the cloning of the potassium channel encoded by the Shaker locus in Drosophila has enabled detailed structure­ function studies of several potassium channel subunits. These breakthroughs have also recently enabled studies of the "toxinology" and pharmacology of specific potassium channel subunits expressed heterologously in Xenopus oocytes and other cells. Here we describe the results of some of those efforts, focusing in particular on our work with four members of the Shaker subfamily of potassium channel a-subunits: Kvl.1 through Kvl.4. These subunits are expressed in the central nervous system and other tissues of rodents, and are highly homologous to corresponding subunits expressed in humans. We provide a profile of potency and selectivity for.five snake dendrotoxins as well as several scorpion toxins for these potassium channel subunits expressed in Xenopus oocytes. We also provide similar data for four other peptide toxins and several nonpeptide compounds that had previously been shown to inhibit potassium currents. We discuss several potential clinical applications of potassium channel inhibitors, including demyelinating diseases such as multiple sclerosis, immunosuppression, cardiac arrhythmias, neurodegenerative and psychiatric diseases. Further progress will require, among other things, a greater understanding of the expression patterns of potassium channel subunits in the CNS and elsewhere as well as knowledge of the specific subunit composition of heteromultimeric channels.
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Wrzosek, Antoni, Bartłomiej Augustynek, Monika Żochowska, and Adam Szewczyk. "Mitochondrial Potassium Channels as Druggable Targets." Biomolecules 10, no. 8 (August 18, 2020): 1200. http://dx.doi.org/10.3390/biom10081200.

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Mitochondrial potassium channels have been described as important factors in cell pro-life and death phenomena. The activation of mitochondrial potassium channels, such as ATP-regulated or calcium-activated large conductance potassium channels, may have cytoprotective effects in cardiac or neuronal tissue. It has also been shown that inhibition of the mitochondrial Kv1.3 channel may lead to cancer cell death. Hence, in this paper, we examine the concept of the druggability of mitochondrial potassium channels. To what extent are mitochondrial potassium channels an important, novel, and promising drug target in various organs and tissues? The druggability of mitochondrial potassium channels will be discussed within the context of channel molecular identity, the specificity of potassium channel openers and inhibitors, and the unique regulatory properties of mitochondrial potassium channels. Future prospects of the druggability concept of mitochondrial potassium channels will be evaluated in this paper.
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Gomez-Sanchez, Celso E., and Kenji Oki. "Minireview: Potassium Channels and Aldosterone Dysregulation: Is Primary Aldosteronism a Potassium Channelopathy?" Endocrinology 155, no. 1 (January 1, 2014): 47–55. http://dx.doi.org/10.1210/en.2013-1733.

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Primary aldosteronism is the most common form of secondary hypertension and has significant cardiovascular consequences. Aldosterone-producing adenomas (APAs) are responsible for half the cases of primary aldosteronism, and about half have mutations of the G protein-activated inward rectifying potassium channel Kir3.4. Under basal conditions, the adrenal zona glomerulosa cells are hyperpolarized with negative resting potentials determined by membrane permeability to K+ mediated through various K+ channels, including the leak K+ channels TASK-1, TASK-3, and Twik-Related Potassium Channel 1, and G protein inward rectifying potassium channel Kir3.4. Angiotensin II decreases the activity of the leak K+ channels and Kir3.4 channel and decreases the expression of the Kir3.4 channel, resulting in membrane depolarization, increased intracellular calcium, calcium-calmodulin pathway activation, and increased expression of cytochrome P450 aldosterone synthase (CYP11B2), the last enzyme for aldosterone production. Somatic mutations of the selectivity filter of the Kir3.4 channel in APA results in loss of selectivity for K+ and entry of sodium, resulting in membrane depolarization, calcium mobilization, increased CYP11B2 expression, and hyperaldosteronism. Germ cell mutations cause familial hyperaldosteronism type 3, which is associated with adrenal zona glomerulosa hyperplasia, rather than adenoma. Less commonly, somatic mutations of the sodium-potassium ATPase, calcium ATPase, or the calcium channel calcium channel voltage-dependent L type alpha 1D have been found in some APAs. The regulation of aldosterone secretion is exerted to a significant degree by activation of membrane K+ and calcium channels or pumps, so it is not surprising that the known causes of disorders of aldosterone secretion in APA have been channelopathies, which activate mechanisms that increase aldosterone synthesis.
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Huang, Xi, and Lily Yeh Jan. "Targeting potassium channels in cancer." Journal of Cell Biology 206, no. 2 (July 21, 2014): 151–62. http://dx.doi.org/10.1083/jcb.201404136.

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Potassium channels are pore-forming transmembrane proteins that regulate a multitude of biological processes by controlling potassium flow across cell membranes. Aberrant potassium channel functions contribute to diseases such as epilepsy, cardiac arrhythmia, and neuromuscular symptoms collectively known as channelopathies. Increasing evidence suggests that cancer constitutes another category of channelopathies associated with dysregulated channel expression. Indeed, potassium channel–modulating agents have demonstrated antitumor efficacy. Potassium channels regulate cancer cell behaviors such as proliferation and migration through both canonical ion permeation–dependent and noncanonical ion permeation–independent functions. Given their cell surface localization and well-known pharmacology, pharmacological strategies to target potassium channel could prove to be promising cancer therapeutics.
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Vyas, Vivek K., Palak Parikh, Jonali Ramani, and Manjunath Ghate. "Medicinal Chemistry of Potassium Channel Modulators: An Update of Recent Progress (2011-2017)." Current Medicinal Chemistry 26, no. 12 (July 1, 2019): 2062–84. http://dx.doi.org/10.2174/0929867325666180430152023.

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Background: Potassium (K+) channels participate in many physiological processes, cardiac function, cell proliferation, neuronal signaling, muscle contractility, immune function, hormone secretion, osmotic pressure, changes in gene expression, and are involved in critical biological functions, and in a variety of diseases. Potassium channels represent a large family of tetrameric membrane proteins. Potassium channels activation reduces excitability, whereas channel inhibition increases excitability. Objective: Small molecule K+ channel activators and inhibitors interact with voltage-gated, inward rectifying, and two-pore tandem potassium channels. Due to their involvement in biological functions, and in a variety of diseases, small molecules as potassium channel modulators have received great scientific attention. Methods: : In this review, we have compiled the literature, patents and patent applications (2011 to 2017) related to different chemical classes of potassium channel openers and blockers as therapeutic agents for the treatment of various diseases. Many different chemical classes of selective small molecule have emerged as potassium channel modulators over the past years. Conclusion: This review discussed the current understanding of medicinal chemistry research in the field of potassium channel modulators to update the key advances in this field.
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Zhao, Yonghui, Zongyun Chen, Zhijian Cao, Wenxin Li, and Yingliang Wu. "Diverse Structural Features of Potassium Channels Characterized by Scorpion Toxins as Molecular Probes." Molecules 24, no. 11 (May 29, 2019): 2045. http://dx.doi.org/10.3390/molecules24112045.

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Scorpion toxins are well-known as the largest potassium channel peptide blocker family. They have been successfully proven to be valuable molecular probes for structural research on diverse potassium channels. The potassium channel pore region, including the turret and filter regions, is the binding interface for scorpion toxins, and structural features from different potassium channels have been identified using different scorpion toxins. According to the spatial orientation of channel turrets with differential sequence lengths and identities, conformational changes and molecular surface properties, the potassium channel turrets can be divided into the following three states: open state with less hindering effects on toxin binding, half-open state or half-closed state with certain effects on toxin binding, and closed state with remarkable effects on toxin binding. In this review, we summarized the diverse structural features of potassium channels explored using scorpion toxin tools and discuss future work in the field of scorpion toxin-potassium channel interactions.
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7

Spires, S., and T. Begenisich. "Modification of potassium channel kinetics by histidine-specific reagents." Journal of General Physiology 96, no. 4 (October 1, 1990): 757–75. http://dx.doi.org/10.1085/jgp.96.4.757.

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We have examined the actions of histidine-specific reagents on potassium channels in squid giant axons. External application of 20-500 microM diethylpyrocarbonate (DEP) slowed the opening of potassium channels with little or no effect on closing rates. Sodium channels were not affected by these low external concentrations of DEP. Internal application of up to 2 mM DEP had no effect on potassium channel kinetics. Steady-state potassium channel currents were reduced in an apparently voltage-dependent manner by external treatment with this reagent. The shape of the instantaneous current-voltage relation was not altered. The voltage-dependent probability of channel opening was shifted toward more positive membrane potentials, thus accounting for the apparent voltage-dependent reduction of steady-state current. Histidine-specific photo-oxidation catalyzed by rose bengal produced alterations in potassium channel properties similar to those observed with DEP. The rate of action of DEP was consistent with a single kinetic class of histidine residues. In contrast to the effects on ionic currents, potassium channel gating currents were not modified by treatment with DEP. These results suggest the existence of a histidyl group (or groups) on the external surface of potassium channels important for a weakly voltage-dependent conformational transition. These effects can be reproduced by a simple kinetic model of potassium channels.
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Barman, Scott A. "Potassium channels modulate hypoxic pulmonary vasoconstriction." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 1 (July 1, 1998): L64—L70. http://dx.doi.org/10.1152/ajplung.1998.275.1.l64.

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The role of Ca2+-activated K+-channel, ATP-sensitive K+-channel, and delayed rectifier K+-channel modulation in the canine pulmonary vascular response to hypoxia was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. Under normoxia, the Ca2+-activated K+-channel blocker tetraethylammonium (1 mM), the ATP-sensitive K+-channel inhibitor glibenclamide (10−5 M), and the delayed rectifier K+-channel blocker 4-aminopyridine (10−4 M) elicited a small but significant increase in pulmonary arterial pressure. Hypoxia significantly increased pulmonary arterial and venous resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. Tetraethylammonium, glibenclamide, and 4-aminopyridine potentiated the response to hypoxia on the arterial segments but not on the venous segments and also further decreased pulmonary vascular compliance. In contrast, the ATP-sensitive K+-channel opener cromakalim and the L-type voltage-dependent Ca2+-channel blocker verapamil (10−5 M) inhibited the vasoconstrictor effect of hypoxia on both the arterial and venous vessels. These results indicate that closure of the Ca2+-activated K+ channels, ATP-sensitive K+ channels, and delayed rectifier K+ channels potentiate the canine pulmonary arterial response under hypoxic conditions and that L-type voltage-dependent Ca2+ channels modulate hypoxic vasoconstriction. Therefore, the possibility exists that K+-channel inhibition is a key event that links hypoxia to pulmonary vasoconstriction by eliciting membrane depolarization and subsequent Ca2+-channel activation, leading to Ca2+ influx.
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Sun, Yuan-Kun, Liang-Hao Guo, Kai-Cheng Wang, Shao-Meng Wang, and Yu-Bin Gong. "Molecular dynamics simulation of effect of terahertz waves on the secondary structure of potassium channel proteins." Acta Physica Sinica 70, no. 24 (2021): 248701. http://dx.doi.org/10.7498/aps.70.20211725.

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Potassium channels play an important role in repolarizing the nerve cell action potentials. There are many types of potassium channel proteins, and potassium channels allow potassium ions to specifically pass through the cell membrane, thereby maintaining the resting potential of nerve cells. In this paper, molecular dynamics simulation method is used to simulate the effects of 53.7 THz terahertz wave with different amplitudes on the secondary structure of KcsA potassium channel protein and the potassium ions rate. It is found in this study that under the action of the 53.7 THz terahertz wave, the number of alpha helices in KcsA potassium channel protein decreases, and the number of beta sheets and the number of coils increase. In addition, the 53.7 THz terahertz wave can accelerate potassium ions through the KcsA potassium channel. In this article, the effects of terahertz waves on potassium channel proteins are analyzed through the secondary structure of proteins, and a new perspective for the interaction between terahertz waves and biological functional molecules is presented as well.
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Park, Kang-Sik, Jae-Won Yang, Edward Seikel, and James S. Trimmer. "Potassium Channel Phosphorylation in Excitable Cells: Providing Dynamic Functional Variability to a Diverse Family of Ion Channels." Physiology 23, no. 1 (February 2008): 49–57. http://dx.doi.org/10.1152/physiol.00031.2007.

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Phosphorylation of potassium channels affects their function and plays a major role in regulating cell physiology. Here, we review previous studies of potassium channel phosphorylation, focusing first on studies employing site-directed mutagenesis of recombinant channels expressed in heterologous cells. We then discuss recent mass spectrometric-based approaches to identify and quantify phosphorylation at specific sites on native and recombinant potassium channels, and newly developed mass spectrometric-based techniques that may prove beneficial to future studies of potassium channel phosphorylation, its regulation, and its mechanism of channel modulation.
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Dissertations / Theses on the topic "Potassium channel"

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Mason, Amy. "Single-Channel Characterisation of Potassium Channels with High Temperature Studies." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491373.

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Potassium channels control the conduction of K+ across cell membranes, down their electrochemical gradient. This rapid and highly selective movement of K+ is essential to many biological processes. K+ channels are largely alpha helical, tetrameric proteins that span the lipid bilayer. Diversity in K+ channels arises primarily in the mechanism of gating by various ligands or voltage; however, the basic structural elements, notably the selectivity filter are conserved within the family. Studies ~n this thesis focus on the single-channel behaviour of the K+ channels KcsA and Kcv. KcsA is a proton-activated channel from the bacterium Streptomyces lividans and its crystal structure was the first of a K+ channel to be solved. Kcv expressed by the Paramecium bursaria Chlorella virus is the smallest known K+ channel and thus represents the minimal structural entity necessary to form a functional and selective pore. Studies on the bacterial inward rectifying channels, KirBacs, have also been initiated. The KirBacs are a superfamily of prokaryotic channels homologous to eukaryotic Kir channels. In this work, KcsA and Kcv were found to form stable tetramers, which can be expressed by coupled in vitro transcription and translation and purified by polyacrylamide gel electrophoresis. The purified tetramers were reconstituted into planar lipid bilayers and studied at the single-channel level. Through single-channel recordings the ionic selectivity, gating behaviour, functional effects of site-directed mutagenesis and the interaction between Kcv and blockers have been studied. In addition, single-channel studies at elevated temperatures have revealed the remarkable thermostability of Kcv, as well as insight into the transport of ions through a narrow and selective pore. Through temperature studies, it has been possible to obtain the thermodynamic and kinetic parameters describing Kcv activity.
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Alexander, Sian. "Modulation of voltage-gated potassium channels: a pathophysiological mechanism of potassium channel antibodies in limbic encephalitis?" Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487139.

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Limbic encephalitis (LE) is a central nervous system disorder that is characterised by memory impairments, confusion, agitation and seizures, and associated with hyperintense lesions of the medial temporal lobe, seen with MRI. Anti-voltage-gated potassium channel (VOKC) antibodies have been been detected in the plasma of a subset of LE patients using a 125I-a-dendrotoxin (a-DTX) radioimmunoprecipitation assay, suggesting that the likely antigens are VOKC Kv1.l, 1.2 and 1.6 subunits. Symptoms of the disease improve markedly with immunosuppression, correlating with similarly dramatic falls in the titre of anti-VOKC antibodies, thus implicating anti-VOKC antibodies in the pathogenesis of LE. Circumstantial evidence from studies of inherited channelopathies and animal models of reduced VOKC activity suggests that VOKC dysfunction may contribute to the pathogenesis of LE. This thesis addresses whether anti-VOKC antibodies (i) bind to a-DTX-sensitive subunits and (ii) affect VOKC function. Immunofluorescence data show that binding of LE patient IgO to the surface of primary neurons and Kvl-expressing HEK-293/HEKTSA cells could not be detected with indirect immunofluorescence. Comparison of intracellular labelling with patient and control IgO showed that no additional labelling could be detected with LE patient IgO. Electrophysiological data show first, that a-DTXsensitive currents could not be reliably isolated from primary cultured hippocampal neurons; second, that NMT or LE samples did not affect VOKCs expressed by neuroblastoma-l cells; third, that none of the LE samples affected potassium currents in Kvl-transfected HEK-293 cells. These data suggest that 'anti-VOKC' antibodies may not bind directly to Kv1.111.2/1.6 homomers, or to a range of Kv1.I/1.2/1.6 subunit-containing heteromers in transfected cells. The findings instead suggest that 'anti-VOKC' antibodies in LE patient plasma may bind to a Kvl-associated protein that contributes to a-DTX-sensitive complexes in the radioimmunoprecipitation assay, but is absent from Kv1.111.2/1.6-transfected cells. Future work to characterise whether another antigen is bound by LE patient anti-VOKC antibodies will be important in determining how these antibodies contribute to the pathogenesis of LE.
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Hodge, J. J. L. "Shaw potassium channel genes in Drosophila." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604121.

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Potassium (K+) channels shape the electrical activities of cells by changing the frequency and duration of action potentials and by setting the resting potential. The huge diversity of K+ channels is conserved across species and is thought to be required to uniquely customise both the active excitable and passive properties of different cell types. When this study began, Drosophila voltage-gated K+ currents were thought to be encoded by the four cloned members of this family Shaker, Shab, Shaw and Shal. Mutant analysis had only been performed with Shaker. In order to investigate the in vivo function of another member of the family, a number of methods of making Shaw mutants were used. A more accurate genomic structure and location of Shaw was determined, and I attempted to identify P-element inserts in Shaw. However all the candidate inserts identified were located too far from Shaw to be of practical use for generating mutations affecting Shaw. A dominant negative strategy to remove Shaw function was therefore performed. PCR mutagenesis was used to generate both epitope-tagged full-length and truncated mutant versions of Shaw. Additional control constructs were also made: a full-length wildtype Shaw and a dominant negative version of Shaker. Transgenic lines were generated containing the constructs whose expression was GAL4 inducible. Expression of mutant Shaw, using a number of GAL4 lines, caused an ether-sensitive leg-shaking phenotype.
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Choi, Eun Kyung. "Regulation of KCNQ1 potassium channel trafficking and gating by KCNE1 and KCNE3 /." Access full-text from WCMC, 2009. http://proquest.umi.com/pqdweb?did=1692648191&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Zhang, Hailin. "ATP-sensitive potassium channels and their modulation by nucleotides and potassium channel openers in vascular smooth muscle cells." Thesis, St George's, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309744.

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Ellis, Lee David. "Potassium channel control of neuronal frequency response." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103381.

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The processing of sensory signals is an important, yet complex task in which a system must extract behaviorally relevant stimulus patterns from a vast array of sensory cues. When a neuron within a major sensory area is presented with a stimulus, one of the important characteristics used to distinguish between types of input is frequency. Often sensory neurons are tuned to narrow stimulus frequency ranges and are thus charged with the processing of subtypes of sensory signals. The weakly electric fish Apteronotus lepthorhynchus senses it's environment through modulations of a self-generated electric field. Two main types of sensory signals can be distinguished based on their frequency patterns. Prey stimuli cause low frequency perturbations of the electric field, while communication signals often result in high frequency signals. Pyramidal neurons in the electrosensory lateral line lobe (ELL) encode the low frequency signals with bursts, while the high frequency signals are relayed with single spikes. This thesis describes how a pyramidal neuron's response patterns can be tuned to specific frequencies by the expression of distinct classes of potassium channels.
I have cloned 3 small conductance (SK) calcium activated potassium channels from cDNA libraries created from the brain of Apteronotus. I have subsequently localized the AptSK channels throughout the brain using both in situ hybridization (AptSK1, 2 & 3) and immunohistochemical (AptSK1 & 2) techniques. The 3 channels showed distinct expression patterns, with the AptSK1 & 2 channels showing a partially overlapping expression pattern, while AptSK3 appears to be expressed in unique areas of the brain. In the ELL AptSK1 & 2 show a partially overlapping expression pattern, appearing in similar pyramidal neurons. However, their distribution within individual cell is unique, with AptSK1 showing a dendritic localization, while AptSK2 is primarily somatic. We have demonstrated that the unique expression pattern of the somatic AptSK2 channel in the ELL coincides with the functional SK currents evaluated through in vitro electrophysiology. Further we have shown that neurons that encode low frequencies do not possess functional SK channels. It thus appears that the presence of the AptSK2 channel subtype can predispose a neuron to respond to specific types of sensory signals.
In an attempt to evaluate if second messengers could modify the AptSK control of frequency tuning I investigated the consequences of muscarinic acetylcholine receptor (mAChR) activation on a pyramidal neurons response patterns. While it had been shown in vivo that mAChR activation increased a pyramidal neuron's response to low frequencies, I have found that this was not due to a decrease in AptSK current, but rather appears to be the result of a down-regulation of an A-type potassium channel.
Taken together the studies that comprise this thesis show how the selective expression of a single potassium channel subtype can control a sensory neurons response to specific environmental cues. The secondary modulation of the A-type current highlights the potential for a second messenger to control a neuron's sensory response through the down-regulation of constitutively expressed potassium current.
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Appenrodt, Peter. "Single-channel recordings of potassium channels from guinea-pig inner hair cells." Thesis, University of Sussex, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390054.

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Styrczewska, Katarzyna. "Turnover of voltage-gated potassium channel Kv 1.3." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/456990.

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Voltage-gated K channels (Kv) is large family of channels that are expressed in both excitable and non-excitable cells. In excitable cells they contribute to the control of resting membrane potential and action potentials frequency and duration. In non-excitable tissues they are involved in many processes such as secretion to cell proliferation. Kv1.3 channel plays a key role in a wide range of physiological phenomenon. Regulation of this transmembrane protein is therefore essential for a correct function of the living cell. The balance between synthesis and degradation is highly important and must be tightly regulated. The present dissertation is focused in investigating endocytosis mechanisms of Kv1.3, as a process controlling number of the channel on the cell surface and the possible implication in cell destiny. We deciphered major endocytosis mechanisms triggered by EGF and Adenosine (ADO) in HeLa and HEK 293 heterologous cell systems as well as in native cell lines (macrophages, dendritic or neuronal precursor). These studies pointed out the impact of endocytosis in turnover and homeostasis of Kv1.3 and possible physiological relevance of these finding. Our experiments showed two different ways to control abundance of the Kv1.3 channel by EGF: via tyrosine phosphorylation and unconventional ERK1/2-dependent mechanisms. EGF triggered clathrin-dependent lysosomal degradation of Kv1.3. Moreover, this study show a high physiological relevance, pointing to EGF as a Kv1.3 inhibitor that might therefore reduce radiation-induced brain injury by targeting the key cells involved in the inflammatory process. As next, study was to investigating PMA-induced PKC-dependent endocytosis and ubiquitination. We revealed that PMA triggered PKC-dependent ubiquitin-mediated lysosomal degradation of Kv1.3. Next, we show that adenosine (ADO), which is a potent endogenous modulator, similar to PMA, stimulates PKC, thereby causing immunosuppression. PKC activation triggers down-regulation of Kv1.3 by inducing a clathrin-mediated endocytosis which targets the channel to lysosomal-degradative compartments. Therefore, the abundance of Kv1.3 at the cell surface decreases, which is clearly compatible with an effective anti-inflammatory response. This mechanism requires ubiquitination of Kv1.3, catalyzed by the E3 ubiquitin-ligase Nedd4-2. However, we discover that ADO activates both PKC and PKA signaling pathways. To further investigate the molecular mechanisms of the Kv1.3 internalization in response to ADO, we have examined the effects of PKA antagonists. Our results, for the first time, provided evidence on the effect of PKA activation on the Kv1.3 trafficking. Our findings indicated that PKA adenosine activation triggered Kv1.3 endocytosis redundantly to PKC. In addition, we put a hypothesis that PKA downregulated Kv1.3 in an ubiquitin-independent manner. In the last part of this dissertation we concentrated at molecular determinants involved in Kv1.3 ubiquitination. We found that complementary and redundant lysines participate in the ubiquitin-dependent PKC and PKA regulation of Kv1.3.
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Thomson, Steven James. "Deactivation gating and pharmacology of hERG potassium channel." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/11071.

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hERG (Kv11.1) encodes the α-subunit of the potassium (K+) channel that carries IKr, an important current for repolarisation of the cardiac action potential. Alterations of hERG current, either through inherited mutations that alter gating or through drugs that block the pore, are associated with Long QT syndrome, cardiac arrhythmias and sudden death. The N-terminus has an important role in regulating deactivation, a gating process that is important for timing of the hERG current during cardiac action potentials. Removing the entire N-terminus accelerates deactivation. A crystal structure of part of the N-terminus (residues 26-135) was solved in 1998 and showed it contained a PAS domain, but it did not resolve the structure of the functionally important first 26 residues (NT 1-26). Here we present an NMR structure of residues 1-135. The structure reveals that residues 1-10 are unordered and residues 11-24 form an amphipathic helix one face of which is positively charged. Neutralising the positive charge accelerates deactivation to similar rates as if the whole of the N-terminus has been removed. Neutralising negative charge in the C-terminus also accelerates deactivation. We propose a model where the N and C-termini interact to stabilise the open state of the channel and slow deactivation. Exactly how changes in membrane voltage are transduced into movement of the activation gate is not fully understood. In hERG, the mutation V659A dramatically slows deactivation. Val659 is located in a region where hERG’s activation gate is believed to lie. From the structure of Kv2.1 it can be seen the S4-S5 linker forms a cuff around S6 where the activation gate is thought to be. Using cysteine cross-linking experiments we show that V659C interacts with E544C and Y545C in the S4-S5 linker to lock the channel in the open state. Trapping of drugs in the inner cavity of hERG has been an important model used to help explain why hERG is blocked by so many drugs and with high potency. A series of derivatives of E-4031, a well characterised high-affinity hERG blocker, were made that progressively increased the length of the molecule. Results in this thesis showed these compounds had binding kinetics completely different from E-4031 and none were trapped in the inner cavity. An alternative model of strongly state-dependent drug binding rather than drug-trapping is proposed. Together, the results in this thesis present new insights on the structural basis for deactivation gating and drug binding in hERG channels.
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Alvis, Simon. "Interactions of phospholipids with the potassium channel KcsA." Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417416.

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Books on the topic "Potassium channel"

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Fonseca, Danielle S. Potassium channels: Types, structure, and blockers. Hauppauge, N.Y: Nova Science Publisher's, Inc., 2011.

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Howarth, Gary Stanley. Potassium Channel KcsA and Its Lipid Environment. [New York, N.Y.?]: [publisher not identified], 2019.

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Chadwick, Derek J., and Jamie Goode, eds. The hERG Cardiac Potassium Channel: Structure, Function and Long QT Syndrome. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/047002142x.

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Derek, Chadwick, Goode Jamie, and Novartis Foundation, eds. The hERG cardial potassium channel: Structure, function, and long QT syndrome. New York: J. Wiley, 2005.

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Yao, Tong-Yi. Modulation of ATP-sensitive potassium channel activity by ATP-binding cassette transporters: A model for channel regulation. [New Haven, Conn: s.n.], 1998.

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Xu, Yunyao. Studies of Allostery in the Potassium Channel Kcsa by Solid-state NMR. [New York, N.Y.?]: [publisher not identified], 2018.

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Isaac, Lynne Mari. Studies of potassium channel inhibitors and openers acting on airways smooth muscle. Manchester: University of Manchester, 1995.

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M, Yellon Derek, and Gross Garrett J, eds. Myocardial protection and the KATP channel. Boston: Kluwer Academic Publishers, 1995.

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M, Evans J., ed. Potassium channels and their modulators: From synthesis to clinical experience. London: Taylor & Francis, 1996.

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Studies of the structure of potassium channel KcsA in the open conformation and the effect of anionic lipids on channel inactivation. [New York, N.Y.?]: [publisher not identified], 2019.

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Book chapters on the topic "Potassium channel"

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Meves, H. "Potassium Channel Toxins." In Selective Neurotoxicity, 739–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85117-9_21.

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Hoppe, U. C., H. B. Nuss, B. O’Rourke, E. Marbán, and D. C. Johns. "Potassium channel overexpression." In Molecular Approaches to Heart Failure Therapy, 180–96. Heidelberg: Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-57710-9_14.

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Fozard, John R., and Paul W. Manley. "Potassium Channel Openers." In New Drugs for Asthma, Allergy and COPD, 77–80. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062131.

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Taura, Jaume, Daniel M. Kircher, Isabel Gameiro-Ros, and Paul A. Slesinger. "Comparison of K+ Channel Families." In Pharmacology of Potassium Channels, 1–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/164_2021_460.

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Gallin, Warren J., and Andrew N. Spencer. "Evolution of Potassium Channel Proteins." In Potassium Channels in Cardiovascular Biology, 3–16. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1303-2_1.

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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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Bell, Joan. "The Sarcoplasmic Reticulum Potassium Channel." In Ion Channel Reconstitution, 469–82. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-1361-9_18.

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Cui, Meng, Lucas Cantwell, Andrew Zorn, and Diomedes E. Logothetis. "Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications." In Pharmacology of Potassium Channels, 277–356. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/164_2021_501.

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Sage, Stewart O., and Sergey M. Marchenko. "Single-Channel Properties of Ca2+ -Activated K+Channels in the Vascular Endothelium." In Potassium Channels in Cardiovascular Biology, 651–66. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1303-2_32.

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Janse, Michiel J., and Arthur A. M. Wilde. "Potassium Channel Activation and Arrhythmogenicity." In Myocardial Protection and the KATP Channel, 121–39. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-0453-1_5.

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Conference papers on the topic "Potassium channel"

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Taylor-Wells, Jennina. "Toxicity and potassium channel-directed effects of flonicamid analogs." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.94621.

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Ali Idham Alzaidi, Baqer Turki, Sabah Mohammad Mlkt, Andrew Martin, Omar Hashim, and Navarun Gupta. "Neuron-MOSFET junction with sodium potassium voltage gate channel." In 2014 IEEE Long Island Systems, Applications and Technology Conference (LISAT). IEEE, 2014. http://dx.doi.org/10.1109/lisat.2014.6845223.

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Ramírez, Ana, María de Guadalupe Chávez-López, Eunice Vera, Jaime de la Garza, Patricio Gariglio, and Javier Camacho. "Abstract 2766: Potassium channel expression in cervical cancer models." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2766.

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Venien- Bryan, Catherine. "Gating mechanism of a potassium channel, experimental and theoretical studies." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.741.

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Alfaro-Mora, Y. E., J. Diaz-Chavez, M. Dante-Escobedo, L. A. Herrera, and J. Camacho. "Abstract C13: Human Eag1 potassium channel expression in lung cancer biopsies." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c13.

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Celotto, Chiara, Carlos Sánchez, Pablo Laguna, and Esther Pueyo. "Calcium-Activated Potassium Channel Inhibition in Autonomically Stimulated Human Atrial Myocytes." In 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.334.

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Yam, Yeung, and Chi-Cheung Lo. "A Mathematical Model For Potassium Channel Conductance in Hodgkin-Huxley Experiments." In 2007 American Control Conference. IEEE, 2007. http://dx.doi.org/10.1109/acc.2007.4283106.

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Fang Shen, Li-ping Wu, Yuan Lu, Hua-wei Liang, I. C. Bruce, and Qiang Xia. "Mitochondrial Permeability Transition Dynamics: An Indicator of Mitochondrial Potassium Channel Opener." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616201.

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Le Ribeuz, Hélène, Mélanie Lambert, Angèle Boet, David Montani, Wendy K. Chung, Marc Humbert, and Fabrice Antigny. "SUR1/Kir6.2 potassium channel a new actor involved in pulmonary arterial hypertension." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3561.

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Zyrianova, T., B. Lopez, D. Pham, A. Ye, and A. Schwingshackl. "TREK-1 Potassium Channel Activation Protects Against Influenza-A Induced Lung Injury." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3458.

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Reports on the topic "Potassium channel"

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Murphy, Geoffrey. The Ketogenic Diet and Potassium Channel Function. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada615827.

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Moran, Nava, Richard Crain, and Wolf-Dieter Reiter. Regulation by Light of Plant Potassium Uptake through K Channels: Biochemical, Physiological and Biophysical Study. United States Department of Agriculture, September 1995. http://dx.doi.org/10.32747/1995.7571356.bard.

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The swelling of plant motor cells is regulated by various signals with almost unknown mediators. One of the obligatory steps in the signaling cascade is the activation of K+-influx channels -K+ channels activated by hyperpolarization (KH channels). We thus explored the regulation of these channels in our model system, motor cell protoplasts from Samanea saman, using patch-clamp in the "whole cell" configuration. (a) The most novel finding was that the activity of KH channels in situ varied with the time of the day, in positive correlation with cell swelling: in Extensor cells KH channels were active in the earlier part of the day, while in Flexor cells only during the later part of the day; (b) High internal pH promoted the activity of these channels in Extensor cells, opposite to the behavior of the equivalent channels in guard cells, but in conformity with the predicted behavior of the putative KH channel, cloned from S. saman recently; (c) HIgh external K+ concentration increased (KH channel currents in Flexor cells. BL depolarized the Flexor cells, as detected in cell-attached patch-clamp recording, using KD channels (the K+-efflux channels) as "voltage-sensing devices". Subsequent Red-Light (RL) pulse followed by Darkness, hyperpolarized the cell. We attribute these changes to the inhibition of the H+-pump by BL and its reactivation by RL, as they were abolished by an H+-pump inhibitor. BL increased also the activity KD channels, in a voltage-independent manner - in all probability by an independent signaling pathway. Blue-Light (BL), which stimulates shrinking of Flexor cells, evoked the IP3 signaling cascade (detected directly by IP3 binding assay), known to mobilize cytosolic Ca2+. Nevertheless, cytosolic Ca2+ . did not activate the KD channel in excised, inside-out patches. In this study we established a close functional similarity of the KD channels between Flexor and Extensior cells. Thus the differences in their responses must stem from different links to signaling in both cell types.
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Aachi, Venkat. Preliminary Characterization of Mitochondrial ATP-sensitive Potassium Channel (MitoKATP) Activity in Mouse Heart Mitochondria. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1666.

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Melkoumian, Zaroui. Regulation of C-myc Gene Expression by Potassium Channel Blocker Quindine in MCF-7 Human Breast Cancer Cell Line. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada384096.

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McDonald, Thomas, and Kami Kim. Novel Lishmania and Malaria Potassium Channels: Candidate Therapeutic Targets. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada418746.

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Holdsworth, Clark, Steven Copp, Daniel Hirai, Scott Ferguson, Gabrielle Sims, Sue Hageman, David Poole, and Timothy Musch. Blockade of ATP-sensitive potassium channels impairs vascular control in exercising rats. Peeref, June 2022. http://dx.doi.org/10.54985/peeref.2206p8529370.

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Lichter, Amnon, David Obenland, Nirit Bernstein, Jennifer Hashim, and Joseph Smilanick. The role of potassium in quality of grapes after harvest. United States Department of Agriculture, October 2015. http://dx.doi.org/10.32747/2015.7597914.bard.

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Objectives: The objectives of the proposal were to study how potassium (K) enters the berry and in what tissues it accumulates, to determine what is the sensitive phenological stage that is responsive to K, to study the influence of K on sugar translocation, to determine if K has effects on expression of genes in source and sink organs and to study applied aspects of the responses to K at the vineyard level. During the research it was realized that K acts externally so a major part of the original objectives had to be deserted and new ones, i.e. the role of K in enhancing water loss from the berry, had to be developed. In addition, the US partners developed practical objectives of understanding the interaction of K application and water deficit as well as application of growth regulators. Background: In our preliminary data we showed that application of K at mid-ripening enhanced sugar accumulation of table grapes. This finding is of major implications to both early and late harvested grapes and it was essential to understand the mode of action of this treatment. Our major hypothesis was that K enters the berry and by that increases sugar translocation into the berry. In addition it was important to cover practical issues of the application which may influence its efficacy and its reproducibility. Conclusions: The major conclusion from the research was that our initial hypothesis was wrong. Mineral analysis of pulp tissue indicated that upon application of K there was a significant increase in most of the major minerals. Subsequently, we developed a new hypothesis that K acts by increasing the water loss from the berry. In vitro studies of K-treated berries corroborated this hypothesis showing greater weight-loss of treated berries. This was not necessarily expressed in the vineyard as in some experiments berry weight remained unchanged, suggesting that the vine compensated for the enhanced water loss. Importantly, we also discovered that the efficacy of different K salts was strongly correlated to the pH of the salt solution: basic K salts had better efficacy than neutral or acidic salts and modifying the pH of the same salt changed its efficacy. It was therefore suggested that K changes the properties of the cuticle making it more susceptible to water loss. Of the practical aspects it was found that application of K to the clusters was sufficient to trigger its affect and that dual application of K had a stronger effect than single application. With regard to timing, it was realized that application of K after veraison was affective and the berries responded also when ripe. While the effect of K application was significant at harvest, it was mostly insignificant one week after application, suggesting that prolonged exposure to K was required. Implications: The scientific implications of the study are that the external mineral composition of the berry may have a significant role in sugar accumulation and that water loss may have an important role in sugar accumulation in grapes. It is not entirely clear how K modulates the cuticle but according to the literature its incorporation into the cuticle may increase its polarity and facilitate generation of "water bridges" between the flesh and the environment. The practical implications of this study are very significant because realizing the mode of action of K can facilitate a much more efficient application strategy. For example, it can be understood that sprays must be directed to the clusters rather than the whole vines and it can be predicted that the length of exposure is important. Also, by increasing the pH of simple K salts, the efficacy of the treatment can be enhanced, saving in the costs of the treatment. Finally, the ability of grape growers to apply K in a safe and knowledgeable way can have significant impact on the length of the season of early grape cultivars and improve the flavor of high grape yields which may otherwise have compromised sugar levels.
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Shtienberg, Dan, William Fry, Amos Dinoor, Thomas Zitter, and Uzi Kafkafi. Reduction in Pesticide Use in Plant Disease Control by Integration of Chemical and Non-Chemical Factors. United States Department of Agriculture, May 1995. http://dx.doi.org/10.32747/1995.7613027.bard.

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The long term goal of this research project was to improve control efficiency of Alternaria diseases while reducing fungicide use, by integration of chemical and non-chemical factors. Non-chemical factors were genotype resistance, age-related resistance and fertilizers. The Specific objectives were: 1) To quantify changes in resistance among genotypes and over time in terms of disease development and specific phases of the disease cycle; 2) To quantify the effects of fertilizers applied to the foliage alone, or in combination with a fungicide, on disease development; 3) To quantify the relative contribution of genotype resistance, age-related resistance and fungicide type to the reduction of disease development; 4) To develop a strategy for integration of chemical and non-chemical factors which will achieve optimal disease suppression. The influence of physiological age of cotton plants and of the individual leaves, on disease incidence and on the rate of lesion expansion of A. macrospora was examined on leaves sampled from the field. Both parameters increased with the physiological age of individual leaves but were not affected by the age of the whole plant. The hypothesis that enrichment of the foliage with nitrogen and potassium may enhance host resistance to Alternaria and thus reduce disease severity, was examined for potato and tomato (A. solani ) and for cotton (A. macrospora ). Under controlled environment conditions, application of urea or KNO3 resulted in some reduction in disease development; however, foliar application of both nutrients (8-10 sprays in total) did not affect Alternaria severity in the field. Systemic fungicides against Alternaria (e.g. , tebuconazole and difenoconazole) are more effective than the commonly used protectant fungicides (e.g. mancozeb and chlorothalonil). Concepts for the integration of genotype resistance, age-related resistances and fungicide for the suppression of Alternaria diseases were developed and evaluated. It was found that reduction in host resistance, with age and among genotypes, can be compensated for by adjusting the intensity of fungicide applications, i.e. by increasing the frequency of sprays and by spraying systemic fungicides towards the end of the season. In, moderately resistant cultivars protection can be achieved by spraying at longer intervals than susceptible cultivars. The concepts for integration were evaluated in field trials for cotton, potatoes and tomatoes. By following these concepts it was possible to save up to five sprays out of 8-10 in a growing season.
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Minz, Dror, Stefan J. Green, Noa Sela, Yitzhak Hadar, Janet Jansson, and Steven Lindow. Soil and rhizosphere microbiome response to treated waste water irrigation. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598153.bard.

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Research objectives : Identify genetic potential and community structure of soil and rhizosphere microbial community structure as affected by treated wastewater (TWW) irrigation. This objective was achieved through the examination soil and rhizosphere microbial communities of plants irrigated with fresh water (FW) and TWW. Genomic DNA extracted from soil and rhizosphere samples (Minz laboratory) was processed for DNA-based shotgun metagenome sequencing (Green laboratory). High-throughput bioinformatics was performed to compare both taxonomic and functional gene (and pathway) differences between sample types (treatment and location). Identify metabolic pathways induced or repressed by TWW irrigation. To accomplish this objective, shotgun metatranscriptome (RNA-based) sequencing was performed. Expressed genes and pathways were compared to identify significantly differentially expressed features between rhizosphere communities of plants irrigated with FW and TWW. Identify microbial gene functions and pathways affected by TWW irrigation*. To accomplish this objective, we will perform a metaproteome comparison between rhizosphere communities of plants irrigated with FW and TWW and selected soil microbial activities. Integration and evaluation of microbial community function in relation to its structure and genetic potential, and to infer the in situ physiology and function of microbial communities in soil and rhizospere under FW and TWW irrigation regimes. This objective is ongoing due to the need for extensive bioinformatics analysis. As a result of the capabilities of the new PI, we have also been characterizing the transcriptome of the plant roots as affected by the TWW irrigation and comparing the function of the plants to that of the microbiome. *This original objective was not achieved in the course of this study due to technical issues, especially the need to replace the American PIs during the project. However, the fact we were able to analyze more than one plant system as a result of the abilities of the new American PI strengthened the power of the conclusions derived from studies for the 1ˢᵗ and 2ⁿᵈ objectives. Background: As the world population grows, more urban waste is discharged to the environment, and fresh water sources are being polluted. Developing and industrial countries are increasing the use of wastewater and treated wastewater (TWW) for agriculture practice, thus turning the waste product into a valuable resource. Wastewater supplies a year- round reliable source of nutrient-rich water. Despite continuing enhancements in TWW quality, TWW irrigation can still result in unexplained and undesirable effects on crops. In part, these undesirable effects may be attributed to, among other factors, to the effects of TWW on the plant microbiome. Previous studies, including our own, have presented the TWW effect on soil microbial activity and community composition. To the best of our knowledge, however, no comprehensive study yet has been conducted on the microbial population associated BARD Report - Project 4662 Page 2 of 16 BARD Report - Project 4662 Page 3 of 16 with plant roots irrigated with TWW – a critical information gap. In this work, we characterize the effect of TWW irrigation on root-associated microbial community structure and function by using the most innovative tools available in analyzing bacterial community- a combination of microbial marker gene amplicon sequencing, microbial shotunmetagenomics (DNA-based total community and gene content characterization), microbial metatranscriptomics (RNA-based total community and gene content characterization), and plant host transcriptome response. At the core of this research, a mesocosm experiment was conducted to study and characterize the effect of TWW irrigation on tomato and lettuce plants. A focus of this study was on the plant roots, their associated microbial communities, and on the functional activities of plant root-associated microbial communities. We have found that TWW irrigation changes both the soil and root microbial community composition, and that the shift in the plant root microbiome associated with different irrigation was as significant as the changes caused by the plant host or soil type. The change in microbial community structure was accompanied by changes in the microbial community-wide functional potential (i.e., gene content of the entire microbial community, as determined through shotgun metagenome sequencing). The relative abundance of many genes was significantly different in TWW irrigated root microbiome relative to FW-irrigated root microbial communities. For example, the relative abundance of genes encoding for transporters increased in TWW-irrigated roots increased relative to FW-irrigated roots. Similarly, the relative abundance of genes linked to potassium efflux, respiratory systems and nitrogen metabolism were elevated in TWW irrigated roots when compared to FW-irrigated roots. The increased relative abundance of denitrifying genes in TWW systems relative FW systems, suggests that TWW-irrigated roots are more anaerobic compare to FW irrigated root. These gene functional data are consistent with geochemical measurements made from these systems. Specifically, the TWW irrigated soils had higher pH, total organic compound (TOC), sodium, potassium and electric conductivity values in comparison to FW soils. Thus, the root microbiome genetic functional potential can be correlated with pH, TOC and EC values and these factors must take part in the shaping the root microbiome. The expressed functions, as found by the metatranscriptome analysis, revealed many genes that increase in TWW-irrigated plant root microbial population relative to those in the FW-irrigated plants. The most substantial (and significant) were sodium-proton antiporters and Na(+)-translocatingNADH-quinoneoxidoreductase (NQR). The latter protein uses the cell respiratory machinery to harness redox force and convert the energy for efflux of sodium. As the roots and their microbiomes are exposed to the same environmental conditions, it was previously hypothesized that understanding the soil and rhizospheremicrobiome response will shed light on natural processes in these niches. This study demonstrate how newly available tools can better define complex processes and their downstream consequences, such as irrigation with water from different qualities, and to identify primary cues sensed by the plant host irrigated with TWW. From an agricultural perspective, many common practices are complicated processes with many ‘moving parts’, and are hard to characterize and predict. Multiple edaphic and microbial factors are involved, and these can react to many environmental cues. These complex systems are in turn affected by plant growth and exudation, and associated features such as irrigation, fertilization and use of pesticides. However, the combination of shotgun metagenomics, microbial shotgun metatranscriptomics, plant transcriptomics, and physical measurement of soil characteristics provides a mechanism for integrating data from highly complex agricultural systems to eventually provide for plant physiological response prediction and monitoring. BARD Report
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