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Relevant bibliographies by topics / C-type inactivation

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Academic literature on the topic 'C-type inactivation'

Author: Grafiati

Published: 14 March 2023

Last updated: 31 July 2025

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Journal articles on the topic "C-type inactivation"

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Yan, Jiusheng, Qin Li, and Richard W. Aldrich. "Closed state-coupled C-type inactivation in BK channels." Proceedings of the National Academy of Sciences 113, no. 25 (2016): 6991–96. http://dx.doi.org/10.1073/pnas.1607584113.

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Ion channels regulate ion flow by opening and closing their pore gates. K+ channels commonly possess two pore gates, one at the intracellular end for fast channel activation/deactivation and the other at the selectivity filter for slow C-type inactivation/recovery. The large-conductance calcium-activated potassium (BK) channel lacks a classic intracellular bundle-crossing activation gate and normally show no C-type inactivation. We hypothesized that the BK channel’s activation gate may spatially overlap or coexist with the C-type inactivation gate at or near the selectivity filter. We induced

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Li, Xiaoyan, Glenna C. L. Bett, Xuejun Jiang, Vladimir E. Bondarenko, Michael J. Morales, and Randall L. Rasmusson. "Regulation of N- and C-type inactivation of Kv1.4 by pHo and K+: evidence for transmembrane communication." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 1 (2003): H71—H80. http://dx.doi.org/10.1152/ajpheart.00392.2002.

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Kv1.4 encodes a slowly recovering transient outward current ( I to), which inactivates by a fast N-type (intracellular ball and chain) mechanism but has slow recovery due to C-type inactivation. C-type inactivation of the NH2-terminal deletion mutant (fKv1.4ΔN) was inhibited by 98 mM extracellular K+concentration ([K+]o), whereas N-type was unaffected. In 98 mM [K+]o, removal of intracellular K+ concentration ([K+]i) speeded C-type inactivation but had no effect on N-type inactivation, suggesting that C-type inactivation is sensitive to K+ binding to intracellular sites. C-type inactivation is

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Villalba-Galea, Carlos A., Takeharu Kawano, and Diomedes E. Logothetis. "C-Type Inactivation in KV2.1 Channels." Biophysical Journal 116, no. 3 (2019): 15a. http://dx.doi.org/10.1016/j.bpj.2018.11.122.

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Kurata, Harley T., Zhuren Wang, and David Fedida. "NH2-terminal Inactivation Peptide Binding to C-type–inactivated Kv Channels." Journal of General Physiology 123, no. 5 (2004): 505–20. http://dx.doi.org/10.1085/jgp.200308956.

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In many voltage-gated K+ channels, N-type inactivation significantly accelerates the onset of C-type inactivation, but effects on recovery from inactivation are small or absent. We have exploited the Na+ permeability of C-type–inactivated K+ channels to characterize a strong interaction between the inactivation peptide of Kv1.4 and the C-type–inactivated state of Kv1.4 and Kv1.5. The presence of the Kv1.4 inactivation peptide results in a slower decay of the Na+ tail currents normally observed through C-type–inactivated channels, an effective blockade of the peak Na+ tail current, and also a d

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Claydon, T. W., M. R. Boyett, A. Sivaprasadarao, and C. H. Orchard. "Two pore residues mediate acidosis-induced enhancement of C-type inactivation of the Kv1.4 K+ channel." American Journal of Physiology-Cell Physiology 283, no. 4 (2002): C1114—C1121. http://dx.doi.org/10.1152/ajpcell.00542.2001.

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Acidosis inhibits current through the Kv1.4 K+ channel, perhaps as a result of enhancement of C-type inactivation. The mechanism of action of acidosis on C-type inactivation has been studied. A mutant Kv1.4 channel that lacks N-type inactivation (fKv1.4 Δ2–146) was expressed in Xenopus oocytes, and currents were recorded using two-microelectrode voltage clamp. Acidosis increased fKv1.4 Δ2–146 C-type inactivation. Replacement of a pore histidine with cysteine (H508C) abolished the increase. Application of positively charged thiol-specific methanethiosulfonate to fKv1.4 Δ2–146 H508C increased C-

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Trefilov, B. B., N. V. Nikitina, and I. K. Leonov. "THE KINETICS OF THE INACTIVATION OF THE HEPATITIS VIRUS TYPE I (AVIHEPATOVIRUS, PICORNAVIRIDAE)." Problems of Virology, Russian journal 63, no. 3 (2018): 135–38. http://dx.doi.org/10.18821/0507-4088-2018-63-3-135-138.

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Experimental data on the kinetics of the inactivation of the vaccine strain of the duckling hepatitis virus of the type I with increased temperature and aminoethyl ethylenimine are presented. It was shown that the vaccine strain 3M-UNIIP of the hepatitis virus of ducklings of type I was comparatively thermostable at 56°C and sensitive to the action of aminoethyl ethylenimine; the time of complete inactivation of the virus at a final concentration of 0.1% at 37°C was 24 h. The obtained results suggest that aminoethyl ethylenimine can be used as an inactivator in manufacturing inactivated vaccin

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Mathes, Chris, Joshua J. C. Rosenthal, Clay M. Armstrong, and William F. Gilly. "Fast Inactivation of Delayed Rectifier K Conductance in Squid Giant Axon and Its Cell Bodies." Journal of General Physiology 109, no. 4 (1997): 435–48. http://dx.doi.org/10.1085/jgp.109.4.435.

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Inactivation of delayed rectifier K conductance (gK) was studied in squid giant axons and in the somata of giant fiber lobe (GFL) neurons. Axon measurements were made with an axial wire voltage clamp by pulsing to VK (∼−10 mV in 50–70 mM external K) for a variable time and then assaying available gK with a strong, brief test pulse. GFL cells were studied with whole-cell patch clamp using the same prepulse procedure as well as with long depolarizations. Under our experimental conditions (12–18°C, 4 mM internal MgATP) a large fraction of gK inactivates within 250 ms at −10 mV in both cell bodies

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Ogielska, Eva M., and Richard W. Aldrich. "Functional Consequences of a Decreased Potassium Affinity in a Potassium Channel Pore." Journal of General Physiology 113, no. 2 (1999): 347–58. http://dx.doi.org/10.1085/jgp.113.2.347.

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Ions bound near the external mouth of the potassium channel pore impede the C-type inactivation conformational change (Lopez-Barneo, J., T. Hoshi, S. Heinemann, and R. Aldrich. 1993. Receptors Channels. 1:61– 71; Baukrowitz, T., and G. Yellen. 1995. Neuron. 15:951–960). In this study, we present evidence that the occupancy of the C-type inactivation modulatory site by permeant ions is not solely dependent on its intrinsic affinity, but is also a function of the relative affinities of the neighboring sites in the potassium channel pore. The A463C mutation in the S6 region of Shaker decreases th

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Starkus, John G., Lioba Kuschel, Martin D. Rayner, and Stefan H. Heinemann. "Ion Conduction through C-Type Inactivated Shaker Channels." Journal of General Physiology 110, no. 5 (1997): 539–50. http://dx.doi.org/10.1085/jgp.110.5.539.

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C-type inactivation of Shaker potassium channels involves entry into a state (or states) in which the inactivated channels appear nonconducting in physiological solutions. However, when Shaker channels, from which fast N-type inactivation has been removed by NH2-terminal deletions, are expressed in Xenopus oocytes and evaluated in inside-out patches, complete removal of K+ ions from the internal solution exposes conduction of Na+ and Li+ in C-type inactivated conformational states. The present paper uses this observation to investigate the properties of ion conduction through C-type inactivate

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Biagi, B. A., and J. J. Enyeart. "Multiple calcium currents in a thyroid C-cell line: biophysical properties and pharmacology." American Journal of Physiology-Cell Physiology 260, no. 6 (1991): C1253—C1263. http://dx.doi.org/10.1152/ajpcell.1991.260.6.c1253.

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The whole cell version of the patch-clamp technique was used to characterize voltage-gated Ca2+ channels in the calcitonin-secreting rat thyroid C-cell line 6-23 (clone 6). Three types of Ca2+ channels could be distinguished based on differences in voltage dependence, kinetics, and pharmacological sensitivity. T-type current was half-maximal at -31 mV, showed steady-state voltage-dependent inactivation that was half-maximal at -57 mV, inactivated with a voltage-dependent time constant that reached a minimum of 20 ms at potentials positive to -20 mV, and deactivated with a single time constant

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Dissertations / Theses on the topic "C-type inactivation"

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Nikouee, Azadeh [Verfasser]. "Structural changes of the outer and inner vestibule of hKv1.3 channels during C type inactivation / Azadeh Nikouee." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1024534308/34.

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Pettini, Francesco. "Molecular Dynamics simulation of the hERG channel assisting Precision Medicine in Channelopathies." Doctoral thesis, Università di Siena, 2023. https://hdl.handle.net/11365/1227475.

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In the last two decades, a revolution in biology has shifted the traditional reductive approach to a bottom-up study of virtual models. This discipline, known as System Biology, integrates information coming from individual components, in order to predict the functioning of biological systems, with the idea that complex systems are made up of many independent components that can interact within well-structured networks changing over time, and that the functional properties of biological systems emerge as a consequence of interactions among their components. This paradigm shift is enabled by ra

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Pang, Chunyan. "REGULATION OF L-TYPE VOLTAGE-DEPENDNET CALCIUM CHANNELS BY THE REM GTPASE." UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/656.

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The Rem, Rem2, Rad, and Gem/Kir GTPases, comprise a novel subfamily of the small Ras-related GTP-binding proteins known as the RGK GTPases, and have been shown to function as potent negative regulators of high voltage-activated (HVA) Ca2+ channels upon overexpression. HVA Ca2+ channels modulate Ca2+ influx in response to membrane depolarization to regulate a wide variety of cellular functions and they minimally consist of a pore-forming α1 subunit, an intracellular β subunit, and a transmembrane complex α2/δ subunit. While the mechanisms underlying RGK-mediated Ca2+ channel regulation remain p

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Lin, Chia-Huei, та 林佳慧. "Dependence of 6β-acetoxy-7α-hydroxyroyleanone block of Kv1.2 channel on C-type inactivation". Thesis, 2009. http://ndltd.ncl.edu.tw/handle/86944920781987811088.

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碩士<br>中國醫藥大學<br>神經科學與認知科學研究所<br>97<br>Voltage-gated K+ (Kv) channels repolarize excitable cells by providing a pathway for K+ efflux. Kv1.2 channels are present in many neurons and exhibit slow inactivation during continuous depolarization. Here we reported that 6β-acetoxy-7α-hydroxyroyleanone (AHR) could affect slow inactivation of Kv1.2 channels heterologously expressed in HEK293 cells. Extracellular AHR (50 μM) dramatically speeded up the slow decay of Kv currents and left-shifted the steady-state inactivation curve. Intracellular dialysis of AHR did not accelerate the slow current decay, s

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Book chapters on the topic "C-type inactivation"

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"C-Type Inactivation." In Encyclopedia of Biophysics. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_100205.

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Barstead, Robert J. "Reverse genetics." In C.elegans. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780199637393.003.0006.

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Abstract The nematode Caenorhabditis elegans has about 19000 genes. Approximately 2000 of these have been identified in forward genetic screens for animals with mutant phenotypes. The generation and analysis of such mutants has been the key to the success of the C. elegans model because the in vivo function of a gene can be inferred from its mutant phenotype. In principle, it is possible to identify mutations in the remaining 17000 genes using various forward genetic screens. In practice, however, it is unlikely that forward genetics will lead to such an end in the foreseeable future. Further,

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Wybranska, Iwona. "Genetic Markers of Endothelial Dysfunction." In Endothelial Dysfunction - A Novel Paradigm [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.109272.

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The rate of endothelial dysfunction is influenced by genetic variation and thus inherited in families. Genetic disorders, such as familial hypercholesterolemia and homocystinuria, are at risk for premature atherosclerosis, and exhibit early endothelial dysfunction. The known spectrum of mutations in LDL receptor, APOB and PCSK9 gene represent the monogenic dominant hypercholesterolemia. An autosomal recessive form of hypercholesterolaemia in the caused by homozygous mutations in the LDL-R adaptor protein. The polygenic hypercholesterolaemia for patients with a clinical diagnosis of FH is based

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Aparecida Matoso, Daniele, Maelin da Silva, Hallana Cristina Menezes da Silva, Eliana Feldberg, and Roberto Ferreira Artoni. "Heterochromatin Dynamics in Response to Environmental Stress in Amazonian Fish." In Cytogenetics - Classical and Molecular Strategies for Analysing Heredity Material. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.94929.

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Transcriptionally inactive portions of genomic DNA, condensed with histones and architectural proteins, are known as heterochromatic regions, often positive C band. The advent of epigenetics and new methodological approaches, showed that these regions are extremely dynamic and responsive to different types of environmental stress. The relationship of the constitutive heterochromatin with the transposable elements inactivation, especially from the Rex family, seems to be a frequent condition in fish. In this manuscript we review the existing knowledge of the nature and function of these genomic

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Conference papers on the topic "C-type inactivation"

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Pittman, Debra D., Louise C. Wasley, Beth L. Murray, Jack H. Wang, and Randal J. Kaufman. "ANALYSIS OF STRUCTURAL REQUIREMENTS FOR FACTOR VIII FUNCTION USING SITE-DIRECTED MUTAGENESIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644044.

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Factor VIII (fVIII) functions in the intrinsic pathway of coagulation as the cofactor for Factor IXa proteolytic activation of Factor X. fVIII contains multiple sites which are susceptible to cleavage by thrombin, Factor Xa, and activate) protein C. Proteolytic cleavage is required for cofactor activity and may be responsible for inactivation of cofactor activity. In order to identify the role ofthe individual cleavages of fVIII in its activation and inactivation, site-directed DNA mediated mutagenesis of fVIII was performed and the altered forms of fVIII produced and characterized. Conversion

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Fong, K. L. L., K. E. Boyle, C. S. Crysler, M. S. Landi, H. E. Griffin, and R. K. Lynn. "EXTRAHEPATIC METABOLISM OF RECOMBINANT TISSUE-TYPE PLASMINOGEN ACTIVATOR (tPA) IN DOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644398.

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Hepatic uptake has been proposed as the major mechanism of tPA clearance from systemic circulation. However, our recent studies demonstrated that tPA was rapidly Inactivated through complexation with protease Inhibitors in dog plasma In vitro, and that tPA-inhibitor complexes were present in plasma of dogs receiving tPA. Therefore, the present work was undertaken to differentiate hepatic from extrahepatlc clearance of tPA. Pharmacokinetics of tPA were determined in anesthetized beagle dogs with either Intact hepatic circulation or with Interrupted hepatic blood flow achieved by hepatic artery

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Elbashir, Israa, Aisha Aisha Nasser J. M. Al-Saei, Paul Thornalley, and Naila Rabbani. "Evaluation of antiviral activity of Manuka honey against SARS-CoV-2." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0113.

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Background and aims: In 2020 a global pandemic was declared caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2). The pandemic is still ongoing and continues to cause considerable mortality and morbidity world-wide and new variants of the virus are emerging. Rapid development and rollout of vaccines for SARS-CoV-2 is in progress to counter the pandemic but has been tempered by the emergence of new SARS-CoV-2 variants, many of which exhibit reduced vaccine effectiveness. To date there is no approved antiviral treatment for coronavirus disease 2019 (COVID-19). Several studies

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Nicham, F., and J. L. Martinoli. "AMIDOLYTIC DETERMINATION OF ANTI-ACTIVATED PROTEIN C ACTIVITY IN PLASMA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644316.

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Anti-activated protein C (anti-APC) potency of plasma was studied using purified bovine activated protein C (Bovine APC) and the chromogenic peptide substrate CBS 65.25. The choice of bovine instead of human APC was justified by a better sensitivity (Km = 0.14 and 0.42 mM respectively). Inhibition was shown to be dramatically enhanced by the presence of Heparin and calcium. No significant difference occurred for pH values up to 8.2 for both inhibition and hydrolysis reactions.In the final test, O.l ml of 1:5 diluted plasma (Tris buffer saline, pH 8.4, containing 5 U/ml of Heparin) were incubat

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Leung, L., K. Saigo, and D. Grant. "HEPARIN BINDING TO HUMAN MONOCYTES: MODULATION BY HISTIDINE-RICH GLYCOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643847.

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Heparin and its related glycosaminoglycans interact with a variety of cell types and, irrespective of their anticoagulant activities, have a complex and biologically important influence in blood vessel wall biology. In this study, the binding of heparin to the human monocytoid cell line U937 was characterized. 35s-Heparin bound to U937 cells in a specific, concentration-dependent, and saturable manner, while binding to human erythrocytes was minimal. The binding was rapid, reaching a steady state at 30 min at 4°C and was reversible. Excess unlabeled heparin, but not chondroitin sulfate or derm

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Reports on the topic "C-type inactivation"

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Ohad, Itzhak, and Himadri Pakrasi. Role of Cytochrome B559 in Photoinhibition. United States Department of Agriculture, 1995. http://dx.doi.org/10.32747/1995.7613031.bard.

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The aim of this research project was to obtain information on the role of the cytochrome b559 in the function of Photosystem-II (PSII) with special emphasis on the light induced photo inactivation of PSII and turnover of the photochemical reaction center II protein subunit RCII-D1. The major goals of this project were: 1) Isolation and sequencing of the Chlamydomonas chloroplast psbE and psbF genes encoding the cytochrome b559 a and b subunits respectively; 2) Generation of site directed mutants and testing the effect of such mutation on the function of PSII under various light conditions; 3)

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VanderGheynst, Jean, Michael Raviv, Jim Stapleton, and Dror Minz. Effect of Combined Solarization and in Solum Compost Decomposition on Soil Health. United States Department of Agriculture, 2013. http://dx.doi.org/10.32747/2013.7594388.bard.

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In soil solarization, moist soil is covered with a transparent plastic film, resulting in passive solar heating which inactivates soil-borne pathogen/weed propagules. Although solarization is an effective alternative to soil fumigation and chemical pesticide application, it is not widely used due to its long duration, which coincides with the growing season of some crops, thereby causing a loss of income. The basis of this project was that solarization of amended soil would be utilized more widely if growers could adopt the practice without losing production. In this research we examined three

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Bryant, C. A., S. A. Wilks, and C. W. Keevil. Survival of SARS-CoV-2 on the surfaces of food and food packaging materials. Food Standards Agency, 2022. http://dx.doi.org/10.46756/sci.fsa.kww583.

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COVID-19, caused by the SARS-CoV-2 virus, was first reported in China in December 2019. The virus has spread rapidly around the world and is currently responsible for 500 million reported cases and over 6.4 million deaths. A risk assessment published by the Foods Standards Agency (FSA) in 2020 (Opens in a new window) concluded that it was very unlikely that you could catch coronavirus via food. This assessment included the worst-case assumption that, if food became contaminated during production, no significant inactivation of virus would occur before consumption. However, the rate of inactiva

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