2024 |
Gochman A, Do TQ, Kim K, Schwarz JA, Thorpe MP, Blackwell DJ, et al., 'ent-Verticilide B1 Inhibits Type 2 Ryanodine Receptor Channels and is Antiarrhythmic in Casq2 -/- Mice.', Mol Pharmacol, 105 194-201 (2024) [C1]
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2023 |
Maxwell MJ, Thekkedam C, Lamboley C, Chin YKY, Crawford T, Smith JJ, et al., 'A bivalent remipede toxin promotes calcium release via ryanodine receptor activation', Nature Communications, 14 (2023) [C1]
Multivalent ligands of ion channels have proven to be both very rare and highly valuable in yielding unique insights into channel structure and pharmacology. Here, we describe a b... [more]
Multivalent ligands of ion channels have proven to be both very rare and highly valuable in yielding unique insights into channel structure and pharmacology. Here, we describe a bivalent peptide from the venom of Xibalbanus tulumensis, a troglobitic arthropod from the enigmatic class Remipedia, that causes persistent calcium release by activation of ion channels involved in muscle contraction. The high-resolution solution structure of f-Xibalbin3-Xt3a reveals a tandem repeat arrangement of inhibitor-cysteine knot (ICK) domains previously only found in spider venoms. The individual repeats of Xt3a share sequence similarity with a family of scorpion toxins that target ryanodine receptors (RyR). Single-channel electrophysiology and quantification of released Ca2+ stores within skinned muscle fibers confirm Xt3a as a bivalent RyR modulator. Our results reveal convergent evolution of RyR targeting toxins in remipede and scorpion venoms, while the tandem-ICK repeat architecture is an evolutionary innovation that is convergent with toxins from spider venoms.
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Nova |
2023 |
Gopaul U, Laver D, Carey L, Matyas T, van Vliet P, Callister R, 'Measures of Maximal Tactile Pressures during a Sustained Grasp Task Using a TactArray Device Have Satisfactory Reliability and Concurrent Validity in People with Stroke', Sensors, 23 (2023) [C1]
Sensor-based devices can record pressure or force over time during grasping and therefore offer a more comprehensive approach to quantifying grip strength during sustained contrac... [more]
Sensor-based devices can record pressure or force over time during grasping and therefore offer a more comprehensive approach to quantifying grip strength during sustained contractions. The objectives of this study were to investigate the reliability and concurrent validity of measures of maximal tactile pressures and forces during a sustained grasp task using a TactArray device in people with stroke. Participants with stroke (n = 11) performed three trials of sustained maximal grasp over 8 s. Both hands were tested in within- and between-day sessions, with and without vision. Measures of maximal tactile pressures and forces were measured for the complete (8 s) grasp duration and plateau phase (5 s). Tactile measures are reported using the highest value among three trials, the mean of two trials, and the mean of three trials. Reliability was determined using changes in mean, coefficients of variation, and intraclass correlation coefficients (ICCs). Pearson correlation coefficients were used to evaluate concurrent validity. This study found that measures of reliability assessed by changes in means were good, coefficients of variation were good to acceptable, and ICCs were very good for maximal tactile pressures using the average pressure of the mean of three trials over 8 s in the affected hand with and without vision for within-day sessions and without vision for between-day sessions. In the less affected hand, changes in mean were very good, coefficients of variations were acceptable, and ICCs were good to very good for maximal tactile pressures using the average pressure of the mean of three trials over 8 s and 5 s, respectively, in between-day sessions with and without vision. Maximal tactile pressures had moderate correlations with grip strength. The TactArray device demonstrates satisfactory reliability and concurrent validity for measures of maximal tactile pressures in people with stroke.
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Nova |
2023 |
Walweel K, Beard N, van Helden DF, Laver DR, 'Dantrolene inhibition of ryanodine channels (RyR2) in artificial lipid bilayers depends on FKBP12.6.', J Gen Physiol, 155 (2023) [C1]
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Nova |
2023 |
Vysma M, Welsh JS, Laver D, 'Computationally Efficient Simulation of Calcium Signaling in Cardiomyocytes', IEEE Transactions on Biomedical Engineering, 70 1298-1309 (2023) [C1]
The objective of this paper is to develop a computationally efficient simulation model of Calcium signalling in cardiomyocytes. The model considered here consists of more than two... [more]
The objective of this paper is to develop a computationally efficient simulation model of Calcium signalling in cardiomyocytes. The model considered here consists of more than two million stiff, nonlinear, and stochastic systems, each of which is composed of 62 state equations. The size of the model, combined with the broad numerical scale, non-continuous stochastic state-transitions, and underlying physiological constraints, presents a significant implementation challenge. The method involves development of specialised algorithms for parallelisation, which include fully-implicit Runge-Kutta integration with both L-stability and step-size control, Newton's root finding method with exception handling, and Conjugate Residual Squared for solving linear systems not of full-rank within available computational precision. Parallelisation of the problem across the systems is employed to allow for practical scaling with computing resources. The results produce sparks and waves akin to those observed in actual laboratory experiments within an acceptable timeframe. Performance measures of the simulation model with respect to accuracy and computation time are also given. The conclusion is that the methodologies utilised in this work are can simulate cardiomyocyte's calcium signalling in a computationally efficient manner with the results produced replicating those in the laboratory. The significance of this paper is that computational models such as the one developed here provide a way to simulate and understand the complex biological interactions operating in organisms. Accurate simulations are extremely computationally intensive and this pursuit is considered as the grand challenge for computational science into the 21st century.
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Nova |
2022 |
Jin R, He S, Black KA, Clarke OB, Wu D, Bolla JR, et al., 'Ion currents through Kir potassium channels are gated by anionic lipids', NATURE COMMUNICATIONS, 13 (2022) [C1]
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Nova |
2021 |
Kryshtal DO, Blackwell DJ, Egly CL, Smith AN, Batiste SM, Johnston JN, et al., 'RYR2 Channel Inhibition Is the Principal Mechanism of Flecainide Action in CPVT', CIRCULATION RESEARCH, 128 321-331 (2021) [C1]
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Nova |
2020 |
Ashna A, van Helden DF, Dos Remedios C, Molenaar P, Laver DR, 'Phenytoin Reduces Activity of Cardiac Ryanodine Receptor 2; A Potential Mechanism for Its Cardioprotective Action.', Mol Pharmacol, 97 250-258 (2020) [C1]
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Nova |
2020 |
Black KA, He S, Jin R, Miller DM, Bolla JR, Clarke OB, et al., 'A constricted opening in Kir channels does not impede potassium conduction', Nature Communications, 11 (2020) [C1]
The canonical mechanistic model explaining potassium channel gating is of a conformational change that alternately dilates and constricts a collar-like intracellular entrance to t... [more]
The canonical mechanistic model explaining potassium channel gating is of a conformational change that alternately dilates and constricts a collar-like intracellular entrance to the pore. It is based on the premise that K+ ions maintain a complete hydration shell while passing between the transmembrane cavity and cytosol, which must be accommodated. To put the canonical model to the test, we locked the conformation of a Kir K+ channel to prevent widening of the narrow collar. Unexpectedly, conduction was unimpaired in the locked channels. In parallel, we employed all-atom molecular dynamics to simulate K+ ions moving along the conduction pathway between the lower cavity and cytosol. During simulations, the constriction did not significantly widen. Instead, transient loss of some water molecules facilitated K+ permeation through the collar. The low free energy barrier to partial dehydration in the absence of conformational change indicates Kir channels are not gated by the canonical mechanism.
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Nova |
2019 |
Ottesen AH, Carlson CR, Eken OS, Sadredini M, Myhre PL, Shen X, et al., 'Secretoneurin Is an Endogenous Calcium/Calmodulin-Dependent Protein Kinase II Inhibitor That Attenuates Ca
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Nova |
2019 |
Nikolaev YA, Cox CD, Ridone P, Rohde PR, Cordero-Morales JF, Vasquez V, et al., 'Mammalian TRP on channels are insensitive to membrane stretch', JOURNAL OF CELL SCIENCE, 132 (2019) [C1]
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Nova |
2019 |
Gopaul U, Laver D, Carey L, Matyas TA, van Vliet P, Callister R, 'Measures of maximal tactile pressures of a sustained grasp task using a TactArray device have satisfactory reliability and validity in healthy people', SOMATOSENSORY AND MOTOR RESEARCH, 36 249-261 (2019) [C1]
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Nova |
2019 |
Walweel K, Gomez-Hurtado N, Rebbeck RT, Oo YW, Beard NA, Molenaar P, et al., 'Calmodulin inhibition of human RyR2 channels requires phosphorylation of RyR2-S2808 or RyR2-S2814', Journal of Molecular and Cellular Cardiology, 130 96-106 (2019) [C1]
Calmodulin (CaM) is a Ca-binding protein that binds to, and can directly inhibit cardiac ryanodine receptor calcium release channels (RyR2). Animal studies have shown that RyR2 hy... [more]
Calmodulin (CaM) is a Ca-binding protein that binds to, and can directly inhibit cardiac ryanodine receptor calcium release channels (RyR2). Animal studies have shown that RyR2 hyperphosphorylation reduces CaM binding to RyR2 in failing hearts, but data are lacking on how CaM regulates human RyR2 and how this regulation is affected by RyR2 phosphorylation. Physiological concentrations of CaM (100 nM) inhibited the diastolic activity of RyR2 isolated from failing human hearts by ~50% but had no effect on RyR2 from healthy human hearts. Using FRET between donor-FKBP12.6 and acceptor-CaM bound to RyR2, we determined that CaM binds to RyR2 from healthy human heart with a K d = 121 ± 14 nM. Ex-vivo phosphorylation/dephosphorylation experiments suggested that the divergent CaM regulation of healthy and failing human RyR2 was caused by differences in RyR2 phosphorylation by protein kinase A and Ca-CaM-dependent kinase II. Ca 2+ -spark measurements in murine cardiomyocytes harbouring RyR2 phosphomimetic or phosphoablated mutants at S2814 and S2808 suggest that phosphorylation of residues corresponding to either human RyR2-S2808 or S2814 is both necessary and sufficient for RyR2 regulation by CaM. Our results challenge the current concept that CaM universally functions as a canonical inhibitor of RyR2 across species. Rather, CaM's biological action on human RyR2 appears to be more nuanced, with inhibitory activity only on phosphorylated RyR2 channels, which occurs during exercise or in patients with heart failure.
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Nova |
2018 |
Laver DR, 'Regulation of the RyR channel gating by Ca
Ryanodine receptors (RyRs) are the Ca2+ release channels in the sarcoplasmic reticulum in striated muscle which play an important role in excitation-contraction coupling and cardi... [more]
Ryanodine receptors (RyRs) are the Ca2+ release channels in the sarcoplasmic reticulum in striated muscle which play an important role in excitation-contraction coupling and cardiac pacemaking. Single channel recordings have revealed a wealth of information about ligand regulation of RyRs from mammalian skeletal and cardiac muscle (RyR1 and RyR2, respectively). RyR subunit has a Ca2+ activation site located in the luminal and cytoplasmic domains of the RyR. These sites synergistically feed into a common gating mechanism for channel activation by luminal and cytoplasmic Ca2+. RyRs also possess two inhibitory sites in their cytoplasmic domains with Ca2+ affinities of the order of 1¿µM and 1¿mM. Magnesium competes with Ca2+ at these sites to inhibit RyRs and this plays an important role in modulating their Ca2+-dependent activity in muscle. This review focuses on how these sites lead to RyR modulation by Ca2+ and Mg2+ and how these mechanisms control Ca2+ release in excitation-contraction coupling and cardiac pacemaking.
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Nova |
2018 |
Korol SV, Jin Z, Jin Y, Bhandage AK, Tengholm A, Gandasi NR, et al., 'Functional Characterization of Native, High-Affinity GABA
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Nova |
2017 |
van Helden DF, Kamiya A, Kelsey S, Laver DR, Jobling P, Mitsui R, Hashitani H, 'Nerve-induced responses of mouse vaginal smooth muscle', Pflugers Archiv European Journal of Physiology, 469 1373-1385 (2017) [C1]
Neural and agonist-induced contractions of proximal (i.e. upper half adjacent to the cervix) and distal mouse vaginal smooth muscle strips were investigated. We hypothesised that ... [more]
Neural and agonist-induced contractions of proximal (i.e. upper half adjacent to the cervix) and distal mouse vaginal smooth muscle strips were investigated. We hypothesised that nerve-mediated vaginal contractions arise through activity of cholinergic nerves. Nerve activation by bursts of electrical field stimulation (EFS) caused a primary transient contraction often accompanied by a secondary transient contraction, both larger in proximal than distal tissues (i.e. primary: 7-fold larger; secondary: 3-fold larger). Our hypothesis was supported as we found that cholinergic nerves mediated the primary transient contraction in both proximal and distal vaginal strips, as EFS responses were enhanced by neostigmine an anticholinesterase, massively inhibited by the competitive muscarinic receptor antagonist atropine and not affected by the non-selective a-adrenergic receptor antagonist phentolamine. Primary transient contractions were halved in amplitude by the L-type Ca2+ channel blocker nifedipine and markedly inhibited by the sarco-endoplasmic reticulum calcium ATPase (SERCA) inhibitor cyclopiazonic acid (CPA). Resultant secondary transient contractions were abolished by nifedipine. Notably, the selective a1-adrenergic receptor agonist phenylephrine caused tonic contracture in distal but not proximal strips. Low-frequency EFS often initiated recurrent transient contractions similar to those elicited by CCh. Immunohistochemical studies demonstrated innervation of the smooth muscle. Findings of enhanced proximal cholinergic nerve-induced transient contractions, evidence that maintained nerve stimulation could cause recurrent contractions and the finding of distal phenylephrine-mediated tonic contraction have implications on insemination.
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Nova |
2017 |
Walweel K, Oo YW, Laver DR, 'The emerging role of calmodulin regulation of RyR2 in controlling heart rhythm, the progression of heart failure and the antiarrhythmic action of dantrolene', Clinical and Experimental Pharmacology and Physiology, 44 135-142 (2017) [C1]
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Nova |
2017 |
Walweel K, Gomez-Hurtado N, Oo YW, Beard NA, dos Remedios C, Johnson CN, et al., 'Calmodulin Mutants Linked to Catecholaminergic Polymorphic Ventricular Tachycardia Fail to Inhibit Human RyR2 Channels', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 70 115-117 (2017)
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2017 |
Laver DR, Attia J, Oldmeadow C, Quail AW, 'Cardiac Calcium Release Channel (Ryanodine Receptor 2) Regulation by Halogenated Anesthetics', Anesthesiology, 126 495-506 (2017) [C1]
Background: Halogenated anesthetics activate cardiac ryanodine receptor 2-mediated sarcoplasmic reticulum Ca 2+ release, leading to sarcoplasmic reticulum Ca 2+ depletion, reduced... [more]
Background: Halogenated anesthetics activate cardiac ryanodine receptor 2-mediated sarcoplasmic reticulum Ca 2+ release, leading to sarcoplasmic reticulum Ca 2+ depletion, reduced cardiac function, and providing cell protection against ischemia-reperfusion injury. Anesthetic activation of ryanodine receptor 2 is poorly defined, leaving aspects of the protective mechanism uncertain. Methods: Ryanodine receptor 2 from the sheep heart was incorporated into artificial lipid bilayers, and their gating properties were measured in response to five halogenated anesthetics. Results: Each anesthetic rapidly and reversibly activated ryanodine receptor 2, but only from the cytoplasmic side. Relative activation levels were as follows: halothane (approximately 4-fold; n = 8), desflurane and enflurane (approximately 3-fold,n = 9), and isoflurane and sevoflurane (approximately 1.5-fold, n = 7, 10). Half-activating concentrations (K a) were in the range 1.3 to 2.1 mM (1.4 to 2.6 minimum alveolar concentration [MAC]) with the exception of isoflurane (5.3 mM, 6.6 minimum alveolar concentration). Dantrolene (10 µM with 100 nM calmodulin) inhibited ryanodine receptor 2 by 40% but did not alter the K a for halothane activation. Halothane potentiated luminal and cytoplasmic Ca 2+ activation of ryanodine receptor 2 but had no effect on Mg 2+ inhibition. Halothane activated ryanodine receptor 2 in the absence and presence (2 mM) of adenosine triphosphate (ATP). Adenosine, a competitive antagonist to ATP activation of ryanodine receptor 2, did not antagonize halothane activation in the absence of ATP. Conclusions: At clinical concentrations (1 MAC), halothane desflurane and enflurane activated ryanodine receptor 2, whereas isoflurane and sevoflurane were ineffective. Dantrolene inhibition of ryanodine receptor 2 substantially negated the activating effects of anesthetics. Halothane acted independently of the adenine nucleotide-binding site on ryanodine receptor 2. The previously observed adenosine antagonism of halothane activation of sarcoplasmic reticulum Ca 2+ release was due to competition between adenosine and ATP, rather than between halothane and ATP.
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Nova |
2017 |
Walweel K, Molenaar P, Imtiaz MS, Denniss A, dos Remedios C, van Helden DF, et al., 'Ryanodine receptor modification and regulation by intracellular Ca
Rationale Heart failure is a multimodal disorder, of which disrupted Ca2¿+ homeostasis is a hallmark. Central to Ca2¿+ homeostasis is the major cardiac Ca2¿+ release channel ¿ the... [more]
Rationale Heart failure is a multimodal disorder, of which disrupted Ca2¿+ homeostasis is a hallmark. Central to Ca2¿+ homeostasis is the major cardiac Ca2¿+ release channel ¿ the ryanodine receptor (RyR2) ¿ whose activity is influenced by associated proteins, covalent modification and by Ca2¿+ and Mg2¿+. That RyR2 is remodelled and its function disturbed in heart failure is well recognized, but poorly understood. Objective To assess Ca2¿+ and Mg2¿+ regulation of RyR2 from left ventricles of healthy, cystic fibrosis and failing hearts, and to correlate these functional changes with RyR2 modifications and remodelling. Methods and results The function of RyR2 from left ventricular samples was assessed using lipid bilayer single-channel measurements, whilst RyR2 modification and protein:protein interactions were determined using Western Blots and co-immunoprecipitation. In all failing hearts there was an increase in RyR2 activity at end-diastolic cytoplasmic Ca2¿+ (100¿nM), a decreased cytoplasmic [Ca2¿+] required for half maximal activation (Ka) and a decrease in inhibition by cytoplasmic Mg2¿+. This was accompanied by significant hyperphosphorylation of RyR2 S2808 and S2814, reduced free thiol content and a reduced interaction with FKBP12.0 and FKBP12.6. Either dephosphorylation of RyR2 using PP1 or thiol reduction using DTT eliminated any significant difference in the activity of RyR2 from healthy and failing hearts. We also report a subgroup of RyR2 in failing hearts that were not responsive to regulation by intracellular Ca2¿+ or Mg2¿+. Conclusion Despite different aetiologies, disrupted RyR2 Ca2¿+ sensitivity and biochemical modification of the channel are common constituents of failing heart RyR2 and may underlie the pathological disturbances in intracellular Ca2¿+ signalling.
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Nova |
2016 |
Laver DR, 'Balancing SR Ca2+ uptake and release in the cycle of heart rhythm', JOURNAL OF PHYSIOLOGY-LONDON, 594 2779-2780 (2016)
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2015 |
Zhang HM, Imtiaz MS, Laver DR, McCurdy DW, Offler CE, Van Helden DF, Patrick JW, 'Polarized and persistent Ca
Transfer cell morphology is characterized by a polarized ingrowth wall comprising a uniform wall upon which wall ingrowth papillae develop at right angles into the cytoplasm. The ... [more]
Transfer cell morphology is characterized by a polarized ingrowth wall comprising a uniform wall upon which wall ingrowth papillae develop at right angles into the cytoplasm. The hypothesis that positional information directing construction of wall ingrowth papillae is mediated by Ca2+ signals generated by spatiotemporal alterations in cytosolic Ca2+ ([Ca2+]cyt) of cells trans-differentiating to a transfer cell morphology was tested. This hypothesis was examined using Vicia faba cotyledons. On transferring cotyledons to culture, their adaxial epidermal cells synchronously trans-differentiate to epidermal transfer cells. A polarized and persistent Ca2+ signal, generated during epidermal cell trans-differentiation, was found to co-localize with the site of ingrowth wall formation. Dampening Ca2+ signal intensity, by withdrawing extracellular Ca2+ or blocking Ca2+ channel activity, inhibited formation of wall ingrowth papillae. Maintenance of Ca2+ signal polarity and persistence depended upon a rapid turnover (minutes) of cytosolic Ca2+ by co-operative functioning of plasma membrane Ca2+-permeable channels and Ca2+-ATPases. Viewed paradermally, and proximal to the cytosol-plasma membrane interface, the Ca2+ signal was organized into discrete patches that aligned spatially with clusters of Ca2+-permeable channels. Mathematical modelling demonstrated that these patches of cytosolic Ca2+ were consistent with inward-directed plumes of elevated [Ca2+]cyt. Plume formation depended upon an alternating distribution of Ca2+-permeable channels and Ca2+-ATPase clusters. On further inward diffusion, the Ca2+ plumes coalesced into a uniform Ca2+ signal. Blocking or dispersing the Ca2+ plumes inhibited deposition of wall ingrowth papillae, while uniform wall formation remained unaltered. A working model envisages that cytosolic Ca2+ plumes define the loci at which wall ingrowth papillae are deposited.
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Nova |
2015 |
Nikolaev YA, Dosen PJ, Laver DR, Van Helden DF, Hamill OP, 'Single mechanically-gated cation channel currents can trigger action potentials in neocortical and hippocampal pyramidal neurons', Brain Research, 1608 1-13 (2015) [C1]
The mammalian brain is a mechanosensitive organ that responds to different mechanical forces ranging from intrinsic forces implicated in brain morphogenesis to extrinsic forces th... [more]
The mammalian brain is a mechanosensitive organ that responds to different mechanical forces ranging from intrinsic forces implicated in brain morphogenesis to extrinsic forces that can cause concussion and traumatic brain injury. However, little is known of the mechanosensors that transduce these forces. In this study we use cell-attached patch recording to measure single mechanically-gated (MG) channel currents and their affects on spike activity in identified neurons in neonatal mouse brain slices. We demonstrate that both neocortical and hippocampal pyramidal neurons express stretch-activated MG cation channels that are activated by suctions of ~25 mm Hg, have a single channel conductance for inward current of 50-70 pS and show weak selectivity for alkali metal cations (i.e., Na+<K+<Cs+). Significantly, single MG channel currents activated on the soma trigger spiking/action potentials in both neocortical and hippocampal pyramidal neurons. Not all neuron types studied here expressed MG channel currents. In particular, locus coeruleus and cerebellar Purkinje neurons showed no detectable MG channel activity. Moreover their robust rhythmic spike activity was resistant to mechanical modulation. Our observation that a single MG channel current can trigger spiking predicates the need for reassessment of the long held view that the impulse output of central neurons depends only upon their intrinsic voltage-gated channels and/or their integrated synaptic input.
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Nova |
2015 |
Walweel K, Laver DR, 'Mechanisms of SR calcium release in healthy and failing human hearts.', Biophys Rev, 7 33-41 (2015)
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2015 |
Oo YW, Gomez-Hurtado N, Walweel K, van Helden DF, Imtiaz MS, Knollmann BC, Laver DR, 'Essential Role of Calmodulin in RyR Inhibition by Dantrolene', MOLECULAR PHARMACOLOGY, 88 57-63 (2015) [C1]
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Nova |
2015 |
Walweel K, Laver DR, 'Mechanisms of SR calcium release in healthy and failing human hearts', Biophysical Reviews, 7 33-41 (2015) [C1]
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Nova |
2014 |
van Helden DF, Thomas PA, Dosen PJ, Imtiaz MS, Laver DR, Isbister GK, 'Pharmacological approaches that slow lymphatic flow as a snakebite first aid.', PLoS Negl Trop Dis, 8 e2722 (2014) [C1]
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Nova |
2014 |
Walweel K, Li J, Molenaar P, Imtiaz MS, Quail A, dos Remedios CG, et al., 'Differences in the regulation of RyR2 from human, sheep, and rat by Ca² and Mg² in the cytoplasm and in the lumen of the sarcoplasmic reticulum.', J Gen Physiol, 144 263-271 (2014) [C1]
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Nova |
2014 |
Hwang HS, Nitu FR, Yang Y, Walweel K, Pereira L, Johnson CN, et al., 'Divergent Regulation of Ryanodine Receptor 2 Calcium Release Channels by Arrhythmogenic Human Calmodulin Missense Mutants', CIRCULATION RESEARCH, 114 1114-1124 (2014) [C1]
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Nova |
2014 |
Mehra D, Imtiaz MS, Van Helden DF, Knollmann BC, Laver DR, 'Multiple modes of ryanodine receptor 2 inhibition by flecainide', Molecular Pharmacology, 86 696-706 (2014) [C1]
Catecholaminergic polymorphic ventricular tachycardia (CPVT) causes sudden cardiac death due to mutations in cardiac ryanodine receptors (RyR2), calsequestrin, or calmodulin. Flec... [more]
Catecholaminergic polymorphic ventricular tachycardia (CPVT) causes sudden cardiac death due to mutations in cardiac ryanodine receptors (RyR2), calsequestrin, or calmodulin. Flecainide, a class I antiarrhythmic drug, inhibits Na<sup>+</sup> and RyR2 channels and prevents CPVT. The purpose of this study is to identify inhibitory mechanisms of flecainide on RyR2. RyR2 were isolated from sheep heart, incorporated into lipid bilayers, and investigated by singlechannel recording under various activating conditions, including the presence of cytoplasmic ATP (2mM) and a range of cytoplasmic [Ca<sup>2+</sup>], [Mg<sup>2+</sup>], pH, and [caffeine]. Flecainide applied to either the cytoplasmic or luminal sides of the membrane inhibited RyR2 by two distinct modes: 1) a fast block consisting of brief substate and closed events with a mean duration of ~1 ms, and 2) a slow block consisting of closed events with a mean duration of ~1 second. Both inhibition modes were alleviated by increasing cytoplasmic pH from 7.4 to 9.5 but were unaffected by luminal pH. The slow block was potentiated in RyR2 channels that had relatively low open probability, whereas the fast block was unaffected by RyR2 activation. These results show that these two modes are independent mechanisms for RyR2 inhibition, both having a cytoplasmic site of action. The slow mode is a closed-channel block, whereas the fast mode blocks RyR2 in the open state. At diastolic cytoplasmic [Ca<sup>2+</sup>] (100 nM), flecainide possesses an additional inhibitory mechanism that reduces RyR2 burst duration. Hence, multiple modes of action underlie RyR2 inhibition by flecainide.
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Nova |
2013 |
Li J, Imtiaz MS, Beard NA, Dulhunty AF, Thorne R, vanHelden DF, Laver DR, 'ß-Adrenergic stimulation increases RyR2 activity via intracellular Ca2+ and Mg2+ regulation.', PLoS One, 8 e58334 (2013) [C1]
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2013 |
Cannell MB, Kong CHT, Imtiaz MS, Laver DR, 'Control of Sarcoplasmic Reticulum Ca2+ Release by Stochastic RyR Gating within a 3D Model of the Cardiac Dyad and Importance of Induction Decay for CICR Termination', BIOPHYSICAL JOURNAL, 104 2149-2159 (2013) [C1]
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Nova |
2013 |
Laver DR, Kong CHT, Imtiaz MS, Cannell MB, 'Termination of calcium-induced calcium release by induction decay: An emergent property of stochastic channel gating and molecular scale architecture', JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 54 98-100 (2013) [C1]
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Nova |
2013 |
Kong CHT, Laver DR, Cannell MB, 'Extraction of Sub-microscopic Ca Fluxes from Blurred and Noisy Fluorescent Indicator Images with a Detailed Model Fitting Approach', PLOS COMPUTATIONAL BIOLOGY, 9 (2013) [C1]
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Nova |
2012 |
Seymour VAL, Curmi JP, Howitt SM, Casarotto MG, Laver DR, Tierney ML, 'Selective modulation of different GABA A receptor isoforms by diazepam and etomidate in hippocampal neurons', International Journal of Biochemistry and Cell Biology, 44 1491-1500 (2012) [C1]
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Nova |
2011 |
Hwang HS, Hasdemir C, Laver DR, Mehra DR, Turhan K, Faggioni M, et al., 'Inhibition of Cardiac Ca2+ Release Channels (RyR2) Determines Efficacy of Class I Antiarrhythmic Drugs in Catecholaminergic Polymorphic Ventricular Tachycardia', Circulation: Arrhythmia and Electrophysiology, 4 128-135 (2011) [C1]
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Nova |
2011 |
Laver DR, Van Helden DF, 'Three independent mechanisms contribute to tetracaine inhibition of cardiac calcium release channels', Journal of Molecular and Cellular Cardiology, 51 357-369 (2011) [C1]
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Nova |
2010 |
Hwang HS, Hasdemir C, Laver D, Mehra D, Turhan K, Faggioni M, et al., 'Inhibition of Cardiac Ca2+ Release Channels (RyR2) Determines Efficacy of Class I Antiarrhythmic Drugs in Catecholaminergic Polymorphic Ventricular Tachycardia', CIRCULATION, 122 (2010) [C3] |
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2010 |
Imtiaz MS, Von Der Weid P-Y, Laver DR, Van Helden DF, 'SR Ca2+ store refill-a key factor in cardiac pacemaking', Journal of Molecular and Cellular Cardiology, 49 412-426 (2010) [C1]
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Nova |
2010 |
Hilliard FA, Steele DS, Laver DR, Yang Z, Le Marchand SJ, Chopra N, et al., 'Flecainide inhibits arrhythmogenic Ca2+ waves by open state block of ryanodine receptor Ca2+ release channels and reduction of Ca2+ spark mass', Journal of Molecular and Cellular Cardiology, 48 293-301 (2010) [C1]
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Nova |
2010 |
Shtifman A, Ward CW, Laver DR, Bannister ML, Lopez JR, Kitazawa M, et al., 'Amyloid-ß protein impairs Ca2+ release and contractility in skeletal muscle', Neurobiology of Aging, 31 2080-2090 (2010) [C1]
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Nova |
2010 |
Van Helden DF, Laver DR, Holdsworth JL, Imtiaz MS, 'Generation and propagation of gastric slow waves', Clinical and Experimental Pharmacology and Physiology, 37 516-524 (2010) [C1]
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Nova |
2009 |
Chopra N, Laver DR, Davies SS, Knollmann BC, 'Amitriptyline activates cardiac ryanodine channels and causes spontaneous sarcoplasmic reticulum calcium release', Molecular Pharmacology, 75 183-195 (2009) [C1]
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Nova |
2009 |
Laver DR, 'Luminal Ca2+ activation of cardiac ryanodine receptors by luminal and cytoplasmic domains', European Biophysics Journal, 39 19-26 (2009) [C1]
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Nova |
2009 |
Everitt AB, Seymour VAL, Curmi J, Laver DR, Gage PW, Tierney ML, 'Protein interactions involving the gamma 2 large cytoplasmic loop of GABA(A) receptors modulate conductance', FASEB Journal, 23 4361-4369 (2009) [C1]
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Nova |
2009 |
Watanabe H, Chopra N, Laver DR, Hwang HS, Davies SS, Roach DE, et al., 'Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans', Nature Medicine, 15 380-383 (2009) [C1]
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Nova |
2008 |
Laver DR, Honen BN, 'Luminal Mg2+, a key factor controlling RYR2-mediated Ca2+ release: Cytoplasmic and luminal regulation modeled in a tetrameric channel', Journal of General Physiology, 132 429-446 (2008) [C1]
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Nova |
2008 |
Laver DR, Honen BN, Lamb GD, Ikemoto N, 'A domain peptide of the cardiac ryanodine receptor regulates channel sensitivity to luminal Ca2+ via cytoplasmic Ca2+ sites', European Biophysics Journal with Biophysics Letters, 37 455-467 (2008) [C1]
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Nova |
2007 |
Laver DR, 'Ca2+ stores regulate ryanodine receptor Ca2+ release channels via luminal and cytosolic Ca2+ sites', Clinical and Experimental Pharmacology and Physiology, 34 889-896 (2007) [C1]
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Nova |
2007 |
Laver DR, 'Ca2+ stores regulate ryanodine receptor Ca2+ release channels via luminal and cytosolic Ca2+ sites', Biophysical Journal, 92 3541-3555 (2007) [C1]
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Nova |
2007 |
Laver DR, Hamada T, Fessenden JD, Ikemoto N, 'The ryanodine receptor pore blocker neomycin also inhibits channel activity via a previously undescribed high-affinity Ca2+ binding site', Journal of Membrane Biology, 220 11-20 (2007) [C1]
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Nova |
2006 |
Lindquist CEL, Laver DR, Birnir B, 'The mechanism of SR95531 inhibition at GABA(A) receptors examined in human alpha(1)beta(1) and alpha(1)beta(1)gamma(2S) receptors (vol 94, pg 491, 2005)', JOURNAL OF NEUROCHEMISTRY, 97 302-302 (2006)
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2006 |
Laver DR, 'Regulation of ryanodine receptors from skeletal and cardiac muscle during rest and excitation', Clinical and Experimental Pharmacology & Physiology, 33 1107-1113 (2006) [C1]
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2006 |
Laver DR, Bradley KM, 'Disulfonic stilbene permeation and block of the anion channel from the sarcoplasmic reticulum of rabbit skeletal muscle', American Journal of Physiology-Cell Physiology, 290 C1666-C1677 (2006) [C1]
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Nova |
2006 |
Lindquist CEL, Laver DR, Birnir B, 'The mechanism of SR95531 inhibition at GABA(A) receptors examined in human alpha(1)beta(1) and alpha(1)beta(1)gamma(2S) receptors (vol 94, pg 491, 2005) (Errartum)', Journal of Neurochemistry, 97 302-302 (2006) [C3]
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2005 |
Haarmann CS, Dulhunty AF, Laver DR, 'Regulation of skeletal ryanodine receptors by dihydropyridine receptor II-III loop C-region peptides: relief of Mg2+ inhibition', Biochemical Journal, 387 429-436 (2005) [C1]
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2005 |
Laver DR, 'Coupled calcium release channels and their regulation by luminal and cytosolic ions', European Biophysics Journal with Biophysics Letters, 34 359-368 (2005) [C1]
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Nova |
2005 |
Lindquist CEL, Laver DR, Birnir B, 'The mechanism of SR95531 inhibition at GABA(A) receptors examined in human alpha(1)beta(1) and alpha(1)beta(1)gamma(2S) receptors', Journal of Neurochemistry, 94 491-501 (2005) [C1] |
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Nova |
2005 |
Beard NA, Casarotto MG, Wei L, Varsanyi M, Laver DR, Dulhunty AF, 'Regulation of ryanodine receptors by calsequestrin: Effect of high luminal Ca2+ and phosphorylation', Biophysical Journal, 88 3444-3454 (2005) [C1]
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Nova |
2004 |
Laver DR, O'Neill ER, Lamb GD, 'Luminal Ca2+ - regulated Mg2+ inhibition of skeletal RyRs reconstituted as isolated channels or coupled clusters', J Gen Physiol, 124 741-758 (2004) [C1]
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Nova |
2004 |
Beard NA, Laver DR, Dulhunty AF, 'Calsequestrin and the calcium release challen of skeletal and cardiac muscle', Progress in Biophysics & Molecular Biology, 85 33-69 (2004) [C1]
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2003 |
O'Neill ER, Sakowska MM, Laver DR, 'Regulation of the Calcium Release Channel from Skeletal Muscle by Suramin and the Disulfonated Stilbene Derivatives DIDS, DBDS, and DNDS', Biophysical Journal, 84 1674-1689 (2003) [C1]
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Nova |
2003 |
Honen BN, Saint DA, Laver DR, 'Supression of Calcium Sparks in Rat Ventricular Myocytes and Direct Inhitition of Sheep Cardiac RyR Channels by EPA, DHA and Oleic Acid', Journal of Membrane Biology, 196 95-103 (2003) [C1]
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2003 |
Haarmann C, Green D, Casarotto MG, Laver DR, Dalhunty AF, 'The Random-Coil 'C' fragment of the dihydropyridine receptor II-III loop can activate or inhibit native skeletal ryanodine receptors', Biochemical journal, 375 305-316 (2003) [C1]
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2002 |
Dulhunty AF, Haarmann CS, Green D, Laver DR, Board PG, Casarotto MG, 'Interactions between dihydropyridine receptors and ryanodine receptors in striated muscle', PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY, 79 45-75 (2002)
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2002 |
Beard NA, Sakowska MM, Dulhunty AF, Laver DR, 'Calsequestrin is an Inhibitor of Skeletal Muscle Ryanodine Receptor Calcium Release Channels', Biophysical Journal, 82 310-320 (2002) [C1]
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2001 |
Dulhunty AF, Laver D, Curtis SM, Pace S, Haarmann C, Gallant EM, 'Characteristics of irreversible ATP activation suggest that native skeletal ryanodine receptors can be phosphorylated via an endogenous CaMKII', BIOPHYSICAL JOURNAL, 81 3240-3252 (2001)
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2001 |
Laver DR, 'The power of single channel recording and analysis: Its application to ryanodine receptors in lipid bilayers', CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 28 675-686 (2001)
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2001 |
Laver DR, Lenz GKE, Dulhunty AF, 'Phosphate ion channels in sarcoplasmic reticulum of rabbit skeletal muscle', JOURNAL OF PHYSIOLOGY-LONDON, 535 715-728 (2001)
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2001 |
Laver DR, Lenz GKE, Lamb GD, 'Regulation of the calcium release channel from rabbit skeletal muscle by the nucleotides ATP, AMP, IMP and adenosine', JOURNAL OF PHYSIOLOGY-LONDON, 537 763-778 (2001)
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Nova |
2000 |
Laver DR, Eager KR, Taoube L, Lamb GD, 'Effects of cytoplasmic and luminal pH on Ca2+ release channels from rabbit skeletal muscle', BIOPHYSICAL JOURNAL, 78 1835-1851 (2000)
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2000 |
Lamb GD, Laver DR, Stephenson DG, 'Perspective - Questions about adaptation in ryanodine receptors', JOURNAL OF GENERAL PHYSIOLOGY, 116 883-890 (2000)
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2000 |
Panter S, Thomson R, de Bruxelles G, Laver D, Trevaskis B, Udvardi M, 'Identification with proteomics of novel proteins associated with the peribacteroid membrane of soybean root nodules', MOLECULAR PLANT-MICROBE INTERACTIONS, 13 325-333 (2000)
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2000 |
Lamb GD, Laver DR, Stephenson DG, 'Questions about adaptation in ryanodine receptors', Journal of General Physiology, 116 883-890 (2000)
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1999 |
Laver DR, Eager KR, Taoube L, Lamb GD, 'Regulation of the skeletal muscle calcium release channel (RyR1) by luminal and cytosolic pH.', BIOPHYSICAL JOURNAL, 76 A303-A303 (1999) |
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1999 |
Dulhunty AF, Laver DR, Gallant EM, Casarotto MG, Pace SM, Curtis S, 'Activation and inhibition of skeletal RyR channels by a part of the skeletal DHPR II-III loop: Effects of DHPR Ser(687) and FKBP12', BIOPHYSICAL JOURNAL, 77 189-203 (1999)
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1998 |
Ahern GP, Laver DR, 'ATP inhibition and rectification of a Ca2+-activated anion channel in sarcoplasmic reticulum of skeletal muscle', BIOPHYSICAL JOURNAL, 74 2335-2351 (1998)
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1998 |
Laver DR, Lamb GD, 'Inactivation of Ca2+ release channels (ryanodine receptors RyR1 and RyR2) with rapid steps in [Ca2+] and voltage', BIOPHYSICAL JOURNAL, 74 2352-2364 (1998)
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1997 |
Laver DR, Owen VJ, Junankar PR, Taske NL, Dulhunty AF, Lamb GD, 'Reduced inhibitory effect of Mg2+ on ryanodine receptor Ca2+ release channels in malignant hyperthermia', BIOPHYSICAL JOURNAL, 73 1913-1924 (1997)
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1997 |
Laver DR, Owen VJ, Junankar PR, Taske NL, Dulhunty AF, Lamb GD, 'Ca2+- and Mg2+-Regulation of Calcium Release Channels from Normal and Malignant Hyperthermia Susceptible Pigs', Biophysical Journal, 73 1913-1924 (1997) [C1] |
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1997 |
McCulloch SR, Laver DR, Walker NA, 'Anion channel activity in the Chara plasma membrane: Co-operative subunit phenomena and a model', JOURNAL OF EXPERIMENTAL BOTANY, 48 383-397 (1997)
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1997 |
Laver DR, Cherry CA, Walker NA, 'The actions of calmodulin antagonists W-7 and TFP and of calcium on the gating kinetics of the calcium-activated large conductance potassium channel of the Chara protoplasmic drop: A substate-sensitive analysis', JOURNAL OF MEMBRANE BIOLOGY, 155 263-274 (1997)
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1997 |
Laver DR, Baynes TM, Dulhunty AF, 'Mg2+-Inhibition of Ryanodine-sensitive Ca2+ Channels: Evidence for Two Independent Mechanisms', Journal of Membrane Biology, 156 213-229 (1997) [C1]
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1997 |
Laver DR, Gage PW, 'Interpretation of substates in ion channels: Unipores or multipores?', PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY, 67 99-140 (1997)
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1996 |
Dulhunty AF, Junankar PR, Eager KR, Ahern GP, Laver DR, 'Ion channels in the sarcoplasmic reticulum of striated muscle', ACTA PHYSIOLOGICA SCANDINAVICA, 156 375-385 (1996)
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Nova |
1996 |
Kourie JI, Laver DR, Junankar PR, Gage PW, Dulhunty AF, 'Characteristics of two types of chloride channel in sarcoplasmic reticulum vesicles from rabbit skeletal muscle', BIOPHYSICAL JOURNAL, 70 202-221 (1996)
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1996 |
Laver D, Curtis B, 'Rapid solution change activates ryanodine receptors within 20 ms.', BIOPHYSICAL JOURNAL, 70 WPO48-WPO48 (1996)
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1996 |
Laver DR, Curtis BA, 'Surface potentials measure ion concentrations near lipid bilayers during rapid solution changes', BIOPHYSICAL JOURNAL, 71 722-731 (1996)
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1996 |
Laver DR, Curtis BA, 'Response of ryanodine receptor channels to Ca2+ steps produced by rapid solution', BIOPHYSICAL JOURNAL, 71 732-741 (1996)
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1996 |
Laver DR, Baynes TM, 'Characterisation of two Mg2+-inhibition mechanisms in ryanodine receptor Ca2+ channels', BIOPHYSICAL JOURNAL, 70 WPO59-WPO59 (1996) |
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1996 |
Kourie JI, Laver DR, Ahern GP, Dulhunty AF, 'A calcium-activated chloride channel in sarcoplasmic reticulum vesicles from rabbit skeletal muscle', AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 270 C1675-C1686 (1996)
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1995 |
Laver DR, Roden LD, Ahem GP, Eager KR, Junankar PR, Dulhunty AF, 'Cytoplasmic Ca2+ Inhibits the Ryanodine Receptor from Cardiac Muscle', Journal of Membrane Biology, 147 7-22 (1995) [C1]
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1994 |
LAVER DR, 'THE BARREL-STAVE MODEL AS APPLIED TO ALAMETHICIN AND ITS ANALOGS REEVALUATED', BIOPHYSICAL JOURNAL, 66 355-359 (1994)
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1994 |
LAVER DR, FAIRLEYGRENOT KA, 'SURFACE-POTENTIALS NEAR THE MOUTH OF THE LARGE-CONDUCTANCE K+ CHANNEL FROM CHARA-AUSTRALIS - A NEW METHOD OF TESTING FOR DIFFUSION-LIMITED ION FLOW', JOURNAL OF MEMBRANE BIOLOGY, 139 149-165 (1994)
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Nova |
1992 |
LAVER DR, 'DIVALENT-CATION BLOCK AND COMPETITION BETWEEN DIVALENT AND MONOVALENT CATIONS IN THE LARGE-CONDUCTANCE K+ CHANNEL FROM CHARA-AUSTRALIS', JOURNAL OF GENERAL PHYSIOLOGY, 100 269-300 (1992)
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Nova |
1991 |
LAVER DR, WALKER NA, 'ACTIVATION BY CA2+ AND BLOCK BY DIVALENT IONS OF THE K+-CHANNEL IN THE MEMBRANE OF CYTOPLASMIC DROPS FROM CHARA-AUSTRALIS', JOURNAL OF MEMBRANE BIOLOGY, 120 131-139 (1991)
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1991 |
FAIRLEY K, LAVER D, WALKER NA, 'WHOLE-CELL AND SINGLE-CHANNEL CURRENTS ACROSS THE PLASMALEMMA OF CORN SHOOT SUSPENSION CELLS', JOURNAL OF MEMBRANE BIOLOGY, 121 11-22 (1991)
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1991 |
LAVER DR, 'A SURGICAL METHOD FOR ACCESSING THE PLASMAMEMBRANE OF CHARA-AUSTRALIS', PROTOPLASMA, 161 79-84 (1991)
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1990 |
LAVER DR, 'COUPLING OF K+-GATING AND PERMEATION WITH CA-2+ BLOCK IN THE CA-2+-ACTIVATED K+ CHANNEL IN CHARA-AUSTRALIS', JOURNAL OF MEMBRANE BIOLOGY, 118 55-67 (1990)
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Nova |
1990 |
GENTLE IR, LAVER DR, RITCHIE GLD, 'TEMPERATURE AND PRESSURE-DEPENDENCE OF THE ELECTROOPTICAL KERR EFFECT OF SULFUR-DIOXIDE', JOURNAL OF PHYSICAL CHEMISTRY, 94 3434-3437 (1990)
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1989 |
LAVER DR, FAIRLEY KA, WALKER NA, 'ION PERMEATION IN A K+ CHANNEL IN CHARA-AUSTRALIS - DIRECT EVIDENCE FOR DIFFUSION LIMITATION OF ION FLOW IN A MAXI-K CHANNEL', JOURNAL OF MEMBRANE BIOLOGY, 108 153-164 (1989)
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Nova |
1989 |
CRAVEN IE, HESLING MR, LAVER DR, LUKINS PB, RITCHIE GLD, VRBANCICH J, 'POLARIZABILITY ANISOTROPY, MAGNETIC-ANISOTROPY, AND QUADRUPOLE-MOMENT OF CYCLOHEXANE', JOURNAL OF PHYSICAL CHEMISTRY, 93 627-631 (1989)
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Nova |
1989 |
GENTLE IR, LAVER DR, RITCHIE GLD, '2ND HYPERPOLARIZABILITY AND STATIC POLARIZABILITY ANISOTROPY OF CARBON-DIOXIDE', JOURNAL OF PHYSICAL CHEMISTRY, 93 3035-3038 (1989)
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1987 |
LAVER DR, WALKER NA, 'STEADY-STATE VOLTAG-DEPENDENT GATING AND CONDUCTION KINETICS OF SINGLE K+ CHANNELS IN THE MEMBRANE OF CYTOPLASMIC DROPS OF CHARA-AUSTRALIS', JOURNAL OF MEMBRANE BIOLOGY, 100 31-42 (1987)
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Nova |
1986 |
COSTER HGL, LAVER DR, 'THE EFFECT OF TEMPERATURE ON LIPID NORMAL-ALKANE INTERACTIONS IN LIPID BILAYERS', BIOCHIMICA ET BIOPHYSICA ACTA, 857 95-104 (1986)
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Nova |
1986 |
COSTER HGL, LAVER DR, 'THE EFFECT OF BENZYL ALCOHOL AND CHOLESTEROL ON THE ACYL CHAIN ORDER AND ALKANE SOLUBILITY OF BIMOLECULAR PHOSPHATIDYLCHOLINE MEMBRANES', BIOCHIMICA ET BIOPHYSICA ACTA, 861 406-412 (1986)
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Nova |
1985 |
SMITH JR, COSTER HGL, LAVER DR, 'THE DEPENDENCE OF THE CONDUCTANCE OF PHOSPHATIDYLCHOLINE BILAYERS UPON THE CONCENTRATION AND COMPOSITION OF THE EXTERNAL ELECTROLYTE', BIOCHIMICA ET BIOPHYSICA ACTA, 812 181-192 (1985)
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1985 |
LUKINS PB, LAVER DR, BUCKINGHAM AD, RITCHIE GLD, 'COTTON-MOUTON EFFECT, MAGNETIC-ANISOTROPY, AND CHARGE-DISTRIBUTION OF CYCLOPROPANE', JOURNAL OF PHYSICAL CHEMISTRY, 89 1309-1312 (1985)
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1984 |
LAVER DR, SMITH JR, COSTER HGL, 'THE THICKNESS OF THE HYDROPHOBIC AND POLAR-REGIONS OF GLYCEROL MONOOLEATE BILAYERS DETERMINED FROM THE FREQUENCY-DEPENDENCE OF BILAYER CAPACITANCE', BIOCHIMICA ET BIOPHYSICA ACTA, 772 1-9 (1984)
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1984 |
SMITH JR, LAVER DR, COSTER HGL, 'THE CONDUCTANCE OF LECITHIN BILAYERS - THE DEPENDENCE UPON TEMPERATURE', CHEMISTRY AND PHYSICS OF LIPIDS, 34 227-236 (1984)
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Nova |
1983 |
ASHCROFT RG, COSTER HGL, LAVER DR, SMITH JR, 'THE EFFECTS OF CHOLESTEROL INCLUSION ON THE MOLECULAR-ORGANIZATION OF BIMOLECULAR LIPID-MEMBRANES', BIOCHIMICA ET BIOPHYSICA ACTA, 730 231-238 (1983)
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1982 |
COSTER HGL, LAVER DR, SCHOENBORN BP, 'EFFECT OF 2H2O/H2O REPLACEMENT ON THE DIELECTRIC STRUCTURE OF LIPID BILAYER-MEMBRANES', BIOCHIMICA ET BIOPHYSICA ACTA, 686 141-143 (1982)
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Nova |