Sentences with phrase «for sodium channels»

«We thought that the conflicting results for sodium channels might be related to difficulties in existing methods to control the calcium concentrations that might affect these channels,» Ben - Johny says.

Not exact matches

In a major breakthrough several years ago, two research groups, the Zuker group at Columbia and the Bachmanov group at the Monell Center for Chemical Senses, each got around this problem by finding drugs that could temporarily block a certain type of sodium channel in mice's mouths.

That suggests that this sodium channel could be a target for the development of drugs to prevent the pain caused by acid build - up — which happens in arthritis and other inflammatory disorders.

Approximately 80 % of Dravet patients have mutations in the gene SCN1A which encodes the Nav1.1 sodium channel, however for the remaining 20 % of patients the underlying genetic cause has yet to be determined.

For instance, the KscA pore, a potassium channel found in soil bacteria, is thought to select potassium using its speed to distinguish it from the very similar sized and charged sodium.

The mutation resulted in a lower single channel conductance for calcium and a strongly increased conductance for sodium and potassium, indicating that glutamic acid - 95 is a crucial constituent of the ion selectivity filter.

Researchers at Johns Hopkins have spotted a strong family trait in two distant relatives: The channels that permit entry of sodium and calcium ions into cells turn out to share similar means for regulating ion intake, they say.

Further, the interleaved and porous structure of the paper electrode offers smooth channels for sodium to diffuse in and out as the cell is charged and discharged quickly.

Researchers have known for decades that some microorganisms, such as single - celled green algae, have proteins that respond to light by opening a channel in the microbe's membranes, allowing the passage of electrically charged ions (such as calcium and sodium).

Dr Chirgadze added: «Our research has important implications for our understanding of the mechanism of sodium channel behaviour.

For instance, sodium channel 1.5 is the heart sodium channel.

Woods published his findings in 2006 in the journal Nature, suggesting that this discovery could «stimulate the search for novel analgesics that selectively target this sodium channel.»

Sodium channels are implicated in many serious conditions such as heart disease, epilepsy and pain, making them an important potential target for drug therapies.

New Cambridge research provides fresh and unexpected insight into the structure of sodium channels and, specifically, one of its components — β - subunit molecules — which are responsible for «fine - tuning» the activity of the channel.

Hund's team identified a phosphorylation site (Serine 571) on the voltage-gated sodium channel targeted by CaM kinase II that serves as a switch for inappropriate «late» sodium influx.

One particular type of sodium channel, called the Nav1.7 subtype, is responsible for sensing pain.

In cells from sick hearts, these channels often don't inactivate properly, allowing for excess sodium entry and a build - up of calcium, which ultimately promotes abnormal heart rate (arrhythmia) and symptoms of heart failure.

«We know dysregulation of a protein enzyme called multifunctional CaM kinase II plays a role in disrupting sodium channel function in cardiac disease, but it was a matter of determining how this occurred and whether we could we prevent it for therapeutic benefit,» said Hund, an associate professor of biomedical engineering at The Ohio State University.

Zheng, being a membrane protein rookie, had what he calls a stroke of beginners luck when he and his team solved the structure for a voltage-gated sodium channel, a channel others in the field had long been working to solve.

Susan Amara, USA - «Regulation of transporter function and trafficking by amphetamines, Structure - function relationships in excitatory amino acid transporters (EAATs), Modulation of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology of G protein - Coupled Receptors; Molecular mechanisms controlling the selectivity and efficacy of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms of Neurotophin Receptor Signaling Mark Coles, UK - Cellular differentiation, human embryonic stem cells, stromal cells, haematopoietic stem cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect of beta adrenergic stimulation; cardiovascular function of cGMP protein kinase Yu Huang, Hong Kong - Endothelial and Metabolic Dysfunction, and Novel Biomarkers in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors, in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) transporters

Discovered that the persistent sodium current, INaP, paradoxically amplifies afterhyperpolarizations and reduces the frequency (f / I) gain, and strongly modulates spike timing (Vervaeke et al., Neuron 2006); that Kv7 / M / KCNQ - type K + channels but not SK channels are essential for excitability control in hippocampal neurons (Gu et al., J Physiol, 2005); that Kv7 / M / KCNQ - type K + channels are essential for spatial learning and prevention of epilepsy (Nature Neuroscience 8: 51 - 60, 2005), that KCa1 / BK - type K + channels are essential for cerebellar learning and motor control (Proc Natl Acad Sci USA 101: 0474 - 8, 2004), the role of postsynaptic voltage-gated K + channels in regulation of synaptic plasticity (LTP) and integration (Proc Natl Acad Sci USA 99:10144, 2002); that Kv7 / M / KCNQ - type K + channels are essential for intrinsic theta resonance in hippocampal neurons (J Physiol 545:783, 2002).

Mutations for mammoth hemoglobin, extra hair growth, fat production, down to nuanced climate adaptations such as slightly altered sodium ion channels in cell membranes have already been engineered into fibroblast cell lines.

Since the mid-2000s, the voltage-gated sodium channel NaV1.7 has emerged as a promising target for a new class of analgesics.

We show that field - collected Ugandan Culex quinquefasciatus display CNV for the voltage-gated sodium channel gene (Vgsc), target - site of pyrethroid and organochlorine insecticides.

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasFor example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasfor example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.