Calcium Channels, L-Type: Long-lasting voltage-gated CALCIUM CHANNELS found in both excitable and nonexcitable tissue. They are responsible for normal myocardial and vascular smooth muscle contractility. Five subunits (alpha-1, alpha-2, beta, gamma, and delta) make up the L-type channel. The alpha-1 subunit is the binding site for calcium-based antagonists. Dihydropyridine-based calcium antagonists are used as markers for these binding sites.Calcium Channels: Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue.Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cellular membranes.Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.Calcium Channels, N-Type: CALCIUM CHANNELS that are concentrated in neural tissue. Omega toxins inhibit the actions of these channels by altering their voltage dependence.Calcium Channels, T-Type: A heterogenous group of transient or low voltage activated type CALCIUM CHANNELS. They are found in cardiac myocyte membranes, the sinoatrial node, Purkinje cells of the heart and the central nervous system.Calcium Signaling: Signal transduction mechanisms whereby calcium mobilization (from outside the cell or from intracellular storage pools) to the cytoplasm is triggered by external stimuli. Calcium signals are often seen to propagate as waves, oscillations, spikes, sparks, or puffs. The calcium acts as an intracellular messenger by activating calcium-responsive proteins.Calcium Channel Agonists: Agents that increase calcium influx into calcium channels of excitable tissues. This causes vasoconstriction in VASCULAR SMOOTH MUSCLE and/or CARDIAC MUSCLE cells as well as stimulation of insulin release from pancreatic islets. Therefore, tissue-selective calcium agonists have the potential to combat cardiac failure and endocrinological disorders. They have been used primarily in experimental studies in cell and tissue culture.Ion Channel Gating: The opening and closing of ion channels due to a stimulus. The stimulus can be a change in membrane potential (voltage-gated), drugs or chemical transmitters (ligand-gated), or a mechanical deformation. Gating is thought to involve conformational changes of the ion channel which alters selective permeability.Potassium Channels, Inwardly Rectifying: Potassium channels where the flow of K+ ions into the cell is greater than the outward flow.Calcium Channels, P-Type: CALCIUM CHANNELS located within the PURKINJE CELLS of the cerebellum. They are involved in stimulation-secretion coupling of neurons.Calcium Channels, Q-Type: CALCIUM CHANNELS located in the neurons of the brain.Dihydropyridines: Pyridine moieties which are partially saturated by the addition of two hydrogen atoms in any position.Calcium Channels, R-Type: CALCIUM CHANNELS located in the neurons of the brain. They are inhibited by the marine snail toxin, omega conotoxin MVIIC.Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.Potassium Channel Blockers: A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.Chloride Channels: Cell membrane glycoproteins that form channels to selectively pass chloride ions. Nonselective blockers include FENAMATES; ETHACRYNIC ACID; and TAMOXIFEN.omega-Conotoxin GVIA: A neurotoxic peptide, which is a cleavage product (VIa) of the omega-Conotoxin precursor protein contained in venom from the marine snail, CONUS geographus. It is an antagonist of CALCIUM CHANNELS, N-TYPE.Electrophysiology: The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.Calcium, Dietary: Calcium compounds used as food supplements or in food to supply the body with calcium. Dietary calcium is needed during growth for bone development and for maintenance of skeletal integrity later in life to prevent osteoporosis.Membrane Potentials: The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).omega-Conotoxins: A family of structurally related neurotoxic peptides from mollusk venom that inhibit voltage-activated entry of calcium into the presynaptic membrane. They selectively inhibit N-, P-, and Q-type calcium channels.Potassium Channels, Voltage-Gated: Potassium channel whose permeability to ions is extremely sensitive to the transmembrane potential difference. The opening of these channels is induced by the membrane depolarization of the ACTION POTENTIAL.Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.KATP Channels: Heteromultimers of Kir6 channels (the pore portion) and sulfonylurea receptor (the regulatory portion) which affect function of the HEART; PANCREATIC BETA CELLS; and KIDNEY COLLECTING DUCTS. KATP channel blockers include GLIBENCLAMIDE and mitiglinide whereas openers include CROMAKALIM and minoxidil sulfate.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.Isradipine: A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.Patch-Clamp Techniques: An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.Potassium Channels, Calcium-Activated: Potassium channels whose activation is dependent on intracellular calcium concentrations.Nitrendipine: A calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.Mibefradil: A benzimidazoyl-substituted tetraline that selectively binds and inhibits CALCIUM CHANNELS, T-TYPE.Electric Conductivity: The ability of a substrate to allow the passage of ELECTRONS.Sodium Channel Blockers: A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.Barium: An element of the alkaline earth group of metals. It has an atomic symbol Ba, atomic number 56, and atomic weight 138. All of its acid-soluble salts are poisonous.Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.omega-Agatoxin IVA: A neuropeptide toxin from the venom of the funnel web spider, Agelenopsis aperta. It inhibits CALCIUM CHANNELS, P-TYPE by altering the voltage-dependent gating so that very large depolarizations are needed for channel opening. It also inhibits CALCIUM CHANNELS, Q-TYPE.TRPC Cation Channels: A subgroup of TRP cation channels that contain 3-4 ANKYRIN REPEAT DOMAINS and a conserved C-terminal domain. Members are highly expressed in the CENTRAL NERVOUS SYSTEM. Selectivity for calcium over sodium ranges from 0.5 to 10.Shaker Superfamily of Potassium Channels: Voltage-gated potassium channels whose primary subunits contain six transmembrane segments and form tetramers to create a pore with a voltage sensor. They are related to their founding member, shaker protein, Drosophila.Kinetics: The rate dynamics in chemical or physical systems.Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Large-Conductance Calcium-Activated Potassium Channels: A major class of calcium activated potassium channels whose members are voltage-dependent. MaxiK channels are activated by either membrane depolarization or an increase in intracellular Ca(2+). They are key regulators of calcium and electrical signaling in a variety of tissues.Potassium: An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.Calcium Carbonate: Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.Cyclic Nucleotide-Gated Cation Channels: A subgroup of cyclic nucleotide-regulated ION CHANNELS within the superfamily of pore-loop cation channels. They are expressed in OLFACTORY NERVE cilia and in PHOTORECEPTOR CELLS and some PLANTS.Oocytes: Female germ cells derived from OOGONIA and termed OOCYTES when they enter MEIOSIS. The primary oocytes begin meiosis but are arrested at the diplotene state until OVULATION at PUBERTY to give rise to haploid secondary oocytes or ova (OVUM).Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Calcium Chloride: A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.TRPV Cation Channels: A subgroup of TRP cation channels named after vanilloid receptor. They are very sensitive to TEMPERATURE and hot spicy food and CAPSAICIN. They have the TRP domain and ANKYRIN repeats. Selectivity for CALCIUM over SODIUM ranges from 3 to 100 fold.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.Xenopus laevis: The commonest and widest ranging species of the clawed "frog" (Xenopus) in Africa. This species is used extensively in research. There is now a significant population in California derived from escaped laboratory animals.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Ryanodine Receptor Calcium Release Channel: A tetrameric calcium release channel in the SARCOPLASMIC RETICULUM membrane of SMOOTH MUSCLE CELLS, acting oppositely to SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. It is important in skeletal and cardiac excitation-contraction coupling and studied by using RYANODINE. Abnormalities are implicated in CARDIAC ARRHYTHMIAS and MUSCULAR DISEASES.TRPM Cation Channels: A subgroup of TRP cation channels named after melastatin protein. They have the TRP domain but lack ANKYRIN repeats. Enzyme domains in the C-terminus leads to them being called chanzymes.Acid Sensing Ion Channels: A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.Spider Venoms: Venoms of arthropods of the order Araneida of the ARACHNIDA. The venoms usually contain several protein fractions, including ENZYMES, hemolytic, neurolytic, and other TOXINS, BIOLOGICAL.Calcium Phosphates: Calcium salts of phosphoric acid. These compounds are frequently used as calcium supplements.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Epithelial Sodium Channels: Sodium channels found on salt-reabsorbing EPITHELIAL CELLS that line the distal NEPHRON; the distal COLON; SALIVARY DUCTS; SWEAT GLANDS; and the LUNG. They are AMILORIDE-sensitive and play a critical role in the control of sodium balance, BLOOD VOLUME, and BLOOD PRESSURE.Kv1.3 Potassium Channel: A delayed rectifier subtype of shaker potassium channels that is the predominant VOLTAGE-GATED POTASSIUM CHANNEL of T-LYMPHOCYTES.Ether-A-Go-Go Potassium Channels: A family of voltage-gated potassium channels that are characterized by long N-terminal and C-terminal intracellular tails. They are named from the Drosophila protein whose mutation causes abnormal leg shaking under ether anesthesia. Their activation kinetics are dependent on extracellular MAGNESIUM and PROTON concentration.Calcium Isotopes: Stable calcium atoms that have the same atomic number as the element calcium, but differ in atomic weight. Ca-42-44, 46, and 48 are stable calcium isotopes.Kv1.2 Potassium Channel: A delayed rectifier subtype of shaker potassium channels that is selectively inhibited by a variety of SCORPION VENOMS.Kv1.1 Potassium Channel: A delayed rectifier subtype of shaker potassium channels that is commonly mutated in human episodic ATAXIA and MYOKYMIA.Calcium Radioisotopes: Unstable isotopes of calcium that decay or disintegrate emitting radiation. Ca atoms with atomic weights 39, 41, 45, 47, 49, and 50 are radioactive calcium isotopes.Protein Subunits: Single chains of amino acids that are the units of multimeric PROTEINS. Multimeric proteins can be composed of identical or non-identical subunits. One or more monomeric subunits may compose a protomer which itself is a subunit structure of a larger assembly.Amlodipine: A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.Kv1.5 Potassium Channel: A delayed rectifier subtype of shaker potassium channels that conducts a delayed rectifier current. It contributes to ACTION POTENTIAL repolarization of MYOCYTES in HEART ATRIA.Agatoxins: A class of polyamine and peptide toxins which are isolated from the venom of spiders such as Agelenopsis aperta.Xenopus: An aquatic genus of the family, Pipidae, occurring in Africa and distinguished by having black horny claws on three inner hind toes.Myocardium: The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.Small-Conductance Calcium-Activated Potassium Channels: A major class of calcium-activated potassium channels that are found primarily in excitable CELLS. They play important roles in the transmission of ACTION POTENTIALS and generate a long-lasting hyperpolarization known as the slow afterhyperpolarization.Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.Action Potentials: Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Ion Transport: The movement of ions across energy-transducing cell membranes. Transport can be active, passive or facilitated. Ions may travel by themselves (uniport), or as a group of two or more ions in the same (symport) or opposite (antiport) directions.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Adenosine Triphosphate: An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.Mollusk Venoms: Venoms from mollusks, including CONUS and OCTOPUS species. The venoms contain proteins, enzymes, choline derivatives, slow-reacting substances, and several characterized polypeptide toxins that affect the nervous system. Mollusk venoms include cephalotoxin, venerupin, maculotoxin, surugatoxin, conotoxins, and murexine.Transient Receptor Potential Channels: A broad group of eukaryotic six-transmembrane cation channels that are classified by sequence homology because their functional involvement with SENSATION is varied. They have only weak voltage sensitivity and ion selectivity. They are named after a DROSOPHILA mutant that displayed transient receptor potentials in response to light. A 25-amino-acid motif containing a TRP box (EWKFAR) just C-terminal to S6 is found in TRPC, TRPV and TRPM subgroups. ANKYRIN repeats are found in TRPC, TRPV & TRPN subgroups. Some are functionally associated with TYROSINE KINASE or TYPE C PHOSPHOLIPASES.KCNQ Potassium Channels: A family of delayed rectifier voltage-gated potassium channels that share homology with their founding member, KCNQ1 PROTEIN. KCNQ potassium channels have been implicated in a variety of diseases including LONG QT SYNDROME; DEAFNESS; and EPILEPSY.Shab Potassium Channels: A subfamily of shaker potassium channels that shares homology with its founding member, Shab protein, Drosophila. They regulate delayed rectifier currents in the NERVOUS SYSTEM of DROSOPHILA and in the SKELETAL MUSCLE and HEART of VERTEBRATES.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.KCNQ1 Potassium Channel: A voltage-gated potassium channel that is expressed primarily in the HEART.Egtazic Acid: A chelating agent relatively more specific for calcium and less toxic than EDETIC ACID.Electric Stimulation: Use of electric potential or currents to elicit biological responses.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Shaw Potassium Channels: A shaker subfamily that is prominently expressed in NEURONS and are necessary for high-frequency, repetitive firing of ACTION POTENTIALS.Kv1.4 Potassium Channel: A fast inactivating subtype of shaker potassium channels that contains two inactivation domains at its N terminus.Tetrodotoxin: An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.Protein Structure, Tertiary: The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.Models, Biological: Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.Calcium Oxalate: The calcium salt of oxalic acid, occurring in the urine as crystals and in certain calculi.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Chelating Agents: Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS.Gallopamil: Coronary vasodilator that is an analog of iproveratril (VERAPAMIL) with one more methoxy group on the benzene ring.G Protein-Coupled Inwardly-Rectifying Potassium Channels: A family of inwardly-rectifying potassium channels that are activated by PERTUSSIS TOXIN sensitive G-PROTEIN-COUPLED RECEPTORS. GIRK potassium channels are primarily activated by the complex of GTP-BINDING PROTEIN BETA SUBUNITS and GTP-BINDING PROTEIN GAMMA SUBUNITS.Calcium Gluconate: The calcium salt of gluconic acid. The compound has a variety of uses, including its use as a calcium replenisher in hypocalcemic states.Shal Potassium Channels: A shaker subfamily of potassium channels that participate in transient outward potassium currents by activating at subthreshold MEMBRANE POTENTIALS, inactivating rapidly, and recovering from inactivation quickly.Presynaptic Terminals: The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the central and peripheral nervous systems are included.Magnesium: A metallic element that has the atomic symbol Mg, atomic number 12, and atomic weight 24.31. It is important for the activity of many enzymes, especially those involved in OXIDATIVE PHOSPHORYLATION.Fura-2: A fluorescent calcium chelating agent which is used to study intracellular calcium in tissues.Peptides: Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.Thapsigargin: A sesquiterpene lactone found in roots of THAPSIA. It inhibits CA(2+)-TRANSPORTING ATPASE mediated uptake of CALCIUM into SARCOPLASMIC RETICULUM.Heart: The hollow, muscular organ that maintains the circulation of the blood.KCNQ2 Potassium Channel: A very slow opening and closing voltage-gated potassium channel that is expressed in NEURONS and is commonly mutated in BENIGN FAMILIAL NEONATAL CONVULSIONS.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels: A subgroup of cyclic nucleotide-regulated ION CHANNELS of the superfamily of pore-loop cation channels that are opened by hyperpolarization rather than depolarization. The ion conducting pore passes SODIUM, CALCIUM, and POTASSIUM cations with a preference for potassium.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.Tetraethylammonium: A potassium-selective ion channel blocker. (From J Gen Phys 1994;104(1):173-90)Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme UREASE.Neurotransmitter Agents: Substances used for their pharmacological actions on any aspect of neurotransmitter systems. Neurotransmitter agents include agonists, antagonists, degradation inhibitors, uptake inhibitors, depleters, precursors, and modulators of receptor function.Biophysics: The study of PHYSICAL PHENOMENA and PHYSICAL PROCESSES as applied to living things.Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Lanthanum: Lanthanum. The prototypical element in the rare earth family of metals. It has the atomic symbol La, atomic number 57, and atomic weight 138.91. Lanthanide ion is used in experimental biology as a calcium antagonist; lanthanum oxide improves the optical properties of glass.Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to CADMIUM POISONING.Scorpion Venoms: Venoms from animals of the order Scorpionida of the class Arachnida. They contain neuro- and hemotoxins, enzymes, and various other factors that may release acetylcholine and catecholamines from nerve endings. Of the several protein toxins that have been characterized, most are immunogenic.Muscles: Contractile tissue that produces movement in animals.Nisoldipine: A dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina.NAV1.5 Voltage-Gated Sodium Channel: A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of CARDIOMYOCYTES. Defects in the SCN5A gene, which codes for the alpha subunit of this sodium channel, are associated with a variety of CARDIAC DISEASES that result from loss of sodium channel function.Hippocampus: A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Intermediate-Conductance Calcium-Activated Potassium Channels: A major class of calcium-activated potassium channels that were originally discovered in ERYTHROCYTES. They are found primarily in non-excitable CELLS and set up electrical gradients for PASSIVE ION TRANSPORT.Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.Synaptic Transmission: The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.KCNQ3 Potassium Channel: A very slow opening and closing voltage-gated potassium channel that is expressed in NEURONS and is closely related to KCNQ2 POTASSIUM CHANNEL. It is commonly mutated in BENIGN FAMILIAL NEONATAL CONVULSIONS.Large-Conductance Calcium-Activated Potassium Channel alpha Subunits: The pore-forming subunits of large-conductance calcium-activated potassium channels. They form tetramers in CELL MEMBRANES.Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as CATIONS; those with a negative charge are ANIONS.Ganglia, Spinal: Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.Hydrogen-Ion Concentration: The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Cations: Positively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis.Nerve Tissue ProteinsInositol 1,4,5-Trisphosphate Receptors: Intracellular receptors that bind to INOSITOL 1,4,5-TRISPHOSPHATE and play an important role in its intracellular signaling. Inositol 1,4,5-trisphosphate receptors are calcium channels that release CALCIUM in response to increased levels of inositol 1,4,5-trisphosphate in the CYTOPLASM.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.Ryanodine: A methylpyrrole-carboxylate from RYANIA that disrupts the RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL to modify CALCIUM release from SARCOPLASMIC RETICULUM resulting in alteration of MUSCLE CONTRACTION. It was previously used in INSECTICIDES. It is used experimentally in conjunction with THAPSIGARGIN and other inhibitors of CALCIUM ATPASE uptake of calcium into SARCOPLASMIC RETICULUM.Delayed Rectifier Potassium Channels: A group of slow opening and closing voltage-gated potassium channels. Because of their delayed activation kinetics they play an important role in controlling ACTION POTENTIAL duration.Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.NAV1.2 Voltage-Gated Sodium Channel: A voltage-gated sodium channel subtype that mediates the sodium ion permeability of excitable membranes. Defects in the SCN2A gene which codes for the alpha subunit of this sodium channel are associated with benign familial infantile seizures type 3, and early infantile epileptic encephalopathy type 11.Voltage-Gated Sodium Channels: A family of membrane proteins that selectively conduct SODIUM ions due to changes in the TRANSMEMBRANE POTENTIAL DIFFERENCE. They typically have a multimeric structure with a core alpha subunit that defines the sodium channel subtype and several beta subunits that modulate sodium channel activity.Chlorides: Inorganic compounds derived from hydrochloric acid that contain the Cl- ion.Myocytes, Cardiac: Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).Cell Membrane Permeability: A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.Charybdotoxin: A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.OxadiazolesLipid Bilayers: Layers of lipid molecules which are two molecules thick. Bilayer systems are frequently studied as models of biological membranes.Biophysical Phenomena: The physical characteristics and processes of biological systems.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Intracellular Fluid: The fluid inside CELLS.Animals, Newborn: Refers to animals in the period of time just after birth.Cytosol: Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.Strontium: An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62.Flunarizine: Flunarizine is a selective calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity. It is effective in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy.Calcimycin: An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.HEK293 Cells: A cell line generated from human embryonic kidney cells that were transformed with human adenovirus type 5.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.GTP-Binding Proteins: Regulatory proteins that act as molecular switches. They control a wide range of biological processes including: receptor signaling, intracellular signal transduction pathways, and protein synthesis. Their activity is regulated by factors that control their ability to bind to and hydrolyze GTP to GDP. EC 3.6.1.-.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Fluorescent Dyes: Agents that emit light after excitation by light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags.Calcium Compounds: Inorganic compounds that contain calcium as an integral part of the molecule.Protein Isoforms: Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.4-Aminopyridine: One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Cyclic AMP: An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.Cations, Divalent: Positively charged atoms, radicals or groups of atoms with a valence of plus 2, which travel to the cathode or negative pole during electrolysis.Apamin: A highly neurotoxic polypeptide from the venom of the honey bee (Apis mellifera). It consists of 18 amino acids with two disulfide bridges and causes hyperexcitability resulting in convulsions and respiratory paralysis.Protein Kinase C: An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.Cyclic AMP-Dependent Protein Kinases: A group of enzymes that are dependent on CYCLIC AMP and catalyze the phosphorylation of SERINE or THREONINE residues on proteins. Included under this category are two cyclic-AMP-dependent protein kinase subtypes, each of which is defined by its subunit composition.Calcium-Binding Proteins: Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins, or activator proteins. They typically contain EF HAND MOTIFS.Potassium Chloride: A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.Receptors, Drug: Proteins that bind specific drugs with high affinity and trigger intracellular changes influencing the behavior of cells. Drug receptors are generally thought to be receptors for some endogenous substance not otherwise specified.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Felodipine: A dihydropyridine calcium antagonist with positive inotropic effects. It lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Mutagenesis, Site-Directed: Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.Sulfonylurea Receptors: ATP-BINDING CASSETTE PROTEINS that are highly conserved and widely expressed in nature. They form an integral part of the ATP-sensitive potassium channel complex which has two intracellular nucleotide folds that bind to sulfonylureas and their analogs.Muscle, Smooth: Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)Cerebellum: The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.Cricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.Sarcolemma: The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.NAV1.4 Voltage-Gated Sodium Channel: A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of SKELETAL MYOCYTES. Defects in the SCN4A gene, which codes for the alpha subunit of this sodium channel, are associated with several MYOTONIC DISORDERS.Voltage-Dependent Anion Channels: A family of voltage-gated eukaryotic porins that form aqueous channels. They play an essential role in mitochondrial CELL MEMBRANE PERMEABILITY, are often regulated by BCL-2 PROTO-ONCOGENE PROTEINS, and have been implicated in APOPTOSIS.Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable.Extracellular Space: Interstitial space between cells, occupied by INTERSTITIAL FLUID as well as amorphous and fibrous substances. For organisms with a CELL WALL, the extracellular space includes everything outside of the CELL MEMBRANE including the PERIPLASM and the cell wall.Dogs: The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)Azetidinecarboxylic Acid: A proline analog that acts as a stoichiometric replacement of proline. It causes the production of abnormal proteins with impaired biological activity.Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.Mice, Inbred C57BLReceptors, Nicotinic: One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.

Activation of human D3 dopamine receptor inhibits P/Q-type calcium channels and secretory activity in AtT-20 cells. (1/3011)

The D3 dopamine receptor is postulated to play an important role in the regulation of neurotransmitter secretion at both pre- and postsynaptic terminals. However, this hypothesis and the underlying mechanisms remain untested because of the lack of D3-selective ligands, paucity of appropriate model secretory systems, and the weak and inconsistent coupling of D3 receptors to classical signal transduction pathways. The absence of ligands that selectively discriminate between D3 and D2 receptors in vivo precludes the study of D3 receptor function in the brain and necessitates the use of heterologous expression systems. In this report we demonstrate that activation of the human D3 dopamine receptor expressed in the AtT-20 neuroendocrine cell line causes robust inhibition of P/Q-type calcium channels via pertussis toxin-sensitive G-proteins. In addition, using the vesicle trafficking dye FM1-43, we show that D3 receptor activation significantly inhibits spontaneous secretory activity in these cells. Our results not only support the hypothesis that the D3 receptor can regulate secretory activity but also provide insight into the underlying signaling mechanisms. We propose a functional model in which the D3 receptor tightly regulates neurotransmitter release at a synapse by only allowing the propagation of spikes above a certain frequency or burst-duration threshold.  (+info)

Regulation of cardiac L-type Ca2+ channel by coexpression of G(alpha s) in Xenopus oocytes. (2/3011)

Activation of G(alpha s) via beta-adrenergic receptors enhances the activity of cardiac voltage-dependent Ca2+ channels of the L-type, mainly via protein kinase A (PKA)-dependent phosphorylation. Contribution of a PKA-independent effect of G(alpha s) has been proposed but remains controversial. We demonstrate that, in Xenopus oocytes, antisense knockdown of endogenous G(alpha s) reduced, whereas coexpression of G(alpha s) enhanced, currents via expressed cardiac L-type channels, independently of the presence of the auxiliary subunits alpha2/delta or beta2A. Coexpression of G(alpha s) did not increase the amount of alpha1C protein in whole oocytes or in the plasma membrane (measured immunochemically). Activation of coexpressed beta2 adrenergic receptors did not cause a detectable enhancement of channel activity; rather, a small cAMP-dependent decrease was observed. We conclude that coexpression of G(alpha s), but not its acute activation via beta-adrenergic receptors, enhances the activity of the cardiac L-type Ca2+ channel via a PKA-independent effect on the alpha1C subunit.  (+info)

Local control models of cardiac excitation-contraction coupling. A possible role for allosteric interactions between ryanodine receptors. (3/3011)

In cardiac muscle, release of activator calcium from the sarcoplasmic reticulum occurs by calcium- induced calcium release through ryanodine receptors (RyRs), which are clustered in a dense, regular, two-dimensional lattice array at the diad junction. We simulated numerically the stochastic dynamics of RyRs and L-type sarcolemmal calcium channels interacting via calcium nano-domains in the junctional cleft. Four putative RyR gating schemes based on single-channel measurements in lipid bilayers all failed to give stable excitation-contraction coupling, due either to insufficiently strong inactivation to terminate locally regenerative calcium-induced calcium release or insufficient cooperativity to discriminate against RyR activation by background calcium. If the ryanodine receptor was represented, instead, by a phenomenological four-state gating scheme, with channel opening resulting from simultaneous binding of two Ca2+ ions, and either calcium-dependent or activation-linked inactivation, the simulations gave a good semiquantitative accounting for the macroscopic features of excitation-contraction coupling. It was possible to restore stability to a model based on a bilayer-derived gating scheme, by introducing allosteric interactions between nearest-neighbor RyRs so as to stabilize the inactivated state and produce cooperativity among calcium binding sites on different RyRs. Such allosteric coupling between RyRs may be a function of the foot process and lattice array, explaining their conservation during evolution.  (+info)

L-type Ca2+ channels and K+ channels specifically modulate the frequency and amplitude of spontaneous Ca2+ oscillations and have distinct roles in prolactin release in GH3 cells. (4/3011)

GH3 cells showed spontaneous rhythmic oscillations in intracellular calcium concentration ([Ca2+]i) and spontaneous prolactin release. The L-type Ca2+ channel inhibitor nimodipine reduced the frequency of Ca2+ oscillations at lower concentrations (100nM-1 microM), whereas at higher concentrations (10 microM), it completely abolished them. Ca2+ oscillations persisted following exposure to thapsigargin, indicating that inositol 1,4,5-trisphosphate-sensitive intracellular Ca2+ stores were not required for spontaneous activity. The K+ channel inhibitors Ba2+, Cs+, and tetraethylammonium (TEA) had distinct effects on different K+ currents, as well as on Ca2+ oscillations and prolactin release. Cs+ inhibited the inward rectifier K+ current (KIR) and increased the frequency of Ca2+ oscillations. TEA inhibited outward K+ currents activated at voltages above -40 mV (grouped within the category of Ca2+ and voltage-activated currents, KCa,V) and increased the amplitude of Ca2+ oscillations. Ba2+ inhibited both KIR and KCa,V and increased both the amplitude and the frequency of Ca2+ oscillations. Prolactin release was increased by Ba2+ and Cs+ but not by TEA. These results indicate that L-type Ca2+ channels and KIR channels modulate the frequency of Ca2+ oscillations and prolactin release, whereas TEA-sensitive KCa,V channels modulate the amplitude of Ca2+ oscillations without altering prolactin release. Differential regulation of these channels can produce frequency or amplitude modulation of calcium signaling that stimulates specific pituitary cell functions.  (+info)

Beta2-adrenergic receptor overexpression in the developing mouse heart: evidence for targeted modulation of ion channels. (5/3011)

1. We studied the effect of overexpression of the beta2-adrenergic receptor (beta2-AR) in the heart on ion channel currents in single cells isolated from hearts of fetal and neonatal transgenic and wild-type mice. The beta2-AR transgene construct was under the control of the murine alpha-myosin heavy chain (alpha-MHC) promoter, and ion channel activity was measured at distinct developmental stages using whole-cell and perforated patch clamp techniques. 2. We found no change in L-type Ca2+ channel current (ICa) density in early embryonic stages (E11-13) of beta2-AR transgenic positive (TG+) mice, but significant increases in ICa density in intermediate (E14-16, 152 %) and late (E17-19, 173.7 %) fetal and neonatal (1 day post partum, 161 %) TG+ compared with transgenic negative (TG-) mice. This increase in ICa was accompanied by a negative shift in the peak of the current-voltage relationship in TG+ mice. 3. Transient (< 3 min) or prolonged (16-24 h) exposure of TG- neonatal stage myocytes to 8-Br-cAMP (300 microM) increased ICa density and caused a shift in the current-voltage relationship to a similar extent to that seen in TG+ mice. In TG+ myocytes, 8-Br-cAMP had no effect. Exposure of TG+ cells to Rp-cAMPS reversed both the shift in voltage dependence and reduced the peak current density observed in these myocytes. We concluded from these results that the L-type Ca2+ channel is maximally modulated by cAMP-dependent protein kinase (PKA) in TG+ mice and that the alpha-MHC promoter is functional in the ventricle as early as embryonic day 14. 4. In contrast, we found that slow delayed rectifier K+ channels were not changed significantly at any of the developmental stages studied by the overexpression of beta2-ARs compared with TG- mice. The sensitivity of murine slow delayed rectifier K+ channels to cAMP was tested by both transient and prolonged exposure to 8-Br-cAMP (300 microM), which increased the slow delayed rectifier K+ channel current (IK,s) density to a similar extent in both TG- and TG+ neonatal myocytes. In addition, we found that there was no difference in the concentration dependence of the response of ICa and IK,s to 8-Br-cAMP. 5. Thus, overexpression of the beta2-AR in the heart results in distinct modulation of ICa, but not IK,s, and this is not due to differences in the 8-Br-cAMP sensitivity of the two channels. Instead, these results are consistent with both compartmentalization of beta2-AR-controlled cAMP and distinct localization of L-type Ca2+ and slow delayed rectifier K+ channels. This cAMP is targeted preferentially to the L-type Ca2+ channel and is not accessible to the slow delayed rectifier K+ channel.  (+info)

Relationship between L-type Ca2+ current and unitary sarcoplasmic reticulum Ca2+ release events in rat ventricular myocytes. (6/3011)

1. The time courses of Ca2+ current and Ca2+ spark occurrence were determined in single rat ventricular myocytes voltage clamped with patch pipettes containing 0.1 microM fluo-3. Acquisition of line-scan images on a laser scanning confocal microscope was synchronized with measurement of Cd2+-sensitive Ca2+ currents. In most cells, individual Ca2+ sparks were observed by reducing Ca2+ current density with nifedipine (0.1-8 microM). 2. Ca2+ sparks elicited by depolarizing voltage-clamp pulses had a peak [Ca2+] amplitude of 289 +/- 3 nM with a decay half-time of 20.8 +/- 0.2 ms and a full width at half-maximum of 1.40 +/- 0.03 microm (mean +/- s. e.m., n = 345), independent of the membrane potential. 3. The time between the beginning of a depolarization and the initiation of each Ca2+ spark was calculated and data were pooled to construct waiting time histograms. Exponential functions were fitted to these histograms and to the decaying phase of the Ca2+ current. This analysis showed that the time constants describing Ca2+ current and Ca2+ spark occurrence at membrane potentials between -30 mV and +30 mV were not significantly different. At +50 mV, in the absence of nifedipine, the time constant describing Ca2+ spark occurrence was significantly larger than the time constant of the Ca2+ current. 4. A simple model is developed using Poisson statistics to relate macroscopic Ca2+ current to the opening of single L-type Ca2+ channels at the dyad junction and to the time course of Ca2+ spark occurrence. The model suggests that the time courses of macroscopic Ca2+ current and Ca2+ spark occurrence should be closely related when opening of a single L-type Ca2+ channel initiates a Ca2+ spark. By comparison with the data, the model suggests that Ca2+ sparks are initiated by the opening of a single L-type Ca2+ channel at all membrane potentials encountered during an action potential.  (+info)

Kinetics of inactivation and restoration from inactivation of the L-type calcium current in human myotubes. (7/3011)

1. Inactivation and recovery kinetics of L-type calcium currents were measured in myotubes derived from satellite cells of human skeletal muscle using the whole cell patch clamp technique. 2. The time course of inactivation at potentials above the activation threshold was obtained from the decay of the current during 15 s depolarizing pulses. At subthreshold potentials, prepulses of different durations, followed by +20 mV test pulses, were used. The time course could be well described by single exponential functions of time. The time constant decreased from 17.8 +/- 7.5 s at -30 mV to 1.78 +/- 0.15 s at +50 mV. 3. Restoration from inactivation caused by 15 s depolarization to +20 mV was slowed by depolarization in the restoration interval. The time constant increased from 1.11 +/- 0.17 s at -90 mV to 7.57 +/- 2.54 s at -10 mV. 4. Restoration showed different kinetics depending on the duration of the conditioning depolarization. While the time constant was similar at restoration potentials of -90 and -50 mV after a 1 s conditioning prepulse, it increased with increasing prepulse duration at -50 mV and decreased at -90 mV. 5. The experiments showed that the rates of inactivation and restoration of the L-type calcium current in human myotubes were not identical when observed at the same potential. The results indicate the presence of more than one inactivated state and point to different voltage-dependent pathways for inactivation and restoration.  (+info)

Diazepam-binding inhibitor33-50 elicits Ca2+ oscillation and CCK secretion in STC-1 cells via L-type Ca2+ channels. (8/3011)

We recently isolated and characterized 86-amino acid CCK-releasing peptide from porcine intestinal mucosa. The sequence of this peptide is identical to that of porcine diazepam-binding inhibitor (DBI). Intraduodenal administration of DBI stimulates the CCK release and elicits pancreatic secretion in rats. In this study we utilized a murine tumor cell line (STC-1 cells) that contains CCK to examine if DBI directly acts on these cells to stimulate CCK release. We investigated the cellular mechanisms responsible for this action. We showed that DBI33-50, a biologically active fragment of DBI1-86, significantly stimulated CCK secretion in STC-1 cells. This action was abolished by Ca2+-free medium. The mean basal intracellular Ca2+ concentration ([Ca2+]i) was 52 nM in fura 2-loaded STC-1 cells. DBI33-50 (1-1,000 nM) elicited Ca2+ oscillations; DBI33-50 (10 nM) increased the oscillation frequency to 5 cycles/10 min and elicited a net [Ca2+]i increase (peak - basal) to 157 nM. In contrast, bombesin and forskolin caused an initial transient [Ca2+]i followed by a small sustained [Ca2+]i plateau. Withdrawal of extracellular Ca2+ abolished Ca2+ oscillations stimulated by DBI33-50. L-type Ca2+ channel blockers nifedipine and diltiazem (3-10 microM) markedly attenuated DBI-stimulated Ca2+ oscillations. In other cell types L-type Ca2+ channels are activated by cAMP-protein kinase A. DBI33-50 failed to stimulate cAMP formation in STC-1 cells. Similarly, DBI33-50 had no effect on myo-inositol 1,4, 5-trisphosphate concentration ([IP3]), whereas bombesin caused an eightfold increase in [IP3] over basal. In addition, inhibitors of phospholipase C (U-73122), phospholipase A2 (ONO-RS-082), and protein tyrosine kinase (genistein) did not alter the Ca2+ oscillations elicited by DBI33-50. It appears that DBI33-50 acts directly on STC-1 cells to elicit Ca2+ oscillations via the voltage-dependent L-type Ca2+ channels, resulting in the secretion of CCK. Mediation of this action is by intracellular mechanisms independent of the traditional signal transduction pathways, including phospholipase C, phospholipase A2, protein tyrosine kinase, and cAMP systems.  (+info)

*R-type calcium channel

The R-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the α1 subunit forms ... "Entrez Gene: CACNA1E calcium channel, voltage-dependent, R type, alpha 1E subunit". Soong TW, Stea A, Hodson CD, Dubel SJ, ... This α1 subunit is also known as the calcium channel, voltage-dependent, R type, alpha 1E subunit (CACNA1E) or Cav2.3 which in ... They are poorly understood, but like Q-type calcium channels, they appear to be present in cerebellar granule cells. They have ...

*Q-type calcium channel

The Q-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the α1 subunit is the ... They are poorly understood, but like R-type calcium channels, they appear to be present in cerebellar granule cells. They have ... Q-Type Calcium Channel at the US National Library of Medicine Medical Subject Headings (MeSH). ... one that determines most of the channel's properties. ...

*P-type calcium channel

The P-type calcium channel is a type of voltage-dependent calcium channel. Similar to many other high-voltage-gated calcium ... P-type calcium channels play a similar role to the N-type calcium channel in neurotransmitter release at the presynaptic ... There are many different types of calcium channels, so to prove that the P/Q type calcium channels are directly involved, a P/Q ... corresponds to what is functionally defined as the P-type and Q-type isoforms. P-type and Q-type calcium channels are closely ...

*T-type calcium channel

Long-Lasting calcium channels). The new T-type channels were much different from the L-type calcium channels due to their ... T-type calcium channels are low-voltage activated calcium channels that open during membrane depolarization. These channels aid ... Calcium channel blockers (CCB) such as mibefradil can also block L-type calcium channels, other enzymes, as well as other ... Novel T-type calcium channel inhibitors have recently been discovered which more selectively target the CaV3.3 channel sub-type ...

*N-type calcium channel

... which is also similar to another type of calcium channels, known as P-type calcium channels. N-type calcium channels are ... N-type calcium channels are voltage gated calcium channels that are distributed throughout the entire body. These channels are ... The inhibition of this channel by calcium channel blockers can lead to renal microcirculation. N-type calcium channels have ... N-type calcium channels have known functions in the kidney, and heart. There are many known N-type calcium channel blockers, ...

*L-type calcium channel

The L-type calcium channel (also known as the dihydropyridine channel, or DHP channel) is part of the high-voltage activated ... This channel has four subunits (Cav1.1, Cav1.2, Cav1.3, Cav1.4). L-type calcium channels are responsible for the excitation- ... In cardiac myocytes, the L-type calcium channel passes inward Ca2+ current and triggers calcium release from the sarcoplasmic ... Rossier, Michel F. (2016). "T-Type Calcium Channel: A Privileged Gate for Calcium Entry and Control of Adrenal Steroidogenesis ...

*Calcium channel

the receptor-operated calcium channels (in vasoconstriction) P2X receptors L-type calcium channel blockers are used to treat ... T-type calcium channel blockers are used to treat epilepsy. Increased calcium conductance in the neurons leads to increased ... A calcium channel is an ion channel which shows selective permeability to calcium ions. It is sometimes synonymous as voltage- ... "calcium channel" at Dorland's Medical Dictionary Striggow F, Ehrlich BE (August 1996). "Ligand-gated calcium channels inside ...

*Calcium channel blocker

N-type, L-type, and T-type voltage-dependent calcium channels are present in the zona glomerulosa of the human adrenal, and ... Calcium channel blockers (CCB), calcium channel antagonists or calcium antagonists are several medications that disrupt the ... may increase or enhance the effects of calcium channel blockade. N-type calcium channels are found in neurons and are involved ... Calcium channel blockers prevent or reduce the opening of these channels and thereby reduce these effects. Several types of ...

*Calcium-induced calcium release

When an action potential depolarizes the cell membrane, voltage-gated Ca2+ channels (e.g., L-type calcium channels) are ... Calcium-induced calcium release (CICR) describes a biological process whereby calcium is able to activate calcium release from ... Fabiato, A. (1983). "Calcium-induced calcium release from the cardiac sarcoplasmic reticulum". American Journal of Physiology. ... Endo, M (1977). "Calcium release from the sarcoplasmic reticulum". Physiological Reviews. 57 (1): 71-108. PMID 13441. ...

*Cav1.2

"Osteoprotegerin expression and secretion are regulated by calcium influx through the L-type voltage-sensitive calcium channel ... This gene encodes an alpha-1 subunit of a voltage-dependent calcium channel. Calcium channels mediate the influx of calcium ... Calcium channel, voltage-dependent, L type, alpha 1C subunit (also known as Cav1.2) is a protein that in humans is encoded by ... Berger SM, Bartsch D (Aug 2014). "The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and ...

*Childhood absence epilepsy

"Molecular characterization of T-type calcium channels". Cell Calcium. 40 (2): 89-96. doi:10.1016/j.ceca.2006.04.012. PMID ... Seizures are believed to originate in the thalamus, where there is an abundance of T-type calcium channels such as those ... a T-type calcium channel". J Neurosci. 25 (19): 4844-55. doi:10.1523/JNEUROSCI.0847-05.2005. PMID 15888660. Liang J, Zhang Y, ... "Gating effects of mutations in the Cav3.2 T-type calcium channel associated with childhood absence epilepsy". J Biol Chem. 279 ...

*Calcium channel opener

A calcium channel opener is a type of drug which facilitates ion transmission through calcium channels. An example is Bay K8644 ... mucolipin TRP channels (TRPMLs) and purinergic receptors of the P2X channel type. Calcium channel blocker Schramm M, Thomas G, ... Calcium permeable ion channels in lysosomal membranes that may be activated by a luminal pH increase include two pore channels ... which is an analogue of nifedipine that specifically and directly activates L-type voltage-dependent calcium channels. In ...

*CACNA1B

The voltage-dependent N-type calcium channel subunit alpha-1B is a protein that in humans is encoded by the CACNA1B gene. ... subunits for the calcium channel I-II linker in relation to calcium channel function". The Journal of Physiology. 574 (Pt 2): ... Maximov A, Bezprozvanny I (Aug 2002). "Synaptic targeting of N-type calcium channels in hippocampal neurons". The Journal of ... Calabrese B, Tabarean IV, Juranka P, Morris CE (Nov 2002). "Mechanosensitivity of N-type calcium channel currents". Biophysical ...

*CACNG3

Voltage-dependent calcium channel gamma-3 subunit is a protein that in humans is encoded by the CACNG3 gene. L-type calcium ... This gene is a member of the neuronal calcium channel gamma subunit gene subfamily of the PMP-22/EMP/MP20 family. This gene is ... "Entrez Gene: CACNG3 calcium channel, voltage-dependent, gamma subunit 3". Powers PA, Liu S, Hogan K, Gregg RG (1993). " ... It is an integral membrane protein that is thought to stabilize the calcium channel in an inactive (closed) state. This protein ...

*CACNG1

Voltage-dependent calcium channel gamma-1 subunit is a protein that in humans is encoded by the CACNG1 gene. L-type calcium ... 1993). "Localization of the gamma-subunit of the skeletal muscle L-type voltage-dependent calcium channel gene (CACNLG) to ... and gamma-subunits of the human skeletal muscle L-type voltage-dependent calcium channel on chromosome 17q and exclusion as ... This gene is a member of the neuronal calcium channel gamma subunit gene subfamily of the PMP-22/EMP/MP20 family and is located ...

*CACNG4

Voltage-dependent calcium channel gamma-4 subunit is a protein that in humans is encoded by the CACNG4 gene. L-type calcium ... This gene is a member of the neuronal calcium channel gamma subunit gene subfamily of the PMP-22/EMP/MP20 family and is located ... "Entrez Gene: CACNG4 calcium channel, voltage-dependent, gamma subunit 4". Gerhard DS, Wagner L, Feingold EA, et al. (2004). " ... Voltage-dependent calcium channel GRCh38: Ensembl release 89: ENSG00000075461 - Ensembl, May 2017 GRCm38: Ensembl release 89: ...

*CACNG2

L-type calcium channels are composed of five subunits. The protein encoded by this gene represents one of these subunits, gamma ... Calcium channel, voltage-dependent, gamma subunit 2, also known as CACNG2 or stargazin is a protein that in humans is encoded ... This gene is a member of the neuronal calcium channel gamma subunit gene subfamily of the PMP-22/EMP/MP20 family. Stargazin is ... It is an integral membrane protein that is thought to stabilize the calcium channel in an inactive (closed) state. This protein ...

*Neuromuscular junction

Proximal muscle weakness is a product of pathogenic autoantibodies directed against P/Q-type voltage-gated calcium channels, ... which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor ... This type of tumor also expresses voltage-gated calcium channels. Oftentimes, LEMS also occurs alongside myasthenia gravis. ... Upon the arrival of an action potential at the presynaptic neuron terminal, voltage-dependent calcium channels open and Ca2+ ...

*Low-threshold spikes

The T-type calcium channel is found in neurons throughout the brain. These channels produce particularly large currents in ... Recent research has also been conducted on the T-type calcium channel and how modulation of these channels may allow for the ... Antiepileptic drugs can control absence seizures by inhibiting the T-type calcium channels which prevents low-voltage calcium ... T-type calcium channels have been known to play a role in the spike-and-wave discharges of absence seizures. ...

*BRL-32872

Structural model for phenylalkylamine binding to L-type calcium channels. The Journal of Biological Chemistry, 284(41), 28332- ... The drug targets L-type Ca+2 channels, and decreases conduction in cells where Ca+2 is required for action potential upstroke ( ... 1995). Electrophysiological effect of BRL-32872, a novel antiarrhythmic agent with potassium and calcium channel blocking ... BRL-32872's class III activity is directed towards the human ether-a-go-go-related gene (hERG) K+ channel. hERG channels are ...

*Timothy syndrome

... type-1) and atypical (type-2). They are both caused by mutations in CACNA1C, the gene encoding the calcium channel Cav1.2 α ... "Severe arrhythmia disorder caused by cardiac L-type calcium channel mutations". Proc Natl Acad Sci USA. 102 (23): 8089-8096. ... Cav1.2 Calcium channel Marks M, Whisler S, Clericuzio C, Keating M (1995). "A new form of long QT syndrome associated with ... However, it was linked with calcium channel abnormalities in 2004, and the disorder was thence named "Timothy syndrome" in ...

*Efonidipine

... calcium channel blocker, inhibits both L-type and T-type calcium channels. Efonidipine exhibits antihypertensive effect through ... It was launched in 1995, under the brand name Landel (ランデル). The drug blocks both T-type and L-type calcium channels. Drug ... Efonidipine is a dual Calcium Channel Blocker (L & T-type). It has a unique chemical structure. The phosphonate moiety (Figure ... Working on sino atrial node cells by inhibiting T-type calcium channel activation, Efonidipine prolongs the late phase-4 ...

*Bay K8644

Calcium Channels (L-Type). It is the first positive inotropic agent shown to act specifically and directly on calcium channels ... Bay K8644 is a chemical compound that functions as a calcium channel agonist. Bay K8644 is used primarily as a biochemical ... that enhances calcium currents in guinea pig and calf myocardial cells. A new type of positive inotropic agent". Circ Res. 56: ...

*Ical

... an ionic current through the L-type calcium channel. ...

*AH-1058

... is a cardioselective L-type calcium channel blocker. AH-1058 binds to the same sites on the alpha-1 subunit of L-type ... These sites on the alpha-1 subunit differ from the active site of the calcium channel, meaning AH-1058 binds L-type calcium ... L-type calcium channel blockers). Class I antiarrhythmic (sodium channel blocker) characteristics have also been seen, but the ... In addition AH-1058 appears to interact with multiple states of L-type calcium channels (i.e. resting and inactive) to suppress ...

*Metabolism

For example, muscle contraction depends upon the movement of calcium, sodium and potassium through ion channels in the cell ... Reaction centers are classed into two types depending on the type of photosynthetic pigment present, with most photosynthetic ... Three types of photosynthesis occur in plants, C3 carbon fixation, C4 carbon fixation and CAM photosynthesis. These differ by ... Hundreds of separate types of dehydrogenases remove electrons from their substrates and reduce NAD+ into NADH. This reduced ...
Read "Ca2+ Calmodulin Kinase and Calcineurin Mediate IGF-1-induced Skeletal Muscle Dihydropyridine Receptor α1S Transcription, The Journal of Membrane Biology" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Headline: Bitcoin & Blockchain Searches Exceed Trump! Blockchain Stocks Are Next!. "L-Type Calcium Channel Blockers-Pipeline Insights, 2016″, report provides in depth insights on the pipeline drugs and their development activities around the L-Type Calcium Channel Blockers. The Report covers the product profiles in various stages of development including Discovery, Pre-clinical, IND, Phase I, Phase II, Phase III and Preregistration. Report covers the product clinical trials information and other development activities including technology, licensing, collaborations, acquisitions, fundings, patent and USFDA & EMA designations details. Report also provides detailed information on the discontinued and dormant drugs that have gone inactive over the years for L-Type Calcium Channel Blockers. Report also assesses the L-Type Calcium Channel Blockers therapeutics by Monotherapy, Combination products, Molecule type and Route of Administration.. For more information about this report: ...
Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1S gives rise to L-type calcium currents. Long-lasting (L-type) calcium channels belong to the high-voltage activated (HVA) group. They are blocked by dihydropyridines (DHP), phenylalkylamines, benzothiazepines, and by omega-agatoxin-IIIA (omega-Aga-IIIA). They are however insensitive to omega-conotoxin-GVIA (omega-CTx-GVIA) and omega-agatoxin-IVA (omega-Aga-IVA). Calcium channels containing the alpha-1S subunit play an important role in excitation-contraction coupling in skeletal muscle ...
Astrocytes are activated by ciliary neurotrophic factor (CNTF) in vivo and in vitro, however, the consequences on the L-type calcium channel (LCC) of neurons are still poorly understood. Therefore, in the present study, whole-cell patch clamp, western-blot and RT-PCR assay were performed to evaluate the effects of CNTF-treated astrocyte conditioned medium (CNTF-ACM) on LCC current (I(Ca)-L) and the expression of Cav1.2 and Cav1.3 in Sprague-Dawley rat cortical neurons. The results revealed that CNTF-ACM enhanced the amplitude of Ica-L and the expression of Cav1.3 significantly, but had no effects on Cav1.2 expression. We also found an increase in the concentration of fibroblast growth factor-2 (FGF-2) in CNTF-ACM by ELISA assay. Taken together, these findings indicate that CNTF induces the release of factors, including FGF-2, from astrocytes, thereby potentiating the activity of LCC in cortical neurons.. ...
L-type (CaV1.2) voltage-gated calcium channels play critical roles in membrane excitability, gene expression, cardiac and smooth muscle contraction. Alternative splicing enriches the functional diversity of the pore-forming CaV1.2 alpha-1 subunit. Systematic screening of the human CaV1.2 alpha-1 gene by the transcript-scanning method revealed 19 of the 55 exons were subjected to alternative splicing, and two of these were novel exons. A large IVS3-S4 variability resulting from combinatorial utilization of exons 31-33 demonstrated a correlation between increased IVS3-S4 linker length and more depolarized activation potentials.Sixty-four splicing profiles of CaV1.2 alpha-1 subunit were identified from 6 full-length cDNA libraries generated from heart and aortic tissues of the Spontaneously Hypertensive Rats and Wistar Kyoto Rats. The tissue-selective and pathologically induced splicing profiles of 10 alternatively spliced exons assessed indicated a striking alteration in exon utilization and ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
TY - JOUR. T1 - Angiotensin II increases expression of α1C subunit of L-type calcium channel through a reactive oxygen species and cAMP response element-binding protein-dependent pathway in HL-1 myocytes. AU - Tsai, Chia Ti. AU - Wang, Danny Ling. AU - Chen, Wen Pin. AU - Hwang, Juey Jen. AU - Hsieh, Chia Shan. AU - Hsu, Kuan Lih. AU - Tseng, Chuen Den. AU - Lai, Ling Ping. AU - Tseng, Yung Zu. AU - Chiang, Fu Tien. AU - Lin, Jiunn Lee. PY - 2007/5/1. Y1 - 2007/5/1. N2 - Angiotensin II (Ang II) is involved in the pathogenesis of atrial fibrillation (AF). L-type calcium channel (LCC) expression is altered in AF remodeling. We investigated whether Ang II modulates LCC current through transcriptional regulation, by using murine atrial HL-1 cells, which have a spontaneous calcium transient, and an in vivo rat model. Ang II increased LCC α1C subunit mRNA and protein levels and LCC current density, which resulted in an augmented calcium transient in atrial myocytes. An ≈2-kb promoter region of LCC ...
Red-fluorescing cells were visualized on an Olympus 1×51 fluorescent microscope (Olympus, Center Valley, PA). Whole-cell currents were recorded with an Axopatch 200A amplifier (Molecular Devices, Sunnyvale, CA). Data were sampled at 2 to 10 kHz, low pass-filtered at 1 kHz, and analyzed using pClamp v9.2 (Molecular Devices). After pipette and membrane capacitance compensation, the series resistance was corrected by 80 to 90% with a 20- to 100-μs lag time. Cells with a series resistance greater than 20 MΩ were not used for analysis. After whole-cell break-in, Ba2+ currents were elicited in voltage-clamp mode by stepping from a holding potential (Vh) of −80 mV to test potentials (Vt) of 0 (Cav1.2) or −25 mV (Cav1.3) for 200 ms. Current rundown, plotted as total charge transfer elicited at 10-s intervals (or higher frequencies, as indicated), was fitted with a one- or two-phase exponential decay curve. Recordings using this protocol were not leak-subtracted.. Drugs were applied by gravity ...
The present study demonstrated that the opening of the L-type Ca2+ channels was increased in arterial smooth muscle cells from SHR compared with WKY. However, the single-channel conductance and open time did not differ between SHR and WKY. Thus, an increased opening of the single channels would contribute greatly to the increased amplitude of the whole-cell current.. The unitary inward current recorded in the present study was considered to be L-type Ca2+ channel currents from the following findings: (1) single-channel conductance and open time were basically the same as those of the L-type Ca2+ channel in other arterial tissues studied10,11,13; (2) the holding potential was −40 mV, which inactivated the T-type Ca2+ channels as well as Na+ channels10; and (3) the channel opening disappeared with the application of nifedipine, suggesting that the channel is sensitive to dihydropyridines.10 11 Whole-cell amplitude (I) consisted of several parameters, such as the amplitude of the single-channel ...
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With PDEs inactivated by IBMX, we assume that there are two pathways for inhibition of ICa(L) by cGMP/PKG, namely, phosphorylation of the α1c subunit that antagonizes the stimulant effect of cAMP/PKA and/or activation of PP that dephosphorylates the α1c subunit. Can 8-Br-cGMP or CCh suppress Ca2+ current through L-type channels in the presence of ATPγS, which allows kinases to thiophosphorylate substrates that resist phosphatase action? Irreversible suppression by 8-Br-cGMP would indicate that thiophosphorylation of the channel had occurred at a site different from that acted upon by cAMP/PKA (Méry et al., 1991; Sumii and Sperelakis, 1995). Alternatively, failure of 8-Br-cGMP to suppress ICa(L) in ATPγS would indicate that the thiophosphorylated channel was resistant to phosphatase. Our results are consistent with the PP hypothesis for inhibition by cGMP of current through L-type channels in guinea pig ventricular myocytes.. Neurotransmitter regulation of ICa(L) by reversible ...
BioAssay record AID 1084627 submitted by ChEMBL: Inhibition of L-type calcium channel in Rattus norvegicus Wistar (rat) thoracic aorta assessed as relaxation of KCl-induced vasoconstriction at 10-11 M after 30 min relative to control.
We have found that phospholemman (PLM) associates with and modulates the gating of cardiac L-type calcium channels (Wang et al., Biophys J 98: 1149-1159, 2010). The short 17 amino acid extracellular NH2-terminal domain of PLM contains a highly conserved PFTYD sequence that defines it as a member of the FXYD family of ion transport regulators. Although we have learned a great deal about PLM-dependent changes in calcium channel gating, little is known regarding the molecular mechanisms underlying the observed changes. Therefore, we investigated the role of the PFTYD segment in the modulation of cardiac calcium channels by individually replacing Pro-8, Phe-9, Thr-10, Tyr-11, and Asp-12 with alanine (P8A, F9A, T10A, Y11A, D12A). In addition, Asp-12 was changed to lysine (D12K) and cysteine (D12C). As expected, wild-type PLM significantly slows channel activation and deactivation and enhances voltage-dependent inactivation (VDI). We were surprised to find that amino acid substitutions at Thr-10 and ...
Our study demonstrates that myocytes lacking the PTEN gene have elevated cardiac L-type Ca2+ currents accompanied by negative shifts in voltage-dependent channel activation, which were unrelated to incomplete voltage control arising from uncompensated RS. Our results further establish that the elevations in ICa,L observed in PTEN-deficient hearts occur without increases in channel expression but are eliminated by PI3K or PKB inhibitors and by dominant-negative PI3Kα suppression. These findings suggest that ICa,L enhancements and voltage shifts of ICa,L activation in PTEN-deficient myocytes result from elevated PI(3,4,5)P3 levels leading to tonic PKB activation and phosphorylation of target proteins involved in L-type Ca2+ channel regulation. These results are consistent with the conclusion that the dominant physiological function of PTEN is the breakdown of the PI3K-generated second messenger PI(3,4,5)P3 to PI(4,5)P2.21 The increases in ICa,L observed in PTEN-deficient myocytes are similar to ...
It has recently become evident that discrete clusters of L-type Ca2+ channels (LTCCs) exist along the cardiomyocyte sarcolemma in association with distinct membrane structures. Such microdomain-specific localization impact channel function and regulation by a variety of neurohormonal pathways, including adrenergic and adenosine. Disruption in their subcellular targeting may contribute to the pathophysiology of cardiac diseases, including heart failure (HF). We used Ca2+ imaging and super-resolution scanning patch clamp to examine microdomain-specific regulation of LTCCs in atrial myocytes isolated from control and 16-weeks post-MI HF rats. In control, β1 adrenergic receptors (β1ARs) stimulation (ISO 100 nM and β2AR antagonist ICI 50 nM) enhanced spontaneous Ca2+ release events while the following adenosine A1 receptors (AdoA1Rs) stimulation (2-MeCCPA 200 nM) abolished β1ARs effects. Non-localized β1ARs stimulation (ISO 2 μM and ICI 50 nM in external solution) activated single LTCCs in ...
WORKLIST ENTRIES (1): LVDCCALPHA1C View alignment Voltage-dependent L-type calcium channel alpha-1C subunit signature Type of fingerprint: COMPOUND with 13 elements Links: PRINTS; PR00167 CACHANNEL; PR01629 TVDCCALPHA1; PR01630 LVDCCALPHA1 PRINTS; PR01631 NVDCCALPHA1; PR01632 PQVDCCALPHA1; PR01633 RVDCCALPHA1 PRINTS; PR01634 LVDCCALPHA1S; PR01636 LVDCCALPHA1D Creation date 20-DEC-2001 1. WILLIAMS, M.E., BRUST, P.F., FELDMAN, D.H., PATTHI, S., SIMERSON, S., MAROUFI, A., MCCUE, A.F., VELICELBI, G., ELLIS, S.B. AND HARPOLD, M.M. Structure and functional expression of an omega-conotoxin sensitive human N-type calcium channel. SCIENCE 257 389-395 (1992). 2. MORI, Y., FRIEDRICH, T., KIM, MS., MIKAMI, A., NAKAI, J., RUTH, P., BOSSE, E., HOFMANN, F., FLOCKERZI, V., FURUICHI, T., MIKOSHIBA, K., IMOTO, K., TANABE, T. AND NUMA, S. Primary structure and functional expression from complementary DNA of a brain calcium channel. NATURE 350 398-402 (1991). 3. ASHCROFT, F.M. Voltage-gated Ca2+ channels. IN ION ...
ID M9PBC0_DROME Unreviewed; 2023 AA. AC M9PBC0; DT 26-JUN-2013, integrated into UniProtKB/TrEMBL. DT 26-JUN-2013, sequence version 1. DT 22-NOV-2017, entry version 39. DE RecName: Full=Voltage-dependent L-type calcium channel subunit alpha {ECO:0000256,RuleBase:RU003808}; GN Name=Ca-alpha1D {ECO:0000313,EMBL:AGB93018.1, GN ECO:0000313,FlyBase:FBgn0001991}; GN Synonyms=alpha1 {ECO:0000313,EMBL:AGB93018.1}, alpha1D GN {ECO:0000313,EMBL:AGB93018.1}, BG:DS02795.1 GN {ECO:0000313,EMBL:AGB93018.1}, Ca-_1D {ECO:0000313,EMBL:AGB93018.1}, GN Ca-a1D {ECO:0000313,EMBL:AGB93018.1}, Ca-alpha1 GN {ECO:0000313,EMBL:AGB93018.1}, ca-alpha1D GN {ECO:0000313,EMBL:AGB93018.1}, ca-alpha1d GN {ECO:0000313,EMBL:AGB93018.1}, Ca-alpha[[1]]D GN {ECO:0000313,EMBL:AGB93018.1}, Ca_alpha1D GN {ECO:0000313,EMBL:AGB93018.1}, Caalpha1D GN {ECO:0000313,EMBL:AGB93018.1}, cad {ECO:0000313,EMBL:AGB93018.1}, caID GN {ECO:0000313,EMBL:AGB93018.1}, DmCa1alpha1 GN {ECO:0000313,EMBL:AGB93018.1}, DmCa1D {ECO:0000313,EMBL:AGB93018.1}, GN ...
WORKLIST ENTRIES (1): LVDCCALPHA1D View alignment Voltage-dependent L-type calcium channel alpha-1D subunit signature Type of fingerprint: COMPOUND with 5 elements Links: PRINTS; PR00167 CACHANNEL; PR01629 TVDCCALPHA1; PR01630 LVDCCALPHA1 PRINTS; PR01631 NVDCCALPHA1; PR01632 PQVDCCALPHA1; PR01633 RVDCCALPHA1 PRINTS; PR01634 LVDCCALPHA1S; PR01635 LVDCCALPHA1C Creation date 20-DEC-2001 1. WILLIAMS, M.E., BRUST, P.F., FELDMAN, D.H., PATTHI, S., SIMERSON, S., MAROUFI, A., MCCUE, A.F., VELICELBI, G., ELLIS, S.B. AND HARPOLD, M.M. Structure and functional expression of an omega-conotoxin sensitive human N-type calcium channel. SCIENCE 257 389-395 (1992). 2. MORI, Y., FRIEDRICH, T., KIM, MS., MIKAMI, A., NAKAI, J., RUTH, P., BOSSE, E., HOFMANN, F., FLOCKERZI, V., FURUICHI, T., MIKOSHIBA, K., IMOTO, K., TANABE, T. AND NUMA, S. Primary structure and functional expression from complementary DNA of a brain calcium channel. NATURE 350 398-402 (1991). 3. ASHCROFT, F.M. Voltage-gated Ca2+ channels. IN ION ...
Neurons fired as the specific calcium channels at play, called L-type voltage-gated calcium channels (LTCCs), boosted the release of a neurotransmitter called GABA.
Contraction of the heart is a complex process initiated by the electrical excitation of cardiac myocytes (excitation-contraction coupling, ECC). In cardiac myocytes, Ca2+ influx induced by activation of voltage-dependent L-type Ca channels (DHP receptors) upon membrane depolarization triggers the release of Ca2+ via Ca2+ release channels (ryanodine receptors) of sarcoplasmic reticulum (SR) through a Ca2+ -induced Ca release (CICR) mechanism. Ca2+ ions released via the CICR mechanism diffuse through the cytosolic space to contractile proteins to bind to troponinC resulting in the release of inhibition induced by troponinI. The Ca2+ binding to troponinC thereby triggers the sliding of thin and thick filaments, that is, the activation of a crossbridge and subsequent cardiac force development and/or cell shortening. Recovery occurs as Ca2+ is pumped out of the cell by the Na+/Ca2+ exchanger (NCX) or is returned to the sarcoplasmic reticulum (SR) by sarco(endo)plasmic Ca2+ -ATPase (SERCA) pumps on ...
Tetrodotoxin (TTX) is believed to be one of the most selective inhibitors of voltage-gated fast Na+ channels in excitable tissues. Recently, however, TTX has been shown to block L-type Ca2+ current (ICa) in canine cardiac cells. In the present study, the TTX-sensitivity of ICa was studied in isolated canine ventricular myocytes as a function of (1) channel phosphorylation, (2) extracellular pH and (3) the redox potential of the bathing medium using the whole cell voltage clamp technique. Fifty-five micromoles of TTX (IC50 value obtained under physiological conditions) caused 60% ± 2% inhibition of ICa in acidic (pH = 6.4), while only a 26% ± 2% block in alkaline (pH = 8.4) milieu. Similarly, the same concentration of TTX induced 62% ± 6% suppression of ICa in a reductant milieu (containing glutathione + ascorbic acid + dithiothreitol, 1 mM each), in contrast to the 31% ± 3% blockade obtained in the presence of a strong oxidant (100 μM H2O2). Phosphorylation of the channel protein (induced by 3 μM
The effects of RX871024, a compound with an imidazoline structure, on cytoplasmic-free Ca2+ concentration ([Ca2+]i) in mouse pancreatic β-cells were studied. RX871024 modulates [Ca2+]i; by at least two mechanisms. One mechanism involves closure ofATPregulated K+ channels, resulting in membrane depolarization, opening of voltage-gated L-type Ca2+ channels, and a subsequent increase in [Ca2+]i. Another mechanism, reported here for the first time, deals with RX871024-induced mobilization of Ca2+ from nonmitochondrial thapsigargin-sensitive intracellular stores. Reduced glutathione, inhibitors of cytochrome P-450, and monoaminooxidases A and B blocked this Ca2+ mobilization. It is concluded that the mechanism of RX871024-induced Ca2+ mobilization from intracellular stores involves changes in the oxidation/reduction state of the pancreatic β-cell and may be controlled by cytochrome P-450.. ...
This gene encodes beta-2-adrenergic receptor which is a member of the G protein-coupled receptor superfamily. This receptor is directly associated with one of its ultimate effectors, the class C L-type calcium channel Ca(V)1.2. This receptor-channel complex also contains a G protein, an adenylyl cyclase, cAMP-dependent kinase, and the counterbalancing phosphatase, PP2A. The assembly of the signaling complex provides a mechanism that ensures specific and rapid signaling by this G protein-coupled receptor. This gene is intronless. Different polymorphic forms, point mutations, and/or downregulation of this gene are associated with nocturnal asthma, obesity and type 2 diabetes ...
Volume 148, No. 2, August 8, 2016. Pages 91-95.. In the original version of this Commentary, the following text was included in the ninth paragraph:. "Although a left shift of V1/2 upon coexpression of α2δ-1 has consistently been observed in past studies, the magnitude reported here is unprecedented. Even in earlier experiments from the Olcese laboratory, shifts of only −10 mV were reported (Platano et al., 2000). At this time, the reason for this unusually large voltage shift upon coexpression of α2δ-1 remains unknown.". After publication, the author noticed that a −50-mV shift of the voltage dependence of the tail currents in the presence of the α2δ-1 subunit, similar to that found in the paper of reference (Savalli et al., 2016), had been reported in the earlier study by Platano et al. (2000; Fig. 5 E). In contrast, the statement in our Commentary related to the shift of IV curves, which indeed is much smaller (−10 mV) than that determined from the tail currents (Platano et al., ...
Providing blood vessels at the proper situations of nationwide emergencies and war-like scenarios is normally a task towards the blood vessels transfusion companies. hemorrhage and rebuilding sufficient oxygen delivery towards the tissue. Medical procedures and control of coagulopathy must stop hemorrhage in these individuals. Resuscitation with liquids and crimson cells are essential to boost perfusion and air delivery to tissue. Once individuals are resuscitated and further bleeding is halted, use of traditional transfusion triggers is recommended to avoid excessive transfusion and adverse outcomes. A host of new systems are being developed that have the potential of reducing blood loss. These will help in reducing the transfusion requirements in stress patients with massive hemorrhage. delivery system is the need of the hour. This requires a detailed coordination between blood center and GSI-IX reversible enzyme inhibition hospital, with developed communication and info system, transportation ...
Compare calcium channel, voltage-dependent, L type, alpha 1S subunit ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
HEK293-HuCACNA1C/CACNB2/CACNA2D1 cell line is a hypotriploid human cell line, which has been transfected with a human calcium channel, voltage-dependent, L type, alpha 1C subunit (CACNA1C), a human calcium channel, voltage-dependent, alpha 2/delta subunit 1 (CACNA2D1) and a human calcium channel, voltage-dependent, beta 2 subunit (CACNB2) to allow stably express of the human CACNA1C, CACNB2, and CACNA2D1. It is an example of a cell line transfected using our proprietary CBTGS gene screening and amplificatio
PDE4 is the predominant PDE family that controls cAMP and LTCC in rodent cardiomyocytes. In the present study, we show that Pde4a, Pde4b, and Pde4d are expressed in mouse heart, but only PDE4B and PDE4D are associated with CaV1.2 channels. Whereas β-AR stimulation of ICa,L is normal in Pde4a-/- and Pde4d-/- myocytes, the β-AR responses of ICa,L, Ca2+ transients, and contraction are enhanced in myocytes from Pde4b-/- mice, and this is accompanied by an increased propensity for arrhythmia. β-AR stimulation of Ca2+ transients and contraction are also enhanced in myocytes from Pde4d-/- mice independently of ICa,L. For the first time to our knowledge, our results identify PDE4B as a major regulator of ICa,L and cardiac function and suggest that PDE4B and PDE4D regulate ECC by different mechanisms. In mouse ventricular myocytes, pharmacological inhibition of PDE4 does not affect basal ICa,L but strongly enhances the effect of β-AR stimulation (Figure 1). A similar regulation of ICa,L by PDE4 was ...
A phenomenon that has fostered much experimental investigation and theoretical speculation is "gain" in cardiac E-C coupling. So-called "macroscopic" or "whole-cell" gain may be defined as the ratio of the total flux through the SR Ca2+ release channels (RyR) to that through the L-type Ca2+ channels (LCC). Experimentally, gain was found early on to be relatively high, and this observation, together with the seemingly incompatible fact that Ca2+-induced Ca2+ release (CICR) is normally tightly controlled in cardiac muscle, led to the development of the modern understanding of cardiac E-C coupling, the "local control" theory. Gain reflects not only the operation of the fundamental processes that underlie normal E-C coupling, but also those involved in important pathological conditions of the heart, particularly those produced by uncontrolled SR Ca2+ release, such as triggered arrhythmias.1. In the heart, it can be said that "not all Ca2+ currents (ICa) are created equal"; ICa at negative potentials ...
View mouse Cacna1s Chr1:136052805-136119822 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
pep chromosome:GRCm38:6:118593892:119107975:-1 gene:ENSMUSG00000051331 transcript:ENSMUST00000112793 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Cacna1c description:calcium channel, voltage-dependent, L type, alpha 1C subunit [Source:MGI Symbol;Acc:MGI:103013 ...
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TY - JOUR. T1 - L-type voltage-gated calcium channels mediate NMDA-independent associative long-term potentiation at thalamic input synapses to the amygdala. AU - Weisskopf, Marc G.. AU - Bauer, Elizabeth P.. AU - Ledoux, Joseph. PY - 1999/12/1. Y1 - 1999/12/1. N2 - Long-term potentiation (LTP) in the amygdala is a leading candidate mechanism to explain fear conditioning, a prominent model of emotional memory. LTP occurs in the pathway from the auditory thalamus to the lateral amygdala, and during fear conditioning LTP-like changes occur in the synapses of this pathway. Nevertheless, LTP has not been investigated in the thalamoamygdala pathway using in vitro recordings; hence little is known about the underlying mechanisms. We therefore examined thalamoamygdala LTP in vitro using visualized whole-cell patch recording. LTP at these synapses was dependent on postsynaptic calcium entry, similar to synaptic plasticity in other regions of the brain. However, unlike many forms of synaptic plasticity, ...
Looking for online definition of calcium channel, L type, alpha 2 polypeptide in the Medical Dictionary? calcium channel, L type, alpha 2 polypeptide explanation free. What is calcium channel, L type, alpha 2 polypeptide? Meaning of calcium channel, L type, alpha 2 polypeptide medical term. What does calcium channel, L type, alpha 2 polypeptide mean?
TY - JOUR. T1 - Timothy syndrome 1 genotype without syndactyly and major extracardiac manifestations. AU - Sepp, Róbert. AU - Hategan, Lidia. AU - Bácsi, Attila. AU - Cseklye, Judit. AU - Környei, László. AU - Borbás, János. AU - Széll, Márta. AU - Forster, T.. AU - Nagy, István. AU - Hegedűs, Zoltán. PY - 2017/3/1. Y1 - 2017/3/1. N2 - Timothy syndrome 1 (TS1) is a rare genetic disorder characterized by multisystem abnormalities including QT prolongation, congenital heart defects, facial dysmorphism, episodic hypoglycemia, and neurological symptoms. A morphological hallmark of TS1 is syndactyly, present in all cases. TS1 is caused by the canonical p.Gly406Arg mutation in the alternatively spliced exon 8A in the CACNA1C gene, encoding for the main cardiac L-type calcium channel. A variant case of TS1 is reported. The proband had intermittent fetal bradycardia with heart rate of 72 bpm. On the first day of life bradycardia due to 2:1 atrioventricular (AV) block and marked QTc ...
Malignant hyperthermia susceptibility (MHS) is an autosomal dominant disorder of skeletal muscle which manifests as a potentially fatal hypermetabolic crisis triggered by commonly used anaesthetic agents. The demonstration of genetic heterogeneity in MHS prompted the investigation of the roles played by calcium regulatory proteins other than the ryanodine receptor (RYR1), which is known to be linked to MHS in fewer than half of the European MHS families studied to date. Previously, we have excluded the genes encoding the skeletal muscle L-type voltage-dependent calcium channel alpha(1)-, beta(1)- and gamma-subunits as candidates for MHS. In this report, we describe the cloning and partial DNA sequence analysis of the gene encoding the alpha(2)/delta-subunits, CACNL2A, and its localization on the proximal long arm of chromosome 7q. A new dinucleotide repeat marker close to CACNL2A was identified at the D7S849 locus and tested for linkage in six MHS families. D7S849 and flanking genetic markers ...
BioAssay record AID 415111 submitted by ChEMBL: Displacement of [3H]diltiazem from L-type calcium channel in Sprague-Dawley rat cardiac myocytes by liquid scintillation counting.
Background. Small conductance Ca2+-activated K+ (SK) channels play significant roles in regulating the excitability of cardiomyocytes (CMs). SK channels are unique in that they are gated solely by intracellular Ca2+ and hence, function to integrate intracellular Ca2+ and membrane potentials on a beat-to-beat basis in the heart. Our previous studies revealed that cardiac SK2 channels coupled with L-type Ca2+ channels (LTCCs) through a physical bridge, α-actinin2, suggesting that LTCCs may be functionally coupled with SK2 channels by providing local Ca2+ domain to activate the SK channels. However, a recent study suggested that sarcoplasmic reticulum (SR) Ca2+ release is necessary and sufficient for the activation of cardiac SK channels. The objective of the study is to examine the mechanisms of SK channel activation in native CMs.. Methods and Results. By using a voltage-clamp protocol in rabbit CMs to activate LTCCs followed immediately by a test voltage to monitor the SK currents, we recorded ...
In the dorsal horn of the spinal cord, pain-transmitting neurons exhibit action potential windup, a form of short-term plasticity, which consists of a progressive increase in neuronal response during repetitive stimulation of nociceptive input fibers. Windup depends on N-methyl-d-aspartate (NMDA) receptor activation, but previous in vitro studies indicated that windup also relies on intrinsic plateau properties of spinal neurons. In the present study, we considered the possible involvement of these properties in windup in vivo. For this purpose, we first studied a nociceptive flexion reflex in the rat. We showed that windup of the reflex is actually suppressed by blockers of L-type calcium current and Ca2+-activated non-specific cationic current (Ican), the two main depolarizing conductances of plateau potentials. We further showed that, during windup, NMDA receptors provide a critical excitatory component in a dynamic balance of excitatory and inhibitory inputs which ultimately activates L-type ...
The regulation of protein phosphorylation requires a balance in the activity of protein kinases and protein phosphatases. Our previous data indicates that Src can increase ERK activity through Raf kinase in response to ischemic stimuli. This study examined the molecular mechanisms by which Src activates ERK cascade through protein phosphatases following cerebral ischemia. Ischemia-induced Src activation is followed by phosphorylation of PP2A at Tyr307 leading to its inhibition in the rat hippocampus. SU6656, a Src inhibitor, up-regulates PP2A activity, resulting in a significant decreased activity in ERK and its targets, CREB and ERα. In addition, the PP2A inhibitor, cantharidin, led to an up-regulation of ERK activity and was able to counteract Src inhibition during ischemia. Src induces up-regulation of ERK activity and its target transcription factors, CREB and ERα, through attenuation of PP2A activity. Therefore, activation of ERK is the result of a crosstalk between two pathways, Raf-dependent
ID H3BA90_LATCH Unreviewed; 2064 AA. AC H3BA90; DT 18-APR-2012, integrated into UniProtKB/TrEMBL. DT 18-APR-2012, sequence version 1. DT 25-OCT-2017, entry version 39. DE RecName: Full=Voltage-dependent L-type calcium channel subunit alpha {ECO:0000256,RuleBase:RU003808}; GN Name=CACNA1C {ECO:0000313,Ensembl:ENSLACP00000018811}; OS Latimeria chalumnae (West Indian ocean coelacanth). OC Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; OC Coelacanthiformes; Coelacanthidae; Latimeria. OX NCBI_TaxID=7897 {ECO:0000313,Ensembl:ENSLACP00000018811, ECO:0000313,Proteomes:UP000008672}; RN [1] {ECO:0000313,Ensembl:ENSLACP00000018811} RP NUCLEOTIDE SEQUENCE [LARGE SCALE GENOMIC DNA]. RC STRAIN=Wild caught {ECO:0000313,Ensembl:ENSLACP00000018811}; RX PubMed=9215903; RA Zardoya R., Meyer A.; RT "The complete DNA sequence of the mitochondrial genome of a living RT fossil, the coelacanth (Latimeria chalumnae)."; RL Genetics 146:995-1010(1997). RN [2] {ECO:0000313,Ensembl:ENSLACP00000018811} ...
Several lines of evidence suggest that electromechanical alternans is linked to alterations in cellular Ca2+homeostasis (33). Calcium homeostasis is not only important for excitation-contraction coupling but it also significantly influences the action potential (AP) profile and duration (APD). Excitation leads to the opening of voltage-gated L-type Ca2+channels, allowing the entry of a small amount of Ca2+into the cell. The small amount of Ca2+that enters the cell through the L-type Ca2+channel triggers a larger release of Ca2+from the sarcoplasmic reticulum (SR) via Ca2+release channels or ryanodine receptors (so-called calcium-induced calcium release), activating the myofilaments and leading to contraction. During relaxation, Ca2+is sequestered in the SR by the SR Ca2+adenosine triphosphatase and extruded from the cell by the sodium calcium exchanger. The change in intracellular Ca2+during the cardiac cycle or calcium transient has direct and indirect effects on a number of ionic currents in ...
Rem, Rem2, Rad, Gem/Kir (RGK) subfamily of Ras GTPases. RGK subfamily. The RGK (Rem, Rem2, Rad, Gem/Kir) subfamily of Ras GTPases are expressed in a tissue-specific manner and are dynamically regulated by transcriptional and posttranscriptional mechanisms in response to environmental cues. RGK proteins bind to the beta subunit of L-type calcium channels, causing functional down-regulation of these voltage-dependent calcium channels, and either termination of calcium-dependent secretion or modulation of electrical conduction and contractile function. Inhibition of L-type calcium channels by Rem2 may provide a mechanism for modulating calcium-triggered exocytosis in hormone-secreting cells, and has been proposed to influence the secretion of insulin in pancreatic beta cells. RGK proteins also interact with and inhibit the Rho/Rho kinase pathway to modulate remodeling of the cytoskeleton. Two characteristics of RGK proteins cited in the literature are N-terminal and C-terminal extensions beyond the ...
Voltage-dependent calcium channel subunit alpha-2/delta-1 (CA2D1) antibody | P54289 | Voltage-dependent calcium channel subunit alpha-2/delta-1, Voltage-gated calcium channel subunit alpha-2/delta-1, CACNL2A, CCHL2A, MHS3
Voltage-dependent N-type calcium channel subunit alpha-1B (Brain calcium channel III) (BIII) (Calcium channel; L type; alpha-1 polypeptide isoform 5) (Voltage-gated calcium channel subunit alpha Cav2.2 ...
OBJECTIVE: The L-type Ca(2+) current (I(Ca,L)) contributes to the generation and modulation of the pacemaker action potential (AP). We investigated facilitation of I(Ca,L) in sino-atrial cells. METHODS: Facilitation was studied in regularly-beating cells isolated enzymatically from young albino rabbits (0.8-1 kg). We used the whole-cell patch-clamp technique to vary the frequency of the test depolarizations evoked at -10 mV or the conditioning diastolic membrane potential prior to the test pulse. RESULTS: High frequencies (range 0.2-3.5 Hz) slowed the decay kinetics of I(Ca,L) evoked from a holding potential (HP) of -80 mV in 68% of cells resulting in a larger Ca(2+) influx during the test pulse. The amount of facilitation increased progressively between 0.2 and 3.0 Hz. When the frequency was changed from 0.1 to 1 Hz, the averaged increase in the time integral of I(Ca,L) was 27+/-7% (n=22). Application of conditioning voltages between -80 and -50 mV induced similar facilitation of I(Ca,L) in 73% of
RGK regulation of voltage-gated calcium channels. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
The IUPHAR/BPS Guide to Pharmacology. Cav1.3 - Voltage-gated calcium channels. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
The result of purified G protein subunits s and on L-type Ca2+ channels in vascular smooth muscle as well as the possible pathways involved were investigated using freshly isolated smooth muscle cells from rabbit portal vein as well as the whole-cell patch clamp technique. subunits with GDP destined to SIS the subunits. Upon dissociation Tivozanib (AV-951) of subunits from dimers by exchange of GTP for GDP, both GTP-bound subunits and dimers are turned on and connect to their effectors such as for example adenylyl cyclases and ion stations (Hepler & Gilman, 1992). Though it is more developed that subunits of Gs proteins play a significant function in the legislation of L-type Ca2+ stations, there is absolutely no immediate proof for modulation of L-type Ca2+ stations by subunits of G protein. Furthermore, the function of G proteins subunits in the legislation of VSM L-type Ca2+ stations has not however been examined in virtually any detail. In todays study, we looked into the consequences of ...
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Anti-Cav1.2 (CACNA1C) Antibody (#ACC-003) from Alomone Labs is a highly specific rabbit polyclonal Ab directed against rat Cav1.2. Applications: ICC, IFC, IHC, IP, WB. Free samples available. Control antigen included. Lyophilized. Global shipping. Top supplier for L-type voltage-gated Ca2+ channel research!
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BAYK 8644 is a L-type Ca2+ channel activator (EC50 = 17.3 nM). BAYK 8644 has positive inotropic, vasoconstrictive and behavioral effects in vivo.
1 Answer (question resolved) - Posted in: cartia xt, high blood pressure - Answer: Cartia XT is an extended release calcium channel beta blocker. I ...
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Verapamil is only found in individuals that have used or taken this drug. Verapamil is a calcium channel blocker that is a class IV anti-arrhythmia agent. [PubChem]Verapamil inhibits voltage-dependent calcium channels. Specifically, its effect on L-type calcium channels in the heart causes a reduction in ionotropy and chronotropy, thuis reducing heart rate and blood pressure. Verapamils mechanism of effect in cluster headache is thought to be linked to its calcium-channel blocker effect, but which channel subtypes are involved is presently not known. [PubChem] Calcium channel antagonists can be quite toxic. In the management of poisoning, early recognition is critical. Calcium channel antagonists are frequently prescribed, and the potential for serious morbidity and mortality with over dosage is significant. Ingestion of these agents should be suspected in any patient who presents in an overdose situation with unexplained hypotension and conduction abnormalities. The potential for toxicity ...
Timothy Syndromes Alliance wrote - The mission of Timothy Syndromes Alliance (TSA) is to raise physician and public awareness and to improve the health and well-being of those affected by Timothy Syndrome\Long QT8, through education, research and family support. The Alliance was formed by two concerned mothers and Katherine Timothy, for whom the syndrome is named, in association with the SADS Foundation. In 2016 TSA held its first ever family support gathering and a one day conference as part of the SADS International Conference, held in San Diego, California. It was a rare opportunity for patients and families to meet in person and attend a syndrome specific roundtable discussion with Katherine Timothy. Patients traveled from all over the United States, and were represented world-wide, as far away as Hong Kong. In 2016, being fiscally conservative with contributed funds, Timothy Syndromes Alliance was able to provide travel scholarships to families as needed. Your generous gift will
Timothy syndrome is a rare autosomal dominant disorder characterized by physical malformations, as well as neurological and developmental defects, including heart QT-prolongation, heart arrhythmias, structural heart defects, syndactyly (webbing of fingers and toes) and autism spectrum disorders. Timothy syndrome often ends in early childhood death. The most striking sign of Timothy syndrome is the co-occurrence of both syndactyly (~0.03% of births) and long QT syndrome (1% per year) in a single patient. Other common symptoms of Timothy syndrome are cardiac arrhythmia (94%), heart malformations (59%), autism or an autism spectrum disorder (80% who survive long enough for evaluation). Facial dysmorphologies such as flattened noses also occur in approximately half of patients. Children with this disorder have small teeth which, due to poor enamel coating, are prone to dental cavities and often require removal. The average age of death due to complications of these symptoms is 2.5 years. Atypical ...
Voltage-gated calcium channels are multi-subunit membrane proteins which transduce depolarization into cellular functions like excitation-contraction coupling in muscle or neurotransmitter release in neurons. The auxiliary β subunits function in membrane targeting of the channel and modulation of its gating properties. However, whether β subunits can reversibly interact with, and thus differentially modulate channels in the membrane is still unresolved. Here we applied fluorescence recovery after photobleaching (FRAP) of GFP-tagged α1 and β subunits expressed in dysgenic myotubes to study the relative dynamics of these calcium channel subunits for the first time in a native functional signaling complex. Identical fluorescence recovery rates of both subunits indicate stable interactions, distinct rates dynamic interactions. Whereas the skeletal muscle β1a isoform formed stable complexes with CaV1.1 and CaV1.2, the non-skeletal muscle β2a and β4b isoforms dynamically interacted with both ...
TY - JOUR. T1 - Domain III regulates N-type (Ca V2.2) calcium channel closing kinetics. AU - Yarotskyy, Viktor. AU - Gao, Guofeng. AU - Peterson, Blaise Z.. AU - Elmslie, Keith S.. PY - 2012/4/1. Y1 - 2012/4/1. N2 - Ca V2.2 (N-type) and Ca V1.2 (L-type) calcium channels gate differently in response to membrane depolarization, which is critical to the unique physiological functions mediated by these channels. We wondered if the source for these differences could be identified. As a first step, we examined the effect of domain exchange between N-type and L-type channels on activationdeactivation kinetics, which were significantly different between these channels. Kinetic analysis of chimeric channels revealed N-channellike deactivation for all chimeric channels containing N-channel domain III, while activation appeared to be a more distributed function across domains. This led us to hypothesize that domain III was an important regulator of N-channel closing. This idea was further examined with ...
TY - JOUR. T1 - Ca2+ channel subtypes and pharmacology in the kidney. AU - Hayashi, Koichi. AU - Wakino, Shu. AU - Sugano, Naoki. AU - Ozawa, Yuri. AU - Homma, Koichiro. AU - Saruta, Takao. PY - 2007/2/1. Y1 - 2007/2/1. N2 - A large body of evidence has accrued indicating that voltage-gated Ca channel subtypes, including L-, T-, N-, and P/Q-type, are present within renal vascular and tubular tissues, and the blockade of these Ca channels produces diverse actions on renal microcirculation. Because nifedipine acts exclusively on L-type Ca channels, the observation that nifedipine predominantly dilates afferent arterioles implicates intrarenal heterogeneity in the distribution of L-type Ca channels and suggests that it potentially causes glomerular hypertension. In contrast, recently developed Ca channel blockers (CCBs), including mibefradil and efonidipine, exert blocking action on L-type and T-type Ca channels and elicit vasodilation of afferent and efferent arterioles, which suggests the ...
Corticotroph releasing hormone (CRH) is one of the major regulatory hormones associated with the neuroendocrine response to stress. Pituitary corticotroph cells generate repetitive action potentials and associated Ca2+ transients in response to the agonist CRH. The mechanisms underlying this process are complex. CRH is known to activate the adenosine 3,5-cyclic monophosphate (cAMP)-dependent protein kinase A (PKA) pathway. PKA phosphorylates L-type voltage-sensitive Ca2+ channels, activating them and contributing to the generation of an action potential and Ca2+ transients. In an earlier Hodgkin-Huxley type mathematical model of this process, LeBeau et al. showed than an increase in the L-type current was sufficient to generate repetitive action potentials from a resting state in the model (LeBeau et al., 1997). However, they found that the action potential frequency of the model was much higher than the observed experimental action potential frequency. This problem was addressed in the ...
In addition to the shift in the I-V relationship for L-type currents of R163C Het and Hom myotubes, we found that this MH mutation caused an increased responsiveness to the dihydropyridine agonist ±Bay K 8644. In particular, L-type currents of MHS R163C myotubes were potentiated to a greater degree (Hom , Het) than WT myotubes (Fig. 4). This observation suggests that one of the retrograde effects of R163C mutation on the L-type channel activity of the DHPR is to facilitate entry of the channel into the long-open gating state (i.e., mode 2; Nowycky et al., 1985), which might explain the enhanced potentiation by ±Bay K 8644. Interestingly, Bay K 8644 enhances pharmacologically (halothane or isofluorane) induced contractures in both swine and human MHS muscle (Williams et al., 1991; Adnet et al., 1992), consistent with the idea that altered L-type current may contribute to the pathogenesis of this disease.. Compared with previous reports on the inactivation of L-type current in "normal" human ...
TY - JOUR. T1 - Cholinoreceptor autoantibodies in Sjögren sndrome. AU - Reina, S.. AU - Oman, B.. AU - Anaya, J. M.. AU - Sterin-Borda, L.. AU - Borda, E.. PY - 2007/9/1. Y1 - 2007/9/1. N2 - Previous studies have demonstrated that antibodies against cholinoreceptors of exocrine glands correlate with dry mouth in persons with primary Sjögren syndrome (pSS). The aim of the present investigation was to establish if serum IgG antibodies (pSS IgG) were able to interact with cholinoreceptors in rat submandibular gland-dependent stimulation of cyclo-oxygenase 2 (COX-2) mRNA expression and PGE2 production. Our findings indicated that pSS IgG-stimulating M3, M4, and M1 cholinoreceptors exerted an increase in COX-2 mRNA without affecting COX-1 mRNA expression and increased PGE2 production. Inhibitors of phospholipase A2, COX-s, L-type calcium channel currents, and Ca2+-ATPase from sarcoplasmic reticulum prevented the pSS IgG effect on PGE2 production. An ionophore of calcium mimicked pSS IgG action, ...
We have monitored electrical activity, voltage-gated Ca2+ currents, and exocytosis in single rat glucagon-secreting pancreatic A-cells. The A-cells were electrically excitable and generated spontaneous Na+- and Ca2+-dependent action potentials. Under basal conditions, exocytosis was tightly linked to Ca2+ influx through omega-conotoxin-GVIA-sensitive (N-type) Ca2+ channels. Stimulation of the A-cells with adrenaline (via beta-adrenergic receptors) or forskolin produced a greater than fourfold PKA-dependent potentiation of depolarization-evoked exocytosis. This enhancement of exocytosis was due to a 50% enhancement of Ca2+ influx through L-type Ca2+ channels, an effect that accounted for |30% of the total stimulatory action. The remaining 70% of the stimulation was attributable to an acceleration of granule mobilization resulting in a fivefold increase in the number of readily releasable granules near the L-type Ca2+ channels.
The localization of ion channels to caveolae may modulate the function of the channels in multiple ways. For example, the precise lipid composition can potently regulate channel function, and dynamic changes in this composition underlie some forms of regulation. In addition, the caveolar localization of ion channels can provide compartmentalization of signaling networks, enabling rapid and specific regulation of the channels. Caveolar-localized signaling complexes composed of β2-AR, AC, Gαs, and Gαi have previously been observed in rat ventricular myocytes (9, 19), but the present study adds Cav1.2 and PP2A to the complex. Conversely, the molecules associated with Cav1.2 channels in the heart have not been extensively defined. Recent studies have identified AKAP15 and PKA as well as certain PKC isoforms in association with Cav1.2 in cardiac muscle (23, 24); however, whether these molecules are associated with the channels in caveolae is unknown. The present results add to the list of proteins ...
The need for integrative analysis in cardiac physiology and pathophysiology is readily appreciated. Common heart diseases are multi-factorial, multi-genic, and linked to other systemic disorders such as diabetes, hypertension, or thyroid disease. The coupling between the L-type Calcium channels (LCCs, also known as dihydropyridine receptors, or DHPRs) and ryanodine receptors (RyRs) are important in the excitation-contraction (E-C) of cardiac myocytes. The influx of calcium releases the calcium store in the Sarcoplasmic reticulum (SR), a phenomenon known as the calcium induced calcium release (CICR). In fact, the latest ionic models of cardiac myocytes include more than 20 ionic fluxes and 40 ordinary differential equations.1 Computational methods and ionic models for cardiac electromechanics at different scales have also been developed and are available in the software package Continuity. Figure 2 shows an example of how Continuity is used to help develop dual pacemaker systems that are helping ...
Calcium channel blockers are drugs that block the entry of calcium into the cells of the heart and blood vessels walls by interacting with calcium channels. They are primarily used to treat hypertension, angina and arrhythmias. Learn about the different classes of calcium channel blocker medications and how they are used.
Verapamil 180 mg pills, (brand names: Isoptin, Verelan, Calan, Bosoptin), is an L-type calcium channel blocker used in the treatment of hypertension, angina pectoris, cardiac arrhythmia, and most recently, headaches. Not to be used along with beta-blockers. Class 4 antiarrhythmic, more effective than digoxin in controlling ventricular rate. Approved by FDA in 1981. One of its purified isomers does not cause constipation whereas racemic Verapamil does. Used as a vasodilator during cryopreservation of blood vessels. - Stock Image C003/0154
Skeletal muscle excitation-contraction (EC) coupling depends upon interactions at triad junctions between L- type Ca2+ channels (dihydropyridine receptors, DHPR...
To assess evidence for the presence of a mendelian pattern of familial transmission the presence of a rare major mendelian gene for PD for a gene that influences age-dependent penetrance of WD-repeat (GRWD1) belong to WD-repeat proteins that promotes microtubule dynamics activity somewhat still carried out, this may be true as far as mendelian (nuclear) genetic mechanisms are concerned that there was no highly penetrant mendelian pattern of inheritance here they show that DJ-1 and PSF bind and regulate the major interacting-proteins with DJ-1 in dopaminergic neuronal cells which can be reversed by wild-type DJ-1 [Drosophila gain-of-function mutants identified] to regulate the expression of a neuroprotective genetic program [1.] appears to have constrained the evolution of the nonA [diss-dissonance, plus the cacophony (referred to as intron L by them, [AFX1] as are inhibited by the L-type calcium channel blockers Dmca1A (nbA-cac) are both expressed in tubules] promoter. (PSF), paraspeckle ...
Peptides , Prion Protein (PrP) Fragments , PrP (106-126); This peptide increases membrane microviscosity, intracellular Ca2+ concentration and cell migration in circulating leucocytes, and oxygen production in monocytes and neutrophils. It also induces apoptotic cell death and impairment of L-type voltage-sensitive calcium channel activity in the GH3 cell lines. PrP (106 126) stimulates leucocyte migration in a dose-dependent manner.; KTNMKHMAGAAAAGAVVGGLG; H-Lys-Thr-Asn-Met-Lys-His-Met-Ala-Gly-Ala-Ala-Ala-Ala-Gly-Ala-Val-Val-Gly-Gly-Leu-Gly-OH
deletion, revealed that ISL1 within SAN is a requirement for early embryonic viability. RNA-sequencing (RNA-seq) analyses of FACS-purified cells from ISL1-deficient SANs revealed that a number of genes critical for SAN function, including those encoding transcription factors and ion channels, were downstream of ISL1. Chromatin immunoprecipitation assays performed with anti-ISL1 antibodies and chromatin extracts from FACS-purified SAN cells demonstrated that ISL1 directly binds genomic regions within several genes required for normal pacemaker function, including subunits of the L-type calcium channel ...
The PUFAs act by stabilizing electrically every cardiac myocyte by modulating conductance of ion channels in the sarcolemma, particularly the fast, voltage-dependent sodium current and the L-type calcium currents, though other ion currents are also affected. Work in progress suggests that the primary site of action of the PUFAs may be on the phospholipid bilayer of the heart cells in the microdomains through which the ion channels penetrate the membrane bilayer in juxtaposition with the ion channels rather than directly on the channel protein itself ...
Catalysis of facilitated diffusion of a calcium ion (by an energy-independent process) involving passage through a transmembrane aqueous pore or channel without evidence for a carrier-mediated mechanism.
The association of L-type Ca(2+) channels to the secretory granules and its functional significance to secretion was investigated in mouse pancreatic B cells. Nonstationary fluctuation analysis showed that the B cell is equipped with ,500 alpha1(C) L-type Ca(2+) channels, corresponding to a Ca(2+) channel density of 0.9 channels per microm(2). Analysis of the kinetics of exocytosis during voltage-clamp depolarizations revealed an early component that reached a peak rate of 1.1 pFs(-1) (approximately 650 granules/s) 25 ms after onset of the pulse and is completed within approximately 100 ms. This component represents a subset of approximately 60 granules situated in the immediate vicinity of the L-type Ca(2+) channels, corresponding to approximately 10% of the readily releasable pool of granules. Experiments involving photorelease of caged Ca(2+) revealed that the rate of exocytosis was half-maximal at a cytoplasmic Ca(2+) concentration of 17 microM, and concentrations ,25 microM are required to ...
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A calcium channel is an ion channel which shows selective permeability to calcium ions. It is sometimes synonymous as voltage-gated calcium channel, although there are also ligand-gated calcium channels. The following tables explain gating, gene, location and function of different types of calcium channels, both voltage and ligand-gated. the receptor-operated calcium channels (in vasoconstriction) P2X receptors L-type calcium channel blockers are used to treat hypertension. In most areas of the body, depolarization is mediated by sodium influx into a cell; changing the calcium permeability has little effect on action potentials. However, in many smooth muscle tissues, depolarization is mediated primarily by calcium influx into the cell. L-type calcium channel blockers selectively inhibit these action potentials in smooth muscle which leads to dilation of blood vessels; this in turn corrects hypertension. T-type calcium channel blockers are used to treat epilepsy. Increased calcium conductance in ...
Dantrolene and nimodipine dramatically reduce the number of activated microglia in the hippocampus and reduce the expression of various pro-inflammatory cytokines. It is not clear from our data whether the anti-inflammatory effects of dantrolene and nimodipine are due to direct action on the microglia themselves or an indirect effect via normalization of neuronal Ca+2 levels. Neurotoxicity of conditioned media from activated microglia is reduced when drugs blocking L-VDCCs or RyRs are applied to the microglia cultures [12-14]. However, the in vivo anti-inflammatory effects of these drugs are not so clear-cut. Following facial nerve transection, nimodipine treatment improves motor neuron survival without reducing microglia activation [53]. However, after ischemic-reperfusion injury, nimodipine does improve behavioral outcomes while concurrently reducing microglia activation [54]. Similarly, in vivo treatment with dantrolene is neuroprotective and improves behavioral outcomes in various in vivo ...
Dihydropyridines (DHP), which nifedipine is a member of, preferentially block Ca2+ channels of different cell types. Moreover, influx of Ca2+ through L-type Ca2+ channels (LTCCs) activates Ca2+ signaling pathways, which in turn contribute to numerous cellular processes. Although LTCCs are expressed in undifferentiated cells, very little is known about its contributions to the transcriptional regulation of mesodermal and cardiac genes. This study aimed to examine the contribution of LTCCs and the effect of nifedipine on the commitment of pluripotent stem cells toward the cardiac lineage in vitro. The murine embryonic stem (ES, cell line D3) and induced pluripotent stem (iPS, cell clone 09) cells were differentiated into enhanced green fluorescence protein (EGFP) expressing spontaneously beating cardiomyocytes (CMs). Early treatment of differentiating cells with 10 µM nifedipine led to a significant inhibition of the cardiac mesoderm formation and cardiac lineage commitment as revealed by gene regulation
Lethal neurotoxin that blocks neuromuscular transmission by binding to the nicotinic acetylcholine receptor. Possess presynaptic activity that affects the release of neurotransmitters from autonomic nerve endings of both cholinergic and adrenergic neuroeffector junctions. Selectively inhibits N-type calcium channel (Cav2.2/CACNA1B) and has only very weak effect on L-type calcium channel (Cav1/CACNA1).
TY - JOUR. T1 - Role of potassium channels in coronary vasodilation. AU - Dick, Gregory M.. AU - Tune, Johnathan D.. PY - 2010/1/1. Y1 - 2010/1/1. N2 - K+ channels in coronary arterial smooth muscle cells (CASMC) determine the resting membrane potential (Em) and serve as targets of endogenous and therapeutic vasodilators. Em in CASMC is in the voltage range for activation of L-type Ca2+ channels; therefore, when K+ channel activity changes, Ca2+ influx and arterial tone change. This is why both Ca2+ channel blockers and K+ channel openers have such profound effects on coronary blood flow; the former directly inhibits Ca2+ influx through L-type Ca2+ channels, while the latter indirectly inhibits Ca2+influx by hyperpolarizing Em and reducing Ca2+ channel activity. K+ channels in CASMC play important roles in vasodilation to endothelial, ischemic and metabolic stimuli. The purpose of this article is to review the types of K+ channels expressed in CASMC, discuss the regulation of their activity by ...
Voltage-dependent calcium channels represent a major pathway of calcium entry into neurons, where they participate actively to cell excitability and to the molecular processes of synaptic transmission. For that reason, they have been the direct or indirect pharmacological targets of analgesics and this long before their implication in the physiology of nociception had been demonstrated. These last years, the still more refined molecular characterization of these channels and their associated regulatory subunits and the demonstration of their implication in nociceptive processes indicates that these structures are prime pharmacological targets for the management of pain. Herein, we detail the recent breakthroughs on calcium channel structure, function and pharmacology, review the implication of calcium channels in the transmission of nociception, and evaluate their importance as targets for the treatment of pain perception. The search for specific inhibitors of voltage-dependent calcium channels appears
Looking for online definition of calcium channel, voltage-dependent, gamma subunit 6 in the Medical Dictionary? calcium channel, voltage-dependent, gamma subunit 6 explanation free. What is calcium channel, voltage-dependent, gamma subunit 6? Meaning of calcium channel, voltage-dependent, gamma subunit 6 medical term. What does calcium channel, voltage-dependent, gamma subunit 6 mean?
Nitric oxide (NO) has long been implicated in the generation of long-term potentiation (LTP) and other types of synaptic plasticity, a role for which the intimate coupling between NMDA receptors (NMDARs) and the neuronal isoform of NO synthase is likely to be instrumental in many instances. While many types of synaptic plasticity depend on NMDA receptors, others do not, an example of which is LTP triggered by opening of L-type voltage-gated Ca2+ channels (L-VGCCs) in postsynaptic neurons. In CA3-CA1 synapses in the hippocampus, NMDAR-dependent LTP appears to be primarily expressed postsynaptically whereas L-VGCC-dependent LTP, which often coexists with NMDAR-dependent LTP, appears mainly to reflect enhanced presynaptic transmitter release. Since NO is an excellent candidate as a retrograde messenger mediating post-to-presynaptic signaling, we sought to determine if NO functions in L-VGCC-dependent LTP in mouse CA3-CA1 synapses. When elicited by a burst type of stimulation with NMDARs and the associated
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Definition of calcium channel blocking agent in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is calcium channel blocking agent? Meaning of calcium channel blocking agent as a finance term. What does calcium channel blocking agent mean in finance?
TY - JOUR. T1 - Voltage-gated divalent currents in descending vasa recta pericytes. AU - Zhang, Zhong. AU - Lin, Hai. AU - Cao, Chunhua. AU - Khurana, Sandeep. AU - Pallone, Thomas L.. PY - 2010/10/1. Y1 - 2010/10/1. N2 - Multiple voltage-gated Ca2+ channel (CaV) subtypes have been reported to participate in control of the juxtamedullary glomerular arterioles of the kidney. Using the patch-clamp technique, we examined whole cell CaV currents of pericytes that contract descending vasa recta (DVR). The dihydropyridine CaV agonist FPL64176 (FPL) stimulated inward Ca2+ and Ba2+ currents that activated with threshold depolarizations to -40 mV and maximized between -20 and -10 mV. These currents were blocked by nifedipine (1 μM) and Ni2+ (100 and 1,000 μM), exhibited slow inactivation, and conducted Ba2+ , Ca 2+ at a ratio of 2.3:1, consistent with "long-lasting" L-type CaV. In FPL, with 1 mM Ca2+ as charge carrier, Boltzmann fits yielded half-maximal activation potential (V1/2) and slope factors of ...
Here, we report the novel findings that in human adrenal glomerulosa cells both basal and stimulated rates of aldosterone production depend on voltage-gated calcium currents through T-type as well as L-type calcium channels. These findings are surprising because patch-clamp studies consistently report the basal membrane potential of ZG cells to be very hyperpolarized (around −80 mV), a potential at which high threshold L-type calcium channels are not expected to be active. In contrast, low threshold T-type calcium channels are activated at more hyperpolarized potentials and have a permissive window of steady-state activity at more hyperpolarized potentials (Perez-Reyes 2003). When stimulated by low physiological concentrations of Ang II or small increases in extracellular potassium, the membrane potential of ZG cells can rapidly reach the permissive voltage window for persistent T-type, but not L-type, calcium channel activity, that allows steady-state calcium influx (Rossier 2016). Therefore, ...
TY - JOUR. T1 - Restoration of motor defects caused by loss of drosophila TDP-43 by expression of the voltage-gated calcium channel, cacophony, in central neurons. AU - Lembke, Kayly M.. AU - Scudder, Charles. AU - Morton, David. PY - 2017/9/27. Y1 - 2017/9/27. N2 - Defects in the RNA-binding protein, TDP-43, are known to cause a variety of neurodegenerative diseases, including amyotrophic lateral sclerosis and frontotemporal lobar dementia. A variety of experimental systems have shown that neurons are sensitive to TDP-43 expression levels, yet the specific functional defects resulting from TDP-43 dysregulation have not been well described. Using the Drosophila TDP-43 ortholog TBPH, we previously showed that TBPH-null animals display locomotion defects as third instar larvae. Furthermore, loss of TBPH caused a reduction in cacophony, a Type II voltage-gated calcium channel, expression and that genetically restoring cacophony in motor neurons in TBPH mutant animals was sufficient to rescue the ...
The regulation of transmitter release at the neuromuscular junction is tightly regulated by the influx of calcium in the presynaptic nerve terminal. Interestingly, the probability that release sites at the neuromuscular junction will liberate transmitter during each action potential is very low. The reasons for this low probability of release are not well understood. To test the hypothesis that individual N-type calcium channels open with a low probability, single channel recordings of N-type voltage-gated calcium channels were performed. Using this approach I determined the conductance of these channels, their probability of gating during an action potential waveform, and the magnitude of calcium flux during a single channel opening. I conclude from these studies that N-type voltage-gated calcium channels have a very low probability of opening (< 5%) during an action potential and the characteristics of calcium entry during single channel openings can help to explain the low probability of ...
We report the complete sequence of a calcium channel alpha 1 subunit cDNA cloned from a Drosophila head cDNA library. This cDNA encodes a deduced protein containing 2516 amino acids with a predicted molecular weight of 276,493. The deduced protein shares many features with vertebrate homologs, including four repeat structures, each containing six transmembrane domains, a conserved ion selectivity filter region between transmembrane domains 5 and 6, and an EF hand in the carboxy tail. The Drosophila subunit has unusually long initial amino and terminal carboxy tails. The region corresponding to the last transmembrane domain (IVS6) and the adjacent cytoplasmic domain has been postulated to form a phenylalkylamine-binding site in vertebrate calcium channels. This region is conserved in the Drosophila sequence, while domains thought to be involved in dihydropyridine binding show numerous changes. The Drosophila subunit exhibits 78.3% sequence similarity to the rat brain type D calcium channel alpha ...
The weaver mutation impairs migration of the cerebellar granular neurons and induces neuronal death during the first two weeks of postnatal life. To elucidate the molecular mechanisms for the impaired neuronal migration, we investigated the rescue mechanisms of the weaver (wv/wv) granule neurons in vitro. We found that Fab2 fragments of antibodies against a neurite outgrowth domain of the B2 chain of laminin enhanced neurite outgrowth and neuronal migration of the weaver granule neurons on a laminin substratum and in the established cable culture system. The rescue of the weaver granule neurons by antibodies against the B2 chain of laminin may result from the neutralizing effect of these antibodies against the elevated B2 chain levels of the weaver brain. The L-type calcium channel blocker, verapamil (1-5 microM), also rescued the weaver granule neurons. High concentrations of MK-801 (10-20 microM), a glutamate receptor antagonist and voltage-gated calcium channel blocker, rescued the weaver ...
Low-voltage-activated calcium channels in the lamprey locomotor network: simulation and experiment. J. Neurophysiol. 77: 1795-1812, 1997. To evaluate the role of low-voltage-activated (LVA) calcium channels in the lamprey spinal locomotor network, a previous computer simulation model has been extended to include LVA calcium channels. It is also of interest to explore the consequences of a LVA conductance for the electrical behavior of the single neuron. The LVA calcium channel was modeled with voltage-dependent activation and inactivation using the m 3 h form, following a Hodgkin-Huxley paradigm. Experimental data from lamprey neurons was used to provide parameter values of the single cell model. The presence of a LVA calcium conductance in the model could account for the occurrence of a rebound depolarization in the simulation model. The influence of holding potential on the occurrence of a rebound as well the latency at which it is elicited was investigated and compared with previous ...

R-type calcium channel - WikipediaR-type calcium channel - Wikipedia

The R-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the α1 subunit forms ... "Entrez Gene: CACNA1E calcium channel, voltage-dependent, R type, alpha 1E subunit". Soong TW, Stea A, Hodson CD, Dubel SJ, ... This α1 subunit is also known as the calcium channel, voltage-dependent, R type, alpha 1E subunit (CACNA1E) or Cav2.3 which in ... They are poorly understood, but like Q-type calcium channels, they appear to be present in cerebellar granule cells. They have ...
more infohttps://en.wikipedia.org/wiki/R-type_calcium_channel

Selective N-Type Calcium Channel Antagonist Omega Conotoxin MVIIA Is Neuroprotective Against Hypoxic Neurodegeneration in...Selective N-Type Calcium Channel Antagonist Omega Conotoxin MVIIA Is Neuroprotective Against Hypoxic Neurodegeneration in...

Second, if calcium entry through N-type calcium channels is prevented, the delayed generation of damage is prevented. ... Background and Purpose Neuroprotection by antagonists of both L-type and N-type calcium channels occurs in in vivo models of ... that neuroprotection by selective N-type calcium channel antagonists is mediated directly through neuronal calcium channels. In ... and Q-type channels in addition to blocking N-type channels. Valentino et al11 confirmed in vivo that CTX MVIIC was a much more ...
more infohttp://stroke.ahajournals.org/content/27/11/2124

IDEALS @ Illinois: Calcium Influx via the T-Type Calcium Channel Plays a Permissive Role in Proliferation of Mouse Embryonic Hl...IDEALS @ Illinois: Calcium Influx via the T-Type Calcium Channel Plays a Permissive Role in Proliferation of Mouse Embryonic Hl...

... expresses T-type calcium current was employed to show that inhibiting calcium influx through the T-type calcium channel ... L-type, and a low voltage activated (LVA) T-type. Influx of calcium into the cell through the L-type channel is responsible for ... Furthermore, blocking the calcium influx through the T-type calcium channel arrests cells in the G2/M phase of the cell cycle. ... Calcium Influx via the T-Type Calcium Channel Plays a Permissive Role in Proliferation of Mouse Embryonic Hl-1 Cells. Welcome ...
more infohttps://www.ideals.illinois.edu/handle/2142/87230

Synthesis and biological evaluation of 1-(2-hydroxy-3-phenyloxypropyl) piperazine derivatives as T-type calcium channel...Synthesis and biological evaluation of 1-(2-hydroxy-3-phenyloxypropyl) piperazine derivatives as T-type calcium channel...

... piperazine derivatives as T-type calcium channel blockers",. abstract = "To obtain selective and potent inhibitor for T-type ... N2 - To obtain selective and potent inhibitor for T-type calcium channel by ligand based drug design, 2-hydroxy-3-phenoxypropyl ... AB - To obtain selective and potent inhibitor for T-type calcium channel by ligand based drug design, 2-hydroxy-3-phenoxypropyl ... To obtain selective and potent inhibitor for T-type calcium channel by ligand based drug design, 2-hydroxy-3-phenoxypropyl ...
more infohttps://koreauniv.pure.elsevier.com/en/publications/synthesis-and-biological-evaluation-of-1-2-hydroxy-3-phenyloxypro

Amlodipine Besylate ManufacturersAmlodipine Besylate Manufacturers

Amlodipine Besylate is a calcium channel blocker drug. It relaxes blood vessels so blood can flow easily. It is also used to ... In this journey we urge you all to join and support us by reporting any type of counterfeiting of any of our products. You can ... prevent certain types of chest pain.. Cadila Pharmaceuticals Limited is one of the top USFDA approved pharmaceutical companies ...
more infohttp://cadilapharma.com/pharma_api/amlodipine-besylate-manufacturers/

Nimodipine Order Online - Mexico Pharmacy Nimodipine - Nimodipine 100mg Price WalmartNimodipine Order Online - Mexico Pharmacy Nimodipine - Nimodipine 100mg Price Walmart

Effects of calcium channel blockers on in vitro platelet function in whole blood using single platelet counting. Thromb Haemost ... Also tell your health care professional if you have any other types of allergies, such as to foods, dyes, preservatives, or ... Fosphenytoin: Calcium Channel Blockers may increase the serum concentration of Fosphenytoin. Management: Monitor for phenytoin ... Calcium channel agonists and antagonists: effects of chronic treatment on pituitary prolactin synthesis and intracellular ...
more infohttp://nimodipine.vuli.info

Targetable T-type Calcium Channels Drive Glioblastoma | Cancer ResearchTargetable T-type Calcium Channels Drive Glioblastoma | Cancer Research

... which inhibits the T-type calcium channel Cav3.2. This calcium channel was highly expressed in human GBM specimens and enriched ... Targetable T-type Calcium Channels Drive Glioblastoma. Ying Zhang, Nichola Cruickshanks, Fang Yuan, Baomin Wang, Mary Pahuski, ... Targetable T-type Calcium Channels Drive Glioblastoma. Ying Zhang, Nichola Cruickshanks, Fang Yuan, Baomin Wang, Mary Pahuski, ... Targetable T-type Calcium Channels Drive Glioblastoma. Ying Zhang, Nichola Cruickshanks, Fang Yuan, Baomin Wang, Mary Pahuski, ...
more infohttp://cancerres.aacrjournals.org/content/77/13/3479

T-type calcium channels in burst-firing, network synchrony, and epilepsy.  - PubMed - NCBIT-type calcium channels in burst-firing, network synchrony, and epilepsy. - PubMed - NCBI

T-type calcium channels in burst-firing, network synchrony, and epilepsy.. Cain SM1, Snutch TP. ... In this review we summarize recent findings concerning the role of T-type calcium channels in burst-firing and discuss how they ... Low voltage-activated (LVA) T-type calcium channels are well regarded as a key mechanism underlying the generation of neuronal ... Publication types, MeSH terms, Substances, Grant support. Publication types. *Research Support, Non-U.S. Govt ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/22885138?dopt=Abstract

Calmodulin supports both inactivation and facilitation of L-type calcium channels.  - PubMed - NCBICalmodulin supports both inactivation and facilitation of L-type calcium channels. - PubMed - NCBI

Among the many types of voltage-gated Ca2+ channel, L-type Ca2+ channels particularly display inactivation and facilitation, ... Calmodulin supports both inactivation and facilitation of L-type calcium channels.. Zühlke RD1, Pitt GS, Deisseroth K, Tsien RW ... L-type Ca2+ channels support Ca2+ entry into cells, which triggers cardiac contraction, controls hormone secretion from ... Publication types, MeSH terms, Substances. Publication types. *Research Support, Non-U.S. Govt ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/10335846?dopt=Abstract

Voltage-dependent L-type calcium channel - DrugBankVoltage-dependent L-type calcium channel - DrugBank

Voltage-dependent L-type calcium channel subunit alpha-1C. Q13936. Details. Voltage-dependent L-type calcium channel subunit ... Voltage-dependent L-type calcium channel subunit alpha-1F. O60840. Details. Voltage-dependent L-type calcium channel subunit ... Voltage-dependent L-type calcium channel subunit beta-1. Q02641. Details. Voltage-dependent L-type calcium channel subunit beta ... Voltage-dependent L-type calcium channel subunit beta-3. P54284. Details. Voltage-dependent L-type calcium channel subunit beta ...
more infohttps://www.drugbank.ca/bio_entities/BE0008715

Voltage-dependent calcium channel, L-type, alpha-1S subunit (IPR005450) | InterPro | EMBL-EBIVoltage-dependent calcium channel, L-type, alpha-1S subunit (IPR005450) | InterPro | EMBL-EBI

Voltage-dependent calcium channel, L-type, alpha-1 subunit (IPR005446) *Voltage-dependent calcium channel, L-type, alpha-1S ... while the Cav3 family mediates T-type calcium currents.. L-type calcium channels are formed from alpha-1S, alpha-1C, alpha-1D, ... The Cav1 family forms channels mediating L-type calcium currents, the Cav2 family mediates P/Q-, N-, and R-type calcium ... Nomenclature of voltage-gated calcium channels.. Neuron 25 533-5 2000. Triggle DJ. 1,4-Dihydropyridines as calcium channel ...
more infohttps://www.ebi.ac.uk/interpro/entry/IPR005450

Marine Drugs | Free Full-Text | Inhibition of N-Type Calcium Channels by Fluorophenoxyanilide DerivativesMarine Drugs | Free Full-Text | Inhibition of N-Type Calcium Channels by Fluorophenoxyanilide Derivatives

... were prepared and tested for N-type calcium channel inhibition in a SH-SY5Y neuroblastoma FLIPR assay. N-type or Cav2.2 channel ... Keywords: N-type calcium channel; Cav2.2; channel blocker; pain; FLIPR N-type calcium channel; Cav2.2; channel blocker; pain; ... were prepared and tested for N-type calcium channel inhibition in a SH-SY5Y neuroblastoma FLIPR assay. N-type or Cav2.2 channel ... Inhibition of N-Type Calcium Channels by Fluorophenoxyanilide Derivatives. Ellen C. Gleeson 1,2. ...
more infohttp://www.mdpi.com/1660-3397/13/4/2030

Lateral Mobility of Presynaptic L-Type Calcium Channels at Photoreceptor Ribbon Synapses | Journal of NeuroscienceLateral Mobility of Presynaptic L-Type Calcium Channels at Photoreceptor Ribbon Synapses | Journal of Neuroscience

2011) Location of release sites and calcium-activated chloride channels relative to calcium channels at the photoreceptor ... Lateral Mobility of Presynaptic L-Type Calcium Channels at Photoreceptor Ribbon Synapses. Aaron J. Mercer, Minghui Chen and ... 2004) Role of lipid microdomains in P/Q-type calcium channel (Cav2.1) clustering and function in presynaptic membranes. J Biol ... 2004) The CACNA1F gene encodes an L-type calcium channel with unique biophysical properties and tissue distribution. J Neurosci ...
more infohttp://www.jneurosci.org/content/31/12/4397

Voltage-dependent L-type calcium channel subunit alpha-1D - DrugBankVoltage-dependent L-type calcium channel subunit alpha-1D - DrugBank

Voltage-dependent L-type calcium channel subunit alpha-1D. Details. Name. Voltage-dependent L-type calcium channel subunit ... Voltage-dependent L-type calcium channel subunit alpha-1D. Q01668. Details. Drug Relations. Drug Relations. DrugBank ID. Name. ...
more infohttps://www.drugbank.ca/biodb/bio_entities/BE0002359

Selective T-Type Calcium Channel Blockade Alleviates Hyperalgesia in ob/ob Mice | DiabetesSelective T-Type Calcium Channel Blockade Alleviates Hyperalgesia in ob/ob Mice | Diabetes

Reducing agents sensitize C-type nociceptors by relieving high-affinity zinc inhibition of T-type calcium channels J Neurosci ... New evidence that both T-type calcium channels and GABAA channels are responsible for the potent peripheral analgesic effects ... Recent studies have highlighted the importance of T-type calcium channels (T-channels) in peripheral nociception; therefore, ... Silencing of the Cav3.2 T-type calcium channel gene in sensory neurons demonstrates its major role in nociception EMBO J 2005; ...
more infohttp://diabetes.diabetesjournals.org/content/58/11/2656.full

N-Type Calcium Channels
      - N-Type Calcium Channel
     Summary Report | CureHunterN-Type Calcium Channels - N-Type Calcium Channel Summary Report | CureHunter

CALCIUM CHANNELS that are concentrated in neural tissue. Omega toxins inhibit the actions of these channels by altering their ... Channels, N-Type Calcium; Channels, Neural-Type Calcium; N Type Calcium Channel; N Type Calcium Channels; N Type VDCC; N Type ... N-Type Calcium Channel; Calcium Channels, N-Type; N-Type VDCC; N-Type Voltage-Dependent Calcium Channels; Calcium Channel, N- ... Type; Calcium Channels, N Type; Calcium Channels, Neural-Type; Channel, N-Type Calcium; ...
more infohttp://www.curehunter.com/public/keywordSummaryD020864-N-Type-Calcium-Channels-N-Type-Calcium-Channel.do

Q-type calcium channel - WikipediaQ-type calcium channel - Wikipedia

The Q-type calcium channel is a type of voltage-dependent calcium channel. Like the others of this class, the α1 subunit is the ... They are poorly understood, but like R-type calcium channels, they appear to be present in cerebellar granule cells. They have ... Q-Type Calcium Channel at the US National Library of Medicine Medical Subject Headings (MeSH). ... one that determines most of the channels properties. ...
more infohttps://en.wikipedia.org/wiki/Q-type_calcium_channel

Voltage-Dependent T-Type Calcium Channel Blockers -Pipeline Insight, 2019Voltage-Dependent T-Type Calcium Channel Blockers -Pipeline Insight, 2019

"Voltage-Dependent T-Type Calcium Channel Blockers. The report assesses the active Voltage-Dependent T-Type Calcium Channel ... "Voltage-Dependent T-Type Calcium Channel Blockers. • Features the Voltage-Dependent T-Type Calcium Channel Blockers pipeline ... "Voltage-Dependent T-Type Calcium Channel Blockers - Pipeline Insight, 2019" offers comprehensive insights of the pipeline ( ... Voltage-Dependent T-Type Calcium Channel Blockers -Pipeline Insight, 2019. *January 2019 • ...
more infohttps://www.reportbuyer.com/product/5129791/voltage-dependent-t-type-calcium-channel-blockers-pipeline-insight-2019.html

Abstract 16089: Functional Coupling of SK Channels and L-type Calcium Channels in Cardiomyocytes | CirculationAbstract 16089: Functional Coupling of SK Channels and L-type Calcium Channels in Cardiomyocytes | Circulation

Abstract 16089: Functional Coupling of SK Channels and L-type Calcium Channels in Cardiomyocytes. Xiao-Dong Zhang, Wei Chun ... Abstract 16089: Functional Coupling of SK Channels and L-type Calcium Channels in Cardiomyocytes ... Abstract 16089: Functional Coupling of SK Channels and L-type Calcium Channels in Cardiomyocytes ... Abstract 16089: Functional Coupling of SK Channels and L-type Calcium Channels in Cardiomyocytes ...
more infohttp://circ.ahajournals.org/content/132/Suppl_3/A16089

Depolarization-stimulated cholecystokinin secretion is mediated by L-type calcium channels in STC-1 cells | RTIDepolarization-stimulated cholecystokinin secretion is mediated by L-type calcium channels in STC-1 cells | RTI

Barium-induced secretion was inhibited by the L-type calcium-channel blocker, ... Blockade of potassium channels with barium chloride (5 mM) increased the release of CCK by 374.6 +/- 46.6% of control levels. ... To examine the role of calcium channels in depolarization-activated cholecystokinin (CCK) release, studies were performed in an ... To further evaluate a role for L-type calcium channels in the secretion of CCK, the effects of the L-type calcium channel ...
more infohttps://www.rti.org/publication/depolarization-stimulated-cholecystokinin-secretion-mediated-l-type-calcium-channels-stc

Molecular Mechanisms of Lipoic Acid Modulation of T-Type Calcium Channels in Pain Pathway | Journal of NeuroscienceMolecular Mechanisms of Lipoic Acid Modulation of T-Type Calcium Channels in Pain Pathway | Journal of Neuroscience

2007a) Reducing agents sensitize C-type nociceptors by relieving high-affinity zinc inhibition of T-type calcium channels. J ... 2005) Silencing of the CaV3.2 T-type calcium channel gene in sensory neurons demonstrates its major role in nociception. EMBO J ... Molecular Mechanisms of Lipoic Acid Modulation of T-Type Calcium Channels in Pain Pathway. Woo Yong Lee, Peihan Orestes, ... 2001b) Cav3.2 channel is a molecular substrate for inhibition of T-type calcium currents in rat sensory neurons by nitrous ...
more infohttp://www.jneurosci.org/content/29/30/9500

calcium channel, voltage-dependent, L type, alpha 1S subunit ELISA Kits | Biocompare.comcalcium channel, voltage-dependent, L type, alpha 1S subunit ELISA Kits | Biocompare.com

L type, alpha 1S subunit ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and ... calcium channel, voltage-dependent, L type, alpha 1S subunit ELISA Kits. Clear ... calcium channel, voltage-dependent, L type, alpha 1S subunit ELISA Kits. The ELISA (enzyme-linked immunosorbent assay) is a ... Mouse Calcium Channel, Voltage Dependent, L-Type, Alpha 1S Subunit (CACNa1S) ELISA Kit ...
more infohttps://www.biocompare.com/pfu/110627/soids/2-321525/Assay_Kit/ELISA_calcium_channel_voltage-dependent_L_type_alpha_1S_subunit

Estradiol receptor antagonist reduces ventricular arrhythmia via L-type calcium channels in chronic heart failure.Estradiol receptor antagonist reduces ventricular arrhythmia via L-type calcium channels in chronic heart failure.

... Minerva ... Estradiol receptor antagonist reduces ventricular arrhythmia via L-type calcium channels in chronic heart failure.. *. ... Estradiol receptor antagonist reduces ventricular arrhythmia via L-type calcium channels in chronic heart failure. Minerva ... Exendin-4 Reduces Ventricular Arrhythmia Activity and Calcium Sparks-Mediated Sarcoplasmic Reticulum Ca Leak in Rats with Heart ...
more infohttps://medworm.com/759935708/estradiol-receptor-antagonist-reduces-ventricular-arrhythmia-via-l-type-calcium-channels-in-chronic-/

Reversal of Neuropathic Pain in Diabetes by Targeting Glycosylation of Cav3.2 T-Type Calcium Channels | DiabetesReversal of Neuropathic Pain in Diabetes by Targeting Glycosylation of Cav3.2 T-Type Calcium Channels | Diabetes

Reversal of Neuropathic Pain in Diabetes by Targeting Glycosylation of Cav3.2 T-Type Calcium Channels. ... Reversal of Neuropathic Pain in Diabetes by Targeting Glycosylation of Cav3.2 T-Type Calcium Channels ... Reversal of Neuropathic Pain in Diabetes by Targeting Glycosylation of Cav3.2 T-Type Calcium Channels ... Reversal of Neuropathic Pain in Diabetes by Targeting Glycosylation of Cav3.2 T-Type Calcium Channels ...
more infohttp://diabetes.diabetesjournals.org/content/62/11/3828.supplemental

Deletion of T-type calcium channels Cav3.1 or Cav3.2 attenuates endothelial dysfunction in aging mice | SpringerLinkDeletion of T-type calcium channels Cav3.1 or Cav3.2 attenuates endothelial dysfunction in aging mice | SpringerLink

T-type Cav3.1 channels augment nitric oxide and co-localize with eNOS. Therefore, the hypothesis... ... T-type Cav3.1 channels augment nitric oxide and co-localize with eNOS. Therefore, the hypothesis was that T-type channels ... and T-type calcium channels in local and remote calcium responses in rat mesenteric terminal arterioles. J Vasc Res 46:138-151 ... Deletion of T-type calcium channels Cav3.1 or Cav3.2 attenuates endothelial dysfunction in aging mice. ...
more infohttps://link.springer.com/article/10.1007%2Fs00424-017-2068-x
  • To obtain selective and potent inhibitor for T-type calcium channel by ligand based drug design, 2-hydroxy-3-phenoxypropyl piperazine derivatives were synthesized and evaluated for in vitro activities. (elsevier.com)
  • Compound 6m and 6q showed high selectivity over hERG channel (IC 50 ratio of hERG/α 1G 6m = 8.5, 6q = 18.38) and they were subjected to measure pharmacokinetics profiles. (elsevier.com)
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