A sesquiterpene lactone found in roots of THAPSIA. It inhibits CA(2+)-TRANSPORTING ATPASE mediated uptake of CALCIUM into SARCOPLASMIC RETICULUM.
A class of compounds composed of repeating 5-carbon units of HEMITERPENES.
Cation-transporting proteins that utilize the energy of ATP hydrolysis for the transport of CALCIUM. They differ from CALCIUM CHANNELS which allow calcium to pass through a membrane without the use of energy.
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.
A divalent calcium ionophore that is widely used as a tool to investigate the role of intracellular calcium in cellular processes.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)
Intracellular messenger formed by the action of phospholipase C on phosphatidylinositol 4,5-bisphosphate, which is one of the phospholipids that make up the cell membrane. Inositol 1,4,5-trisphosphate is released into the cytoplasm where it releases calcium ions from internal stores within the cell's endoplasmic reticulum. These calcium ions stimulate the activity of B kinase or calmodulin.
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-transporting ATPases that catalyze the active transport of CALCIUM into the SARCOPLASMIC RETICULUM vesicles from the CYTOPLASM. They are primarily found in MUSCLE CELLS and play a role in the relaxation of MUSCLES.
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.
A fluorescent calcium chelating agent which is used to study intracellular calcium in tissues.
A chelating agent relatively more specific for calcium and less toxic than EDETIC ACID.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
Unsaturated derivatives of the ESTRANES with methyl groups at carbon-13, with no carbon at carbon-10, and with no more than one carbon at carbon-17. They must contain one or more double bonds.
A network of tubules and sacs in the cytoplasm of SKELETAL MUSCLE FIBERS that assist with muscle contraction and relaxation by releasing and storing calcium ions.
Chemical agents that increase the permeability of biological or artificial lipid membranes to specific ions. Most ionophores are relatively small organic molecules that act as mobile carriers within membranes or coalesce to form ion permeable channels across membranes. Many are antibiotics, and many act as uncoupling agents by short-circuiting the proton gradient across mitochondrial membranes.
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.
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.
Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS.
A group of compounds that are derivatives of oxo-pyrrolidines. A member of this group is 2-oxo pyrrolidine, which is an intermediate in the manufacture of polyvinylpyrrolidone. (From Merck Index, 11th ed)
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
Inorganic or organic compounds that contain boron as an integral part of the molecule.
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.
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.
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.
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.
The fluid inside CELLS.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
A plant genus of the family APIACEAE. Members contain THAPSIGARGIN and other guaianolides (SESQUITERPENES, GUAIANOLIDE).
Cyclic compounds with a ring size of approximately 1-4 dozen atoms.
An N-acetylglycosamine containing antiviral antibiotic obtained from Streptomyces lysosuperificus. It is also active against some bacteria and fungi, because it inhibits the glucosylation of proteins. Tunicamycin is used as tool in the study of microbial biosynthetic mechanisms.
A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.
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.
A subclass of phospholipases that hydrolyze the phosphoester bond found in the third position of GLYCEROPHOSPHOLIPIDS. Although the singular term phospholipase C specifically refers to an enzyme that catalyzes the hydrolysis of PHOSPHATIDYLCHOLINE (EC 3.1.4.3), it is commonly used in the literature to refer to broad variety of enzymes that specifically catalyze the hydrolysis of PHOSPHATIDYLINOSITOLS.
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.
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.
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.
A trace element with atomic symbol Mn, atomic number 25, and atomic weight 54.94. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver. (From AMA Drug Evaluations Annual 1992, p2035)
Established cell cultures that have the potential to propagate indefinitely.
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).
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.
The rate dynamics in chemical or physical systems.
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.
Various physiological or molecular disturbances that impair ENDOPLASMIC RETICULUM function. It triggers many responses, including UNFOLDED PROTEIN RESPONSE, which may lead to APOPTOSIS; and AUTOPHAGY.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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.
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.
A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.
Oxyvanadium ions in various states of oxidation. They act primarily as ion transport inhibitors due to their inhibition of Na(+)-, K(+)-, and Ca(+)-ATPase transport systems. They also have insulin-like action, positive inotropic action on cardiac ventricular muscle, and other metabolic effects.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
Five-membered heterocyclic ring structures containing an oxygen in the 1-position and a nitrogen in the 3-position, in distinction from ISOXAZOLES where they are at the 1,2 positions.
A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.
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.
Phosphoric acid esters of inositol. They include mono- and polyphosphoric acid esters, with the exception of inositol hexaphosphate which is PHYTIC ACID.
An electrogenic ion exchange protein that maintains a steady level of calcium by removing an amount of calcium equal to that which enters the cells. It is widely distributed in most excitable membranes, including the brain and heart.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
Compounds that bind to and activate PURINERGIC RECEPTORS.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 12 is activated by pro-apoptotic factors that are released during cell stress and by CARD SIGNALING ADAPTOR PROTEINS. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.
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.
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.
Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
Compounds with three aromatic rings in linear arrangement with an OXYGEN in the center ring.
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.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.
An indolocarbazole that is a potent PROTEIN KINASE C inhibitor which enhances cAMP-mediated responses in human neuroblastoma cells. (Biochem Biophys Res Commun 1995;214(3):1114-20)
A CCAAT-enhancer binding protein that is induced by DNA DAMAGE and growth arrest. It serves as a dominant negative inhibitor of other CCAAT-enhancer binding proteins.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
Uridine 5'-(tetrahydrogen triphosphate). A uracil nucleotide containing three phosphate groups esterified to the sugar moiety.
Organic nitrogenous bases. Many alkaloids of medical importance occur in the animal and vegetable kingdoms, and some have been synthesized. (Grant & Hackh's Chemical Dictionary, 5th ed)
Gadolinium. An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A proton ionophore that is commonly used as an uncoupling agent in biochemical studies.
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.
An imidazole derivative that is commonly used as a topical antifungal agent.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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.
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.
An inorganic dye used in microscopy for differential staining and as a diagnostic reagent. In research this compound is used to study changes in cytoplasmic concentrations of calcium. Ruthenium red inhibits calcium transport through membrane channels.
A partitioning within cells due to the selectively permeable membranes which enclose each of the separate parts, e.g., mitochondria, lysosomes, etc.
Elements of limited time intervals, contributing to particular results or situations.

The mammalian endoplasmic reticulum stress response element consists of an evolutionarily conserved tripartite structure and interacts with a novel stress-inducible complex. (1/2135)

When mammalian cells are subjected to calcium depletion stress or protein glycosylation block, the transcription of a family of glucose-regulated protein (GRP) genes encoding endoplasmic reticulum (ER) chaperones is induced to high levels. The consensus mammalian ER stress response element (ERSE) conserved among grp promoters consists of a tripartite structure CCAAT(N9)CCACG, with N being a strikingly GC-rich region of 9 bp. The ERSE, in duplicate copies, can confer full stress inducibility to a heterologous promoter in a sequence-specific but orientation-independent manner. In addition to CBF/NF-Y and YY1 binding to the CCAAT and CCACG motifs, respectively, we further discovered that an ER stress-inducible complex (ERSF) from HeLa nuclear extract binds specifically to the ERSE. Strikingly, the interaction of the ERSF with the ERSE requires a conserved GGC motif within the 9 bp region. Since mutation of the GGC triplet sequence also results in loss of stress inducibility, specific sequence within the 9 bp region is an integral part of the tripartite structure. Finally, correlation of factor binding with stress inducibility reveals that ERSF binding to the ERSE alone is not sufficient; full stress inducibility requires integrity of the CCAAT, GGC and CCACG sequence motifs, as well as precise spacing among these sites.  (+info)

Mechanisms involved in the metabotropic glutamate receptor-enhancement of NMDA-mediated motoneurone responses in frog spinal cord. (2/2135)

1. The metabotropic glutamate receptor (mGluR) agonist trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD) (10-100 microM) depolarized isolated frog spinal cord motoneurones, a process sensitive to kynurenate (1.0 mM) and tetrodotoxin (TTX) (0.783 microM). 2. In the presence of NMDA open channel blockers [Mg2+; (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK801); 3,5-dimethyl-1-adamantanamine hydrochloride (memantine)] and TTX, trans-ACPD significantly potentiated NMDA-induced motoneurone depolarizations, but not alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionate (AMPA)- or kainate-induced depolarizations. 3. NMDA potentiation was blocked by (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) (240 microM), but not by alpha-methyl-(2S,3S,4S)-alpha-(carboxycyclopropyl)-glycine (MCCG) (290 microM) or by alpha-methyl-(S)-2-amino-4-phosphonobutyrate (L-MAP4) (250 microM), and was mimicked by 3,5-dihydroxyphenylglycine (DHPG) (30 microM), but not by L(+)-2-amino-4-phosphonobutyrate (L-AP4) (100 microM). Therefore, trans-ACPD's facilitatory effects appear to involve group I mGluRs. 4. Potentiation was prevented by the G-protein decoupling agent pertussis toxin (3-6 ng ml(-1), 36 h preincubation). The protein kinase C inhibitors staurosporine (2.0 microM) and N-(2-aminoethyl)-5-isoquinolinesulphonamide HCI (H9) (77 microM) did not significantly reduce enhanced NMDA responses. Protein kinase C activation with phorbol-12-myristate 13-acetate (5.0 microM) had no effect. 5. Intracellular Ca2+ depletion with thapsigargin (0.1 microM) (which inhibits Ca2+/ATPase), 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetracetic acid acetyl methyl ester (BAPTA-AM) (50 microM) (which buffers elevations of [Ca2+]i), and bathing spinal cords in nominally Ca2+-free medium all reduced trans-ACPD's effects. 6. The calmodulin antagonists N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W7) (100 microM) and chlorpromazine (100 microM) diminished the potentiation. 7. In summary, group I mGluRs selectively facilitate NMDA-depolarization of frog motoneurones via a G-protein, a rise in [Ca2+]i from the presumed generation of phosphoinositides, binding of Ca2+ to calmodulin, and lessening of the Mg2+-produced channel block of the NMDA receptor.  (+info)

Mouse trp2, the homologue of the human trpc2 pseudogene, encodes mTrp2, a store depletion-activated capacitative Ca2+ entry channel. (3/2135)

Capacitative Ca2+ entry (CCE) is Ca2+ entering after stimulation of inositol 1,4,5-trisphosphate (IP3) formation and initiation of Ca2+ store depletion. One hallmark of CCE is that it can also be triggered merely by store depletion, as occurs after inhibition of internal Ca2+ pumps with thapsigargin. Evidence has accumulated in support of a role of transient receptor potential (Trp) proteins as structural subunits of a class of Ca2+-permeable cation channels activated by agonists that stimulate IP3 formation-very likely through a direct interaction between the IP3 receptor and a Trp subunit of the Ca2+ entry channel. The role of Trp's in Ca2+ entry triggered by store depletion alone is less clear. Only a few of the cloned Trp's appear to enhance this type of Ca2+ entry, and when they do, the effect requires special conditions to be observed, which native CCE does not. Here we report the full-length cDNA of mouse trp2, the homologue of the human trp2 pseudogene. Mouse Trp2 is shown to be readily activated not only after stimulation with an agonist but also by store depletion in the absence of an agonist. In contrast to other Trp proteins, Trp2-mediated Ca2+ entry activated by store depletion is seen under the same conditions that reveal endogenous store depletion-activated Ca2+ entry, i.e., classical CCE. The findings support the general hypothesis that Trp proteins are subunits of store- and receptor-operated Ca2+ channels.  (+info)

Calcium and cAMP are second messengers in the adipokinetic hormone-induced lipolysis of triacylglycerols in Manduca sexta fat body. (4/2135)

We have previously shown that stereospecific hydrolysis of stored triacylglycerol by a phosphorylatable triacylglycerol-lipase is the pathway for the adipokinetic hormone-stimulated synthesis of sn -1, 2-diacylglycerol in insect fat body. The current series of experiments were designed to determine whether cAMP and/or calcium are involved in the signal transduction pathway for adipokinetic hormone in the fat body. After adipokinetic hormone treatment, cAMP-dependent protein kinase activity in the fat body rapidly increased and reached a maximum after 20 min, suggesting that adipokinetic hormone causes an increase in cAMP. Forskolin (0.1 micrometer), an adenylate cyclase activator, induced up to a 97% increase in the secretion of diacylglycerol from the fat body. 8Br-cAMP (a membrane-permeable analog of cAMP) produced a 40% increase in the hemolymph diacylglycerol content. Treatment with cholera toxin, which also stimulates adenylate cyclase, induced up to a 145% increase in diacylglycerol production. Chelation of extracellular calcium produced up to 70% inhibition of the adipokinetic hormone-dependent mobilization of lipids. Calcium-mobilizing agents, ionomycin and thapsigargin, greatly stimulated DG production by up to 130%. Finally, adipokinetic hormone caused a rapid increase of calcium uptake into the fat body. Our findings indicate that the action of adipokinetic hormone in mobilizing lipids from the insect fat body involves both cAMP and calcium as intracellular messengers.  (+info)

Isosmotic modulation of Ca2+-regulated exocytosis in guinea-pig antral mucous cells: role of cell volume. (5/2135)

1. Exocytotic events and changes of cell volume in mucous cells from guinea-pig antrum were examined by video-enhanced optical microscopy. 2. Acetylcholine (ACh) evoked exocytotic events following cell shrinkage, the frequency and extent of which depended on the ACh concentration. ACh actions were mimicked by ionomycin and thapsigargin, and inhibited by Ca2+-free solution and Ca2+ channel blockers (Ni2+, Cd2+ and nifedipine). Application of 100 microM W-7, a calmodulin inhibitor, also inhibited the ACh-induced exocytotic events. These results indicate that ACh actions are mediated by intracellular Ca2+ concentration ([Ca2+]i) in antral mucous cells. 3. The effects of ion channel blockers on exocytotic events and cell shrinkage evoked by ACh were examined. Inhibition of KCl release (quinine, Ba2+, NPPB or KCl solution) suppressed both the exocytotic events and cell shrinkage evoked by ACh. 4. Bumetanide (inhibition of NaCl entry) or Cl--free solution (increasing Cl- release and inhibition of NaCl entry) evoked exocytotic events following cell shrinkage in unstimulated antral mucous cells and caused further cell shrinkage and increases in the frequency of exocytotic events in ACh-stimulated cells. However, Cl--free solution did not evoke exocytotic events in unstimulated cells in the absence of extracellular Ca2+, although cell shrinkage occurred. 5. To examine the effects of cell volume on ACh-evoked exocytosis, the cell volume was altered by increasing the extracellular K+ concentration. The results showed that cell shrinkage increases the frequency of ACh-evoked exocytotic events and cell swelling decreases them. 6. Osmotic shrinkage or swelling caused the frequency of ACh-evoked exocytotic events to increase. This suggests that the effects of cell volume on ACh-evoked exocytosis under anisosmotic conditions may not be the same as those under isosmotic conditions. 7. In antral mucous cells, Ca2+-regulated exocytosis is modulated by cell shrinkage under isosmotic conditions.  (+info)

Mitochondrial regulation of the cytosolic Ca2+ concentration and the InsP3-sensitive Ca2+ store in guinea-pig colonic smooth muscle. (6/2135)

1. Mitochondrial regulation of the cytosolic Ca2+ concentration ([Ca2+]c) in guinea-pig single colonic myocytes has been examined, using whole-cell recording, flash photolysis of caged InsP3 and microfluorimetry. 2. Depolarization increased [Ca2+]c and triggered contraction. Resting [Ca2+]c was virtually restored some 4 s after the end of depolarization, a time when the muscle had shortened to 50 % of its fully relaxed length. The muscle then slowly relaxed (t = 17 s). 3. The decline in the Ca2+ transient was monophasic but often undershot or overshot resting levels, depending on resting [Ca2+]c. The extent of the overshoot or undershoot increased with increasing peak [Ca2+]c. 4. Carbonyl cyanide m-chlorophenyl hydrazone (CCCP; 5 microM), which dissipates the mitochondrial proton electrochemical gradient and therefore prevents mitochondrial Ca2+ accumulation, slowed Ca2+ removal at high ( > 300 nM) but not at lower [Ca2+]c and abolished [Ca2+]c overshoots. Oligomycin B (5 microM), which prevents mitchondrial ATP production, affected neither the rate of decline nor the magnitude of the overshoot. 5. During depolarization, the global rhod-2 signal (which represents the mitochondrial matrix Ca2+ concentration, [Ca2+]m) rose slowly in a CCCP-sensitive manner during and for about 3 s after depolarization had ended. [Ca2+]m then slowly decreased over tens of seconds. 6. Inhibition of sarcoplasmic reticulum Ca2+ uptake with thapsigargin (100 nM) reduced the undershoot and increased the overshoot. 7. Flash photolysis of caged InsP3 (20 microM) evoked reproducible increases in [Ca2+]c. CCCP (5 microM) reduced the magnitude of the [Ca2+]c transients evoked by flash photolysis of caged InsP3. Oligomycin B (5 microM) did not reduce the inhibition of the InsP3-induced Ca2+ transient by CCCP thus minimizing the possibility that CCCP lowered ATP levels by reversing the mitochondrial ATP synthase and so reducing SR Ca2+ refilling. 8. While CCCP reduced the magnitude of the InsP3-evoked Ca2+ signal, the internal Ca2+ store content, as assessed by the magnitude of ionomycin-evoked Ca2+ release, did not decrease significantly. 9. [Ca2+]c decline in smooth muscle, following depolarization, may involve mitochondrial Ca2+ uptake. Following InsP3-evoked Ca2+ release, mitochondrial uptake of Ca2+ may regulate the local [Ca2+]c near the InsP3 receptor so maintaining the sensitivity of the InsP3 receptor to release Ca2+ from the SR.  (+info)

Thapsigargin inhibits a potassium conductance and stimulates calcium influx in the intact rat lens. (7/2135)

1. An increase in lens cell calcium has long been associated with cortical cataract. Recently, it has been shown that thapsigargin induces a rise in lens cell calcium by release from endoplasmic reticulum stores. The effects of this rise on the optical and membrane characteristics of the lens were studied in the isolated rat lens. 2. The electrical characteristics of the isolated, perifused rat lens were measured using a two-internal microelectrode technique that permits measurement of plasma membrane conductance (Gm), membrane potential (Vm) and junctional conductance in the intact lens. 3. Thapsigargin (1 microM) induced a rapid overall depolarization of Vm that was accompanied by first a decrease and then an increase in Gm. 4. Replacing external Na+ with tetraethylammonium (TEA) abolished the decrease in Gm. However, a transient increase phase was still observed. 5. The changes in conductance were further characterized by measuring 22Na+ and 45Ca2+ influxes into the isolated lens. Thapsigargin (1 microM) induced a transient increase in 45Ca2+, but did not affect Na+ influx. 6. The Ca2+ channel blocker La3+ (10 microM) totally inhibited the thapsigargin-induced Ca2+ influx. It also blocked the increase in Gm observed in control and in Na+-free-TEA medium. In the absence of external calcium, thapsigargin induced a small depolarization in Vm. 7. These data indicate that thapsigargin induces both a decrease in K+ conductance and an increase in Ca2+ conductance. These probably result from release of stored Ca2+ and subsequent activation of store-operated Ca2+ channels (capacitative Ca2+ entry). 8. Thapsigargin application over the time course of these experiments (24 h) had no effect on junctional conductance or on the transparency of the lens.  (+info)

Chemical signaling from colonic smooth muscle cells to DRG neurons in culture. (8/2135)

Transduction mechanisms between target cells within the intestinal wall and peripheral terminals of extrinsic primary afferent neurons are poorly understood. The purpose of this study was to characterize the interactions between smooth muscle cells from the rat distal colon and lumbar dorsal root ganglion (DRG) neurons in coculture. DRG neurons visually appeared to make contact with several myocytes. We show that brief mechanical stimulation of these myocytes resulted in intracellular Ca2+ concentration ([Ca2+]i) transients that propagated into 57% of the contacting neurites. Direct mechanical stimulation of DRG neurites cultured without smooth muscle had no effect. We also show that colonic smooth muscle cells express multiple connexin mRNAs and that these connexins formed functional gap junctions, as evidenced by the intercellular transfer of Lucifer yellow. Furthermore, thapsigargin pretreatment and neuronal heparin injection abolished the increase in neurite [Ca2+]i, indicating that the neuronal Ca2+ signal was triggered by inositol 1,4, 5-trisphosphate-mediated Ca2+ release from intracellular stores. Our results provide evidence for intercellular chemical communication between DRG neurites and intestinal smooth muscle cells that mediates the exchange of second messenger molecules between different cell types.  (+info)

The steady-state ATPase activity of sarcoplasmic-reticulum (Ca(2+)-Mg2+)-ATPase is inhibited by thapsigargin at a molar ratio of 1:1, with a dissociation constant for thapsigargin estimated to be in the sub-nanomolar range. In the presence of thapsigargin, only a single Ca2+ ion binds to the ATPase. Similarly, addition of thapsigargin to the ATPase incubated in the presence of Ca2+ results in the release of one of the two originally bound Ca2+ ions. As monitored by the fluorescence of nitrobenzo-2-oxa-1,3-diazole-labelled ATPase, thapsigargin appears to shift the transition between E1 and E2 conformations towards E2. Addition of thapsigargin prevents phosphorylation of the ATPase by P(i) and results in a very low steady-state level of phosphorylation of the ATPase by ATP, as observed previously for nonylphenol. ...
FIG. 2. Dose- and time-dependent effects of SERCA inhibition on CHOP expression, caspase-3 activation, and cell death. Cell death was assayed in real-time by propidium iodide incorporation in MIN6 cells. A: Images illustrating the progressive propidium iodide incorporation in a field of MIN6 cells exposed to 1 μmol/l thapsigargin (Tg). B: Representative time course of cell death in response to various concentrations of thapsigargin. ○, Control; ▪, 0.01 μmol/l thapsigargin; ▴, 0.1 μmol/l thapsigargin; •, 1 μmol/l thapsigargin. C: Dose dependence of the thapsigargin-induced MIN6 cell death, quantified as the area under the curves (IAUC) of the first 24 h of the propidium iodide incorporation profiles (n = 3). D: Induction of CHOP (∼31-kDa band) and cleaved caspase-3 (∼17- to 19-kDa band) in MIN6 cells cultured for 24 h in DMEM containing 25 mmol/l glucose and increasing concentrations of thapsigargin (n = 3). E: Representative real-time imaging of caspase-3 activation in living ...
Hughes AR, Thastrup O, and Putney JW, Jr. Activation of calcium entry by the tumor promoter thapsigargin in parotid acinar cells. Evidence that an intracellular calcium pool and not an inositol phosphate regulate calcium fluxes at the plasma membrane. J Biol Chem 1989;264:12,266- 12,271. 45. Putney JW, Jr. Capacitative calcium entry revisited. Cell Calcium 1990;11:611-624. 46. Putney JW, Jr, Bird GSJ. The inositol phosphate-calcium signaling system in no-excitable cells. Endocr Rev 1993;14:610-631. Putney JW Jr. Type 3 inositol 1,4,5-trisphosphate receptor and capacitative calcium entry. Cell Calcium 1997;21:257-261. 13. Fagan KA, Graf RA, Tolman S, Schaack J, Cooper MF. Regulation of a Ca2+-sensitive adenylyl cyclase in an excitable cell. Role of voltage-gated versus capacitative Ca2+ entry. J Biol Chem 2000;275:40,187- 40,194. 14. Herms I, Schneider J, Dewachter I, Caluwaerts N, Kretzshmar H, Van Leuven F. Capacitative calcium entry is directly activated by mutant presenilin-1 independent of ...
Although other antiapoptotic genes may be implicated in the protection of c-myc-induced cell death, we pursued the potential protective function of Bcl-xL in view of its link with c-myc in β-cell survival and proliferation (Pelengaris et al., 2002). Small increases in Bcl-xL, similar to those observed in our work, were shown to protect β-cells against thapsigargin-induced apoptosis in a transgenic mouse model. Increased levels of this mitochondrially targeted protein were also found to impair insulin secretion (Zhou et al., 2000). Consistent with these studies, we found that glucose-stimulated insulin exocytosis was attenuated by 50% in Pax4-overexpressing islets 48 h after infection. β-Galactosidase-expressing islets and noninfected controls exhibited an expected threefold increase in hormone release (Fig. 5 A). However, inhibition was transient as glucose-induced insulin secretion was restored 6 d after infection (unpublished data). Inclusion of 1 μM forskolin/100 μM IBMX, which modulates ...
Although other antiapoptotic genes may be implicated in the protection of c-myc-induced cell death, we pursued the potential protective function of Bcl-xL in view of its link with c-myc in β-cell survival and proliferation (Pelengaris et al., 2002). Small increases in Bcl-xL, similar to those observed in our work, were shown to protect β-cells against thapsigargin-induced apoptosis in a transgenic mouse model. Increased levels of this mitochondrially targeted protein were also found to impair insulin secretion (Zhou et al., 2000). Consistent with these studies, we found that glucose-stimulated insulin exocytosis was attenuated by 50% in Pax4-overexpressing islets 48 h after infection. β-Galactosidase-expressing islets and noninfected controls exhibited an expected threefold increase in hormone release (Fig. 5 A). However, inhibition was transient as glucose-induced insulin secretion was restored 6 d after infection (unpublished data). Inclusion of 1 μM forskolin/100 μM IBMX, which modulates ...
To investigate the relationship between the nitric oxide (NO) and the endoplasmic reticulum (ER)-related cell death in human astroglioma CRT-MG cells, the cells were treated with S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor and thapsigargin, an ER-stress inducer, respectively. The SNAP as well as thapsigargin increased the cytosolic Ca2+ and led to apoptosis in a dose dependent manner in CRT-MG cells suggesting NO depletes ER Ca2+. The expressions of ER-associated molecules including IRE1, p-eIF2\#945;, ATF-1 and Ero1-\#945; increased in the thapsigargin- or SNAP- treated CRT-MG cells. Among them the expression of IRE1 markedly began to increase at 12 hrs, peaked at 24 hrs, and was still persisted up to 48 hrs on the treatment of cells with thapsigargin or SNAP. Furthermore, the nuclease activity of IRE1 was also detected in the thapsigargin- or SNAP- treated CRT-MG cells. SNAP as well as the thapsigargin induced the formation of the IRE1-TRAF2 complex and the increase of expressions ...
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The mechanism of Ca2+ entry after ligand binding to receptors on the surface of non-excitable cells is a current focus of interest. Considerable attention has been given to Ca2+ influx induced by emptying of intracellular pools. Thapsigargin, an inhibitor of microsomal Ca(2+)-ATPase, is an important tool in inducing store-regulated Ca2+ influx. In the present paper we show that, at concentrations above 500 nM, thapsigargin also has an opposite effect: it inhibits store-regulated Ca2+ influx into Fura-2-loaded human neutrophil granulocytes. As thapsigargin has been frequently applied at concentrations up to 2 microM, its inhibitory action on plasma-membrane Ca2+ fluxes deserves consideration. ...
Pan-embryonic Ca2+ waves during epiboly/gastrula stages are believed to coordinate convergent extension (CE), the lengthening and narrowing of groups of cells, as well as their directed migration to the future dorsal side (Wallingford et al., 2001; Wallingford et al., 2002). Genetic data supports this idea, in that zebrafish homozygous zygotic Wnt-5 mutants (pipetail) display CE defects and have reduced Ca2+ release frequency (Westfall et al., 2003a). In fact, thapsigargin treatment during 30-50% epiboly resulted in cell movement defects and a shortened anterior-posterior axis (data not shown), consistent with previously described thapsigargin-induced phenotypes (Creton, 2004). However, brief thapsigargin treatment of epiboly/gastrula stage zebrafish and Xenopus disrupts laterality without perturbing normal cell movement. Similar laterality defects are generated with additional inhibitors (valproate, to disrupt inositol levels, XeC, to inhibit IP3-induced Ca2+ release and cyclopiazonic acid, to ...
This milestone signifies the advancement in Phytons Plant Cell Fermentation development program that now has begun to define the process by which the Thapsia plant is converted into a preserved, fermentable cell line, thus providing a more sustainable source of high-quality thapsigargin. Phyton is converting the Thapsia plant into thapsigargin in partnership with Inspyr Therapeutics, Inc. , a clinical-stage biotechnology company that has a patented technology platform utilizing thapsigargin for its prodrug delivery system, mipsagargin.. ...
Live-cell imaging allows for the in-depth study of activities occurring within living cells. The understanding of these complex interactions has wide ranging implications to many biomedical applications [1]. As the techniques used in live-cell imaging have improved, they have become an important component of monitoring the interactions within and among cells throughout their lifecycle [2, 3] . Several probes have been developed in relation to these endeavors, [4-6], and in turn, we have created T-Time, a repository of T cell images using a novel tag developed in [7].. T cells are lymphocytes that play a central role in cell-mediated immunity to foreign pathogens. Dysregulated T cell responses are implicated in numerous chronic conditions ranging from severe combined immunodeficiency (SCID) to autoimmunity and cancer. T cells migrate extensively throughout the body to enable proper immune function. This migration is the focus of extensive research and has motivated the development of ...
BioTek Application Notes, 05-Oct-18, Thapsigargin-induced Cellular Stress Response and Inhibition of Gq-dependent Calcium Signaling
Cyclopiazonic acid and thapsigargin induce platelet aggregation resulting from Ca2+ influx through Ca2+ store-activated Ca2+- channels Academic Article ...
TY - JOUR. T1 - Regulation of calreticulin gene expression by calcium. AU - Waser, Mathilde. AU - Mesaeli, Nasrin. AU - Spencer, Charlotte. AU - Michalak, Marek. PY - 1997/8/11. Y1 - 1997/8/11. N2 - We have isolated and characterized a 12-kb mouse genomic DNA fragment containing the entire calreticulin gene and 2.14 kb of the promoter region. The mouse calreticulin gene consists of nine exons and eight introns, and it spans 4.2 kb of genomic DNA. A 1.8-kb fragment of the calreticulin promoter was subcloned into a reporter gene plasmid containing chloramphenicol acetyltransferase. This construct was then used in transient and stable transfection of NIH/3T3 cells. Treatment of transfected cells either with the Ca2+ ionophore A23187, or with the ER Ca2+-ATPase inhibitor thapsigargin, resulted in a five- to sevenfold increase of the expression of chloramphenicol acetyltransferase protein. Transactivation of the calreticulin promoter was also increased by fourfold in NIH/3T3 cells treated with ...
Orai1 antibody (ORAI calcium release-activated calcium modulator 1) for ELISA, ICC/IF, IHC-P, WB. Anti-Orai1 pAb (GTX85057) is tested in Human, Mouse samples. 100% Ab-Assurance.
The molecular nature of calcium (Ca(2+))-dependent mechanisms and the ion channels having a major role in the apoptosis of cancer cells remain a subject of debate. Here, we show that the recently identified Orai1 protein represents the major molecular component of endogenous store-operated Ca(2+) entry (SOCE) in human prostate cancer (PCa) cells, and constitutes the principal source of Ca(2+) influx used by the cell to trigger apoptosis. The downregulation of Orai1, and consequently SOCE, protects the cells from diverse apoptosis-inducing pathways, such as those induced by thapsigargin (Tg), tumor necrosis factor α, and cisplatin/oxaliplatin. The transfection of functional Orai1 mutants, such as R91W, a selectivity mutant, and L273S, a coiled-coil mutant, into the cells significantly decreased both SOCE and the rate of Tg-induced apoptosis. This suggests that the functional coupling of STIM1 to Orai1, as well as Orai1 Ca(2+)-selectivity as a channel, is required for its pro-apoptotic effects. We have
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Calcium (Ca2+) is a fundamental regulator of cell signaling and function. Thapsigargin (Tg) blocks the sarco/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA), disrupts Ca2+ homeostasis, and causes cell death. However, the exact mechanisms whereby SERCA-inhibition induces cell death are incompletely understood. Here, we report that low (0.1 μM) concentrations of Tg and Tg analogs with various long-chain substitutions at the O(8) position extensively inhibit SERCA1a-mediated Ca2+ transport. We also found that in both prostate and breast cancer cells, exposure to Tg or Tg analogs for 1 day caused extensive drainage of the ER Ca2+ stores. This Ca2+ depletion was followed by markedly reduced cell proliferation rates and morphological changes that developed over 2-4 days and culminated in cell death. Interestingly, these changes were not accompanied by bulk increases in cytosolic Ca2+ levels. Moreover, knockdown of two key store-operated Ca2+ entry (SOCE) components, Orai1 and STIM1, did not reduce Tg ...
Dense core granules of exocrine cells are a potential source of calcium, and results to date have been controversial regarding whether the calcium in these organelles is involved in controlling the cytosolic calcium concentration. Mitchell et al. developed a fusion protein between the dense core transmembrane protein VAMP and the calcium-sensitive bioluminescent protein aequorin in order to visualize calcium in the dense core granules of a pancreatic β cell line. Vesicular free [Ca2+] was approximately 50 μM, significantly lower than endoplasmic reticulum (ER) or Golgi free [Ca2+]. Vesicular [Ca2+] increased when calcium was reintroduced to the cells following calcium depletion. Uptake required adenosine triphosphate (ATP) and was inhibited by high concentrations of orthovanadate, but not by the ER Ca2+ ATPase inhibitor thapsigargin or by agents that altered intravesicular pH or elevations in Na+ concentration, suggesting that the uptake does not occur through a Ca2+/H+ exchanger or through a ...
The cytoplasmic free calcium concentration ([Ca2+]i) was studied in Fura-2/AM loaded granule neurones in acutely prepared cerebellar slices isolated from neonatal (6 days old) and adult (30 days old) mice. Bath application of elevated (10-50 mM) KCl-containing extracellular solutions evoked [Ca2+]i rise which was dependent on extracellular Ca2+. The K(+)-induced [Ca2+]i elevation was inhibited to different extends by verapamil, nickel and omega-conotoxin suggesting the coexpression of different subtypes of plasmalemmal voltage-gated Ca2+ channels. Bath application of caffeine (10-40 mM) elevated [Ca2+]i by release of Ca2+ from intracellular stores. Caffeine-induced [Ca2+]i elevation was inhibited by 100 microM ryanodine and 500 nM thapsigargin. Depletion of internal Ca2+ stores by caffeine, or blockade of Ca2+ release channels by ryanodine, did not affect depolarization-induced [Ca2+]i transients, suggesting negligible involvement of Ca(2+)-induced Ca2+ release in [Ca2+]i signal generation following
Although many aspects of capacitative Ca2+ entry remain unknown or controversial, the store-dependent generation of the plasma membrane Ca2+ influx appears to be certain and well documented. The first direct experimental proof of the capacitative Ca2+ entry model was demonstrated by Hallam et al. (5). They determined that depletion of the intracellular stores activated Ca2+ entry by a mechanism independent of receptor occupation or inositol phosphates. Depletion of the intracellular stores by repetitive agonist stimulation in a Ca2+-free environment triggered a large influx of Ca2+ when the ion was returned to the extracellular environment. This large Ca2+ influx or overshoot is now the characteristic trademark of capacitative Ca2+ entry. This influx pathway can also be activated by inhibition of the sarcoplasmic-endoplasmic reticulum Ca2+-ATPase pump using thapsigargin, cyclopiazonic acid, or 2,5-di-tert-butyl-1,4-benzohydroquinone. These inhibitors block the sequestration of Ca2+, thereby ...
Thapsigargin is derived from the plant Thapsia garganica that produces tumor promoters. This effect is a result of emptying the...
Studies in humans and in animal models have shown that high-density lipoprotein, or HDL, reduces the risk of diabetes by decreasing ER stress and beta-cell apoptosis. Researchers also have found that the hedgehog signaling pathway and cholesterol are involved in the fate of pancreatic beta cells and insulin production.. Mustafa Yalcinkaya and colleagues at the University Hospital of Zurich, Switzerland, published a paper in the Journal of Lipid Research on the mechanism by which HDL and the hedgehog signaling molecule Smoothened, or Smo, reduce beta-cell apoptosis induced by ER stress. They treated rat insulinoma beta cells with the ER stress inducer thapsigargin in the presence or absence of native HDL or CSL-111 (an artificially reconstituted HDL). Apoptosis studies such as free nucleosome assay and Caspase-3 activity assay showed that both HDL and CSL-111 reduced apoptosis in these cells.. Similar experiments involving the knockdown of oxysterol-producing enzyme cytochrome P450 and ...
To unravel the evolutionarily conserved genetic network underlying energy homeostasis, we performed a systematic in vivo gene knockdown screen in D...
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Calcium release-activated calcium channels (CRAC) control influx of calcium in human T lymphocytes. Hour-long calcium elevations are necessary for efficient gene expression during T cell activation and proliferation. We report here that, the time course for store-operated Ca2+ entry is short-lived (3-4 min) and therefore, cannot account for the prolonged Ca2+ elevations necessary for NFAT translocation into nucleus. Previous findings strongly suggest that T cell activation is accompanied by cytosolic alkalinization. Here, we show that pH changes in Jurkat T cells following activation with mitogenic lectin, phytohemagglutinin (PHA), depends on the length of time of exposure and the concentration (potency) of the mitogen. For full understanding of ion fluxes involved in this process, it is important to distinguish CRAC channel subtype functions in these cells during activation as well as elucidate the pH mediated changes in Ca2+. In some experiments we show low pH with high concentrations of PHA. We also
title: Regulation of phagocytosis and cytokine secretion by store-operated calcium entry in primary isolated murine microglia, doi: 10.1016/j.cellsig.2014.11.003, category: Article
In this study, we have analysed the relationship between Ca2+ pumps and Ins(1,4,5)P3-sensitive Ca2+ channels in myeloid cells. To study whether sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA)-type Ca2+-ATPases are responsible for Ca2+ uptake into Ins(1,4,5)P3-sensitive Ca2+ stores, we used the three structurally unrelated inhibitors thapsigargin, 2,5-di-t-butylhydroquinone and cyclopiazonic acid. In HL-60 cells, all three compounds precluded formation of the phosphorylated intermediate of SERCA-type Ca2+-ATPases. They also decreased, in parallel, ATP-dependent Ca2+ accumulation and the amount of Ins(1,4,5)P3-releasable Ca2+. Immunoblotting with subtype-directed antibodies demonstrated that HL-60 cells contain the Ca2+ pump SERCA2 (subtype b), and the Ca2+-release-channel type-1 Ins(1,4,5)P3 receptor. In subcellular fractionation studies, SERCA2 and type-1 Ins(1,4,5)P3 receptor co-purified. Immunofluorescence studies demonstrated that both type-1 Ins(1,4,5)P3 receptor and SERCA2 were ...
To test the involvement of the endoplasmic reticulum (ER) in LA-induced Ca2+cytincrease, neurons were pretreated prior to LA addition with 100 nm thapsigargin (Tps), which releases and depletes ER Ca2+by inhibiting the ERs ATP-dependent Ca2+transport. 28 Representative single neuron tracings are depicted in figure 5, while statistical comparisons of the Ca2+cytaverages for 0-10 min and 10-60 min after LA addition are depicted in figure 6. As expected, Tps pretreatment caused a transient increase in Ca2+cytwhich returned to a plateau level slightly higher than pre-Tps Ca2+cytas Ca2+cytreleased from the ER was transported out of the cell and sequestered in other organelles. Subsequent addition of LA equipotent to lidocaine 1 or 2.5% caused minimal increase in Ca2+cyt, consistent with the ER being the origin of the initial transient Ca2+cytpeak seen with these LA concentrations in the absence of Tps. In contrast, Tps pretreatment had no effect on the large increase in Ca2+cytcaused by 5% lidocaine ...
E2F-1 is a transcription factor that is involved in cellular growth and regulates the transition between G1 and S phase during the cell cycle. However, the mechanisms by which E2F-1 regulates endoplasmic reticulum (ER) stress in ventricular myocytes remain poorly defined. ER stress was triggered by tunicamycin or thapsigargin; gene transcription was assessed by polymerase chain reaction and protein expression was detected by western blot. Cell viability and mitochondrial defects were assessed by fluorescent microscopy imaging. During ER stress, E2F-1 repressed signaling molecules of the unfolded protein response (UPR) and sensitized myocytes to cell death triggered by thapsigargin that was inhibited in Bnip3 null fibroblasts. Bnip3Δex3 rescued thapsigargin-induced cardiac apoptosis, blocked mitochondrial defects and rescued hypoxia/ER stress induced cardiac cell death. This study provides evidence that E2F-1 sensitizes ventricular myocytes to ER stress induced apoptosis 1) by repressing the ...
https://doi.org/10.18632/oncotarget.12187 Lisha Qi, Wangzhao Song, Lingmei Li, Lu Cao, Yue Yu, Chunmin Song, Yalei Wang, Fei Zhang, Yang Li, Bin Zhang, Wenfeng Cao
An elevated level of Ca2+ is an important factor in cataract, yet precisely how Ca2+ enters the lens is unknown. Lens epithelial cells contain a range of G-protein-coupled receptors and receptor tyrosine kinases that induce increases in intracellular Ca2+. Receptor-associated Ca2+ influx is, therefore, likely to be an important route for Ca2+ influx to the lens. The authors investigated stimulated and passive Ca2+ influx in in situ human lens epithelium. Ca2+ changes in equatorial (E) and central anterior (CA) epithelial cells were monitored with the use of a Ca2+ indicator (Fluo4) and confocal microscopy. Gene expression was monitored by RT-PCR and immunoblotting. Adenosine triphosphate (ATP) induced Ca2+ responses that were smaller in CA than E. Ca2+ store depletion, using ATP (100 µM) or thapsigargin (1 µM), revealed greater relative store capacity and Ca2+ influx in E. Ca2+ influx was blocked by La3+ (0.5 µM) in both regions. Unstimulated Ca2+ influx was greater in E than CA. Greater ...
The presence of a store-operated or capacitative pathway was first suggested by Putney (Putney, 1990; Putney, 1986) and has since proved to be the most important mechanism for Ca2+ entry into non-excitable cells. In the excitable pancreatic β-cell, this mechanism seems to have only modest direct effects on [Ca2+]i (Liu and Gylfe, 1997) but, by modulating the membrane potential, store-operated fluxes of Ca2+ and Na+ may be significant for the more pronounced Ca2+ influx through the voltage-dependent channels (Worley et al., 1994; Bertram et al., 1995; Liu and Gylfe, 1997; Gilon et al., 1999). The molecular events coupling Ca2+ emptying of the ER to activation of Ca2+ influx have not yet been unequivocally identified (Putney, 1999). More than one mechanism may be involved, explaining why the Ca2+ influx is activated in an all-or-none fashion after almost complete emptying of the intracellular Ca2+ stores in some types of cells (Fierro and Parekh, 2000; Fierro et al., 2000), whereas there is ...
Changes in the cytoplasm free Ca2+ concentration [Ca2+]in regulate a large number of relevant physiological processes and have a major impact on cell development and function. The identification of STIM, the endoplasmic reticulum (ER) Ca2+ sensor, and Orai, a key subunit of the Ca2+ release-activated Ca2+ (CRAC) channel pore, have provided the tools to illuminate the mechanisms of CRAC channel regulation, that play an important role in modulation of the free Ca2+ concentration in non-excitable cells. Store-operated Ca2+ entry (SOCE) is a common and ubiquitous mechanism for regulating Ca2+ influx into cells and is widely expressed in most tissues. ...
SWISS-MODEL Template Library (SMTL) entry for 3nal.1. SR Ca(2+)-ATPase in the HnE2 state complexed with the Thapsigargin derivative DTB
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Calbiochem Thapsigargin, CAS 67526-95-8, is a cell-permeable, tumor-promoting sesquiterpene lactone that releases calcium by ... More,, Thapsigargin, CAS 67526-95-8, is a cell-permeable, tumor-promoting sesquiterpene lactone that releases calcium by non- ... Thapsigargin - CAS 67526-95-8 - Calbiochem MSDS (material safety data sheet) or SDS, CoA and CoQ, dossiers, brochures and other ... Thapsigargin, CAS 67526-95-8, is a cell-permeable, tumor-promoting sesquiterpene lactone that releases calcium by non- ...
Thapsigargin affinity purification of intracellular P2A-type Ca2+ ATPases. Publikation: Bidrag til tidsskrift › ... In a first step, these proteins were purified with the aid of an analogue of the SERCA inhibitor thapsigargin (Tg) coupled to a ... This study shows that it is possible to purify functionally active intracellular Ca(2+) ATPases using successive thapsigargin ...
Thapsigargin (TG; 5-25 nM), cyclopiazonic acid (CPA; 5-20 microM), and tert-butylhydroquinone (tBHQ; 80-200 microM), inhibitors ...
... and compared them with the effects of thapsigargin in the same cells. Our results demonstrate that thapsigargin, CPA, and BHQ ... To determine the specificity of thapsigargins effects, in the present study we have examined the effects on [Ca2+]i in single ... Previous studies have demonstrated in single rat parotid acinar cells that the microsomal Ca(2+)-ATPase inhibitor thapsigargin ... Nevertheless, the IP3-sensitive Ca2+ store remains continuously depleted during thapsigargin-induced oscillations, indicating ...
Incubation with 15 µM thapsigargin in the absence of extracellular calcium (5 mm BAPTA) resulted in a 279-fold increase (P, ... Incubation with 15 µM thapsigargin in the absence of extracellular calcium (5 mm BAPTA) resulted in a 279-fold increase (P, ... Incubation with 15 µM thapsigargin in the absence of extracellular calcium (5 mm BAPTA) resulted in a 279-fold increase (P, ... Incubation with 15 µM thapsigargin in the absence of extracellular calcium (5 mm BAPTA) resulted in a 279-fold increase (P, ...
From Plant to Patient: Thapsigargin, a Tool for Understanding Natural Product Chemistry, Total Syntheses, Biosynthesis, ...
Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis. Hsieh, W.C.; 洪慧芝; Hsu, P.C.; Liao, Y.F.; ...
La3+ or PLC inhibitors obstructed UTP depolarization; PKC inhibitors, thapsigargin or zero Ca2+buffer didnt. UTP activated 5- ...
Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis. Hsieh, W.C.; 洪慧芝; Hsu, P.C.; Liao, Y.F.; ...
Mechanical stimulation of HCD cells evoked a transient increase in [Ca2+]i that was dependent upon thapsigargin-sensitive store ...
Capacitative Ca2+ influx induced by thapsigargin was also significantly enhanced in activated T cells. We conclude that a ... Capacitative Ca2+ influx induced by thapsigargin was also significantly enhanced in activated T cells. We conclude that a ...
Contractile responses to caffeine and IP3 were abolished by the Ca(2+)-ATPase inhibitor, thapsigargin (1 microM). 4. Ca2+ (0.1- ... Contractile responses to caffeine and IP3 were abolished by the Ca(2+)-ATPase inhibitor, thapsigargin (1 microM). 4. Ca2+ (0.1- ...
Chu, H., Smith, J. M., Felding, J., Baran, P. S. Scalable synthesis of (-)-thapsigargin ACS Central Science 2017 3:47-51 DOI: ... Chu, H., Dunstl, G., Felding, J., Baran, P. S. Divergent synthesis of thapsigargin analogs Bioorganic & Medicinal Chemistry ...
... we utilized partial calcium store depletion induced by application of 10 nM thapsigargin (Tg). TRPC1 activation by endogenous ...
ER stress inducer thapsigargin (Tg, 100 and 500 nM) activated gene and protein expression of IL-6 and induced phosphorylation ...
... whereas the response was blocked by thapsigargin and caffeine. Neither the L-type calcium channel blockers, nifedipine and ... whereas the response was blocked by thapsigargin and caffeine. Neither the L-type calcium channel blockers, nifedipine and ...
... whereas the response was blocked by thapsigargin and caffeine. Neither the L-type calcium channel blockers, nifedipine and ... whereas the response was blocked by thapsigargin and caffeine. Neither the L-type calcium channel blockers, nifedipine and ...
Pretreatment having a Ca2+-free of charge remedy, thapsigargin, a Ca2+-ATPase inhibitor from the endoplasmic reticulum, U-73122 ...
... thapsigargin and tomentosin) are presented and discussed, along with some of their derivatives. In the authors opinion, these ...
... depletion of ER-calcium shops with thapsigargin (1.5 M, 5 min) (grey bars), and dealing with with 100 M EGTA and 10 M ruthenium ...
Bodipy Thapsigargin Marker Gene. *Bottles 500 mL Ppco Fb Herolab. *Bovine IgG Solution Equitech Bio ...
Bodipy Thapsigargin Marker Gene. *Bottles 500 mL Ppco Fb Herolab. *Bovine IgG Solution Equitech Bio ...
Bodipy Thapsigargin Marker Gene. *Bottles 500 mL Ppco Fb Herolab. *Bovine IgG Solution Equitech Bio ...
Bodipy Thapsigargin Marker Gene. *Bottles 500 mL Ppco Fb Herolab. *Bovine IgG Solution Equitech Bio ...
Bodipy Thapsigargin Marker Gene. *Bottles 500 mL Ppco Fb Herolab. *Bovine IgG Solution Equitech Bio ...
Bodipy Thapsigargin Marker Gene. *Bottles 500 mL Ppco Fb Herolab. *Bovine IgG Solution Equitech Bio ...
Bodipy Thapsigargin Marker Gene. *Bottles 500 mL Ppco Fb Herolab. *Bovine IgG Solution Equitech Bio ...

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