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.
ISOQUINOLINES with a benzyl substituent.
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.
(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.
A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
Tumors or cancer of the COLON.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.
The inner portion of the adrenal gland. Derived from ECTODERM, adrenal medulla consists mainly of CHROMAFFIN CELLS that produces and stores a number of NEUROTRANSMITTERS, mainly adrenaline (EPINEPHRINE) and NOREPINEPHRINE. The activity of the adrenal medulla is regulated by the SYMPATHETIC NERVOUS SYSTEM.
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
The cells of the body which stain with chromium salts. They occur along the sympathetic nerves, in the adrenal gland, and in various other organs.
Small masses of chromaffin cells found near the SYMPATHETIC GANGLIA along the ABDOMINAL AORTA, beginning cranial to the superior mesenteric artery (MESENTERIC ARTERY, SUPERIOR) or renal arteries and extending to the level of the aortic bifurcation or just beyond. They are also called the organs of Zuckerkandl and sometimes called aortic bodies (not to be confused with AORTIC BODIES in the THORAX). The para-aortic bodies are the dominant source of CATECHOLAMINES in the FETUS and normally regress after BIRTH.
Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds.
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)
A serine endopeptidase that is formed from TRYPSINOGEN in the pancreas. It is converted into its active form by ENTEROPEPTIDASE in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4.
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.
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.
A 90-amino acid peptide derived from post-translational processing of pro-opiomelanocortin (POMC) in the PITUITARY GLAND and the HYPOTHALAMUS. It is the C-terminal fragment of POMC with lipid-mobilizing activities, such as LIPOLYSIS and steroidogenesis. Depending on the species and the tissue sites, beta-LPH may be further processed to yield active peptides including GAMMA-LIPOTROPIN; BETA-MSH; and ENDORPHINS.
A G-protein-coupled, proteinase-activated receptor that is expressed in a variety of tissues including ENDOTHELIUM; LEUKOCYTES; and the GASTROINTESTINAL TRACT. The receptor is activated by TRYPSIN, which cleaves off the N-terminal peptide from the receptor. The new N-terminal peptide is a cryptic ligand for the receptor. The uncleaved receptor can also be activated by the N-terminal peptide present on the activated THROMBIN RECEPTOR and by small synthetic peptides that contain the unmasked N-terminal sequence.
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.
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
A publication issued at stated, more or less regular, intervals.
"The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.
The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).
Publications in any medium issued in successive parts bearing numerical or chronological designations and intended to be continued indefinitely. (ALA Glossary of Library and Information Science, 1983, p203)
All of the divisions of the natural sciences dealing with the various aspects of the phenomena of life and vital processes. The concept includes anatomy and physiology, biochemistry and biophysics, and the biology of animals, plants, and microorganisms. It should be differentiated from BIOLOGY, one of its subdivisions, concerned specifically with the origin and life processes of living organisms.
Round, granular, mononuclear phagocytes found in the alveoli of the lungs. They ingest small inhaled particles resulting in degradation and presentation of the antigen to immunocompetent cells.
Cell-surface receptors that bind LEUKOTRIENES with high affinity and trigger intracellular changes influencing the behavior of cells. The leukotriene receptor subtypes have been tentatively named according to their affinities for the endogenous leukotrienes LTB4; LTC4; LTD4; and LTE4.
One of the biologically active principles of SRS-A. It is generated from LEUKOTRIENE C4 after partial hydrolysis of the peptide chain, i.e., cleavage of the gamma-glutamyl portion. Its biological actions include stimulation of vascular and nonvascular smooth muscle, and increases in vascular permeability. (From Dictionary of Prostaglandins and Related Compounds, 1990)

Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model. (1/3227)

Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin.  (+info)

Relaxation of endothelin-1-induced pulmonary arterial constriction by niflumic acid and NPPB: mechanism(s) independent of chloride channel block. (2/3227)

We investigated the effects of the Cl- channel blockers niflumic acid, 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) and 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) on endothelin-1 (ET-1)-induced constriction of rat small pulmonary arteries (diameter 100-400 microm) in vitro, following endothelium removal. ET-1 (30 nM) induced a sustained constriction of rat pulmonary arteries in physiological salt solution. Arteries preconstricted with ET-1 were relaxed by niflumic acid (IC50: 35.8 microM) and NPPB (IC50: 21.1 microM) in a reversible and concentration-dependent manner. However, at concentrations known to block Ca++-activated Cl- channels, DIDS (+info)

Oxygen-dependent K+ influxes in Mg2+-clamped equine red blood cells. (3/3227)

1. Cl--dependent K+ (86Rb+) influxes were measured in oxygenated and deoxygenated equine red blood cells, whose free [Mg2+]i had been clamped, to examine the effect on O2 dependency of the K+-Cl- cotransporter. 2. Total [Mg2+]i was 2.55 +/- 0.07 mM (mean +/- s.e.m. , n = 6). Free [Mg2+]i was estimated at 0.45 +/- 0.04 and 0.68 +/- 0. 03 mM (mean +/- s.e.m., n = 4) in oxygenated and deoxygenated red cells, respectively. 3. K+-Cl- cotransport was minimal in deoxygenated cells but substantial in oxygenated ones. Cl--dependent K+ influx, inhibited by calyculin A, consistent with mediation via the K+-Cl- cotransporter, was revealed by depleting deoxygenated cells of Mg2+. 4. Decreasing [Mg2+]i stimulated K+ influx, and increasing [Mg2+]i inhibited it, in both oxygenated and deoxygenated red cells. When free [Mg2+]i was clamped, Cl--dependent K+ influxes were always greater in oxygenated cells than in deoxygenated ones, and changes in free [Mg2+]i of the magnitude occurring during oxygenation-deoxygenation cycles had a minimal effect. Physiological fluctuations in free [Mg2+]i are unlikely to provide the primary link coupling activity of the K+-Cl- cotransporter with O2 tension. 5. Volume and H+ ion sensitivity of K+ influx in Mg2+-clamped red cells were increased in O2 compared with those in deoxygenated cells at the same free [Mg2+]i, by about 6- and 2-fold, respectively, but again these features were not responsible for the higher fluxes in oxygenated cells. 6. Regulation of the K+-Cl- cotransporter by O2 is very similar in equine, sheep and in normal human (HbA) red cells, but altered in human sickle cells. Present results imply that, as in sheep red cells, O2 dependence of K+-Cl- cotransport in equine red cells is not mediated via changes in free [Mg2+]i and that cotransport in Mg2+-clamped red cells is still stimulated by O2. This behaviour is contrary to that reported for human sickle (HbS) cells.  (+info)

Acetylcholine-induced membrane potential changes in endothelial cells of rabbit aortic valve. (4/3227)

1. Using a microelectrode technique, acetylcholine (ACh)-induced membrane potential changes were characterized using various types of inhibitors of K+ and Cl- channels in rabbit aortic valve endothelial cells (RAVEC). 2. ACh produced transient then sustained membrane hyperpolarizations. Withdrawal of ACh evoked a transient depolarization. 3. High K+ blocked and low K+ potentiated the two ACh-induced hyperpolarizations. Charybdotoxin (ChTX) attenuated the ACh-induced transient and sustained hyperpolarizations; apamin inhibited only the sustained hyperpolarization. In the combined presence of ChTX and apamin, ACh produced a depolarization. 4. In Ca2+-free solution or in the presence of Co2+ or Ni2+, ACh produced a transient hyperpolarization followed by a depolarization. In BAPTA-AM-treated cells, ACh produced only a depolarization. 5. A low concentration of A23187 attenuated the ACh-induced transient, but not the sustained, hyperpolarization. In the presence of cyclopiazonic acid, the hyperpolarization induced by ACh was maintained after ACh removal; this maintained hyperpolarization was blocked by Co2+. 6. Both NPPB and hypertonic solution inhibited the membrane depolarization seen after ACh washout. Bumetanide also attenuated this depolarization. 7. It is concluded that in RAVEC, ACh produces a two-component hyperpolarization followed by a depolarization. It is suggested that ACh-induced Ca2+ release from the storage sites causes a transient hyperpolarization due to activation of ChTX-sensitive K+ channels and that ACh-activated Ca2+ influx causes a sustained hyperpolarization by activating both ChTX- and apamin-sensitive K+ channels. Both volume-sensitive Cl- channels and the Na+-K+-Cl- cotransporter probably contribute to the ACh-induced depolarization.  (+info)

The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (5/3227)

1. Arachidonic acid (0.01-1 microM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1 microM. Concentrations higher than 1 microM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. 2. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3 microM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. 3. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10 microM) pretreatment. 4. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. 5. In the presence of 1 microM arachidonic acid, venous rings produced 8-10 fold more PGE2 than did aorta whereas 6keto-PGF1alpha and TXB2 productions remained comparable. 6. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100 microM) or indomethacin (10 microM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. 7. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2.  (+info)

Differences in the actions of some blockers of the calcium-activated potassium permeability in mammalian red cells. (6/3227)

1. The actions of some inhibitors of the Ca2+-activated K+ permeability in mammalian red cells have been compared. 2. Block of the permeability was assessed from the reduction in the net loss of K+ that followed the application of the Ca2+ ionophore A23187 (2 microM) to rabbit red cells suspended at a haematocrit of 1% in a low potassium solution ([K]0 0.12-0.17 mM) at 37 degrees C. Net movement of K+ was measured using a K+-sensitive electrode placed in the suspension. 3. The concentrations (microM +/- s.d.) of the compounds tested causing 50% inhibition of K+ loss were: quinine, 37 +/- 3; cetiedil, 26 +/- 1; the cetiedil congeners UCL 1269, UCL 1274 and UCL 1495, approximately 150, 8.2 +/- 0.1, 0.92 +/- 0.03 respectively; clotrimazole, 1.2 +/- 0.1; nitrendipine, 3.6 +/- 0.5 and charybdotoxin, 0.015 +/- 0.002. 4. The characteristics of the block suggested that compounds could be placed in two groups. For one set (quinine, cetiedil, and the UCL congeners), the concentration-inhibition curves were steeper (Hill coefficient, nH, > or = 2.7) than for the other (clotrimazole, nitrendipine, charybdotoxin) for which nH approximately 1. 5. Compounds in the first set alone became less active on raising the concentration of K+ in the external solution to 5.4 mM. 6. The rate of K+ loss induced by A23187 slowed in the presence of high concentrations of cetiedil and its analogues, suggesting a use-dependent component to the inhibitory action. This was not seen with clotrimazole. 7. The blocking action of the cetiedil analogue UCL 1274 could not be overcome by an increase in external Ca2+ and its potency was unaltered when K+ loss was induced by the application of Pb2+ (10 microM) rather than by A23187. 8. These results, taken with the findings of others, suggest that agents that block the red cell Ca2+-activated K+ permeability can be placed in two groups with different mechanisms of action. The differences can be explained by supposing that clotrimazole and charybdotoxin act at the outer face of the channel whereas cetiedil and its congeners may block within it, either at or near the K+ binding site that determines the flow of K+.  (+info)

Arterial flow conditions downregulate thrombomodulin on saphenous vein endothelium. (7/3227)

BACKGROUND: The antithrombogenic properties of venous endothelium may be attenuated when vein is implanted in the arterial circulation. Such changes may facilitate thrombosis, which is the final common pathway for saphenous vein arterial bypass graft occlusion. METHODS AND RESULTS: Using human saphenous vein in a validated ex vivo flow circuit, we investigated (1) the possibility that arterial flow conditions (mean pressure, 100 mm Hg, 90 cpm, approximately 200 mL/min) alter the concentration of proteins involved in regulating thrombosis at the vessel wall and (2) the influence of ion channel blockade on such effects. Concentrations of thrombomodulin and tissue factor were quantified by Western blotting (ratio of von Willebrand factor staining) and immunohistochemistry (as a percentage of CD31-staining area). Thrombomodulin concentrations after 90 minutes of venous and arterial flow conditions were quantified by immunostaining (68.9+/-4.8% and 41.0+/-3.0% CD31, respectively; P<0.01) and by Western blotting (1.35+/-0.20 and 0. 15+/-0.03 ratio of von Willebrand factor, respectively; P<0.01). The ability of endothelial cells to generate activated protein C also decreased from 62+/-14 to 19+/-10 ng. min-1. 1000 cells-1 (P=0.01). The significant reduction in thrombomodulin was attenuated if calcium was removed from the perfusate but not by external vein stenting. Inclusion in the vein perfusate of drugs that reduce calcium entry (including Gd3+, to block stretch-activated ion channels, and nifedipine) abolished the reduction in thrombomodulin concentration observed after arterial flow conditions. In freshly excised vein, negligible concentrations of tissue factor were detected on the endothelium and concentrations did not increase after 90 minutes of arterial flow conditions, although the inclusion of nifedipine caused the immunostaining to increase from 3.0+/-0.4% to 8.5+/-0.7% CD31 (P<0.02). CONCLUSIONS: In saphenous vein endothelium exposed to arterial flow conditions, there is rapid downregulation of thrombomodulin, sufficient to limit protein C activation, by a calcium-dependent mechanism.  (+info)

Bcl-2 alters the balance between apoptosis and necrosis, but does not prevent cell death induced by oxidized low density lipoproteins. (8/3227)

Oxidized low density lipoproteins (oxLDL) participate in atherosclerosis plaque formation, rupture, and subsequent thrombosis. Because oxLDL are toxic to cultured cells and Bcl-2 protein prevents apoptosis, the present work aimed to study whether Bcl-2 may counterbalance the toxicity of oxLDL. Two experimental model systems were used in which Bcl-2 levels were modulated: 1) lymphocytes in which the (high) basal level of Bcl-2 was reduced by antisense oligonucleotides; 2) HL60 and HL60/B (transduced by Bcl-2) expressing low and high Bcl-2 levels, respectively. In cells expressing relatively high Bcl-2 levels (lymphocytes and HL60/B), oxLDL induced mainly primary necrosis. In cells expressing low Bcl-2 levels (antisense-treated lymphocytes, HL60 and ECV-304 endothelial cells), the rate of oxLDL-induced apoptosis was higher than that of primary necrosis. OxLDL evoked a sustained calcium rise, which is a common trigger to necrosis and apoptosis since both types of cell death were blocked by the calcium chelator EGTA. Conversely, a sustained calcium influx elicited by the calcium ionophore A23187 induced necrosis in cells expressing high Bcl-2 levels and apoptosis in cells expressing low Bcl-2 levels. This suggests that Bcl-2 acts downstream from the calcium peak and inhibits only the apoptotic pathway, not the necrosis pathway, thus explaining the apparent shift from oxLDL-induced apoptosis toward necrosis when Bcl-2 is overexpressed.  (+info)

Calcimycin incorporates into the cell membranes : first into plasma membrane and then very slowly into other intracellular membranes i.e. the membranes of mitochondria, nucleus, ER, Lysosomes, Golgi etc. It has to diffuse through the aqueous cytoplasm to reach the latter membranes OR through the continuities of plasma membrane with these membranes. So, the main action of calcimycin will be through its incorporation in the plasma membrane. The result will be a lot of sudden influx of calcium ions into the cytoplasm and resultant dramatic rise of cytoplasmic calcium ion conc. This happens only when the extracellular Calcium ion conc. is much higher than the intracellular conc. This generally is the case. The intracellular Ca ion conc. are less than micromolar (most cells have 0.1 micromolar or less) and extracellular conc. are above millimolar; so the gradient is nearly 10,000 times ...
Calcimycin incorporates into the cell membranes : first into plasma membrane and then very slowly into other intracellular membranes i.e. the membranes of mitochondria, nucleus, ER, Lysosomes, Golgi etc. It has to diffuse through the aqueous cytoplasm to reach the latter membranes OR through the continuities of plasma membrane with these membranes. So, the main action of calcimycin will be through its incorporation in the plasma membrane. The result will be a lot of sudden influx of calcium ions into the cytoplasm and resultant dramatic rise of cytoplasmic calcium ion conc. This happens only when the extracellular Calcium ion conc. is much higher than the intracellular conc. This generally is the case. The intracellular Ca ion conc. are less than micromolar (most cells have 0.1 micromolar or less) and extracellular conc. are above millimolar; so the gradient is nearly 10,000 times ...
Calcium ionophore IV | C52H100N2O3 | CID 601910 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
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Ramsay, E, Alnajim, J, Anantha, M, Zastre, J, Yan, H, Webb, M, Waterhouse, D and Bally, M (2008) A novel liposomal irinotecan formulation with significant anti-tumour activity: use of the divalent cation ionophore A23187 and copper-containing liposomes to improve drug retention. European Journal of Pharmaceutics and Biopharmaceutics, 68 (3). pp. 607-617. ISSN 0939-6411 ...
The Ca2+ ionophore 4-Br A23187 is effective in increasing [Ca2+]i and eliciting secretion when ICRAC is inhibited by SK&F 96365. Antigen (Ag) (1 μg/ml) sti
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Previous studies have shown that local selective in situ injury of pial arteriolar endothelium eliminates the dilations produced by acetylcholine or bradykinin. One means of producing such injury employs a helium-neon laser in the presence of intravascular Evans blue. Since the endothelium-dependent dilations produced by acetylcholine or bradykinin may be initiated by interaction with endothelial surface receptors, it is possible that the light simply inactivates or destroys these receptors. We used calcium ionophore A-23187, another dilating agent known from in vitro studies of large arteries to be endothelium-dependent, which moves calcium into endothelial cells rather than interacting with surface receptors. Our data in 10 mice show that before injury, 10(-5)M A-23187 dilated arterioles to 109 +/- 2% of control diameter. After selective endothelial injury by helium-neon laser, dilation was essentially abolished (101 +/- 1% of baseline diameter; p less than 0.01, Wilcoxon test). Undamaged ...
Ionomycin was isolated from Streptomyces conglobatus as a potent Gram positive antibiotic. During isolation, it was recognised that ionomycin exhibits a very high affinity and selectivity for calcium ions, suggesting the metabolite acts as a calcium ionophore. More recently, ionomycin has been used in cell biology as a universal calcium ionophore to explore the role of calcium regulation in the cell ...
The cross-linking of human peripheral lymphocyte surface Ig results in an early association of cyclic adenosine 3:5-monophosphate (cAMP) and the cell surface Ig patches. Examination of the subsequent stages of cap formation reveals the continued relationship of cAMP and the clustered surface Ig. In addition, the generalized influx of calcium produced by the ionophore A-23187 disrupts human lymphocyte caps. During the process of cap dissolution cAMP is still associated with surface Ig. Therefore, it is hypothesized that the localized concentration of cyclic nucleotide and calcium ion regulates the movement of cell surface constituents by coordinating the function of the cells contractile and structural elements. ...
How is TPA and 1-oleoyl-2-acetyl-glycerol abbreviated? OAG stands for TPA and 1-oleoyl-2-acetyl-glycerol. OAG is defined as TPA and 1-oleoyl-2-acetyl-glycerol very rarely.
ekirdekli h crelerde fosfatidilserinin (PS) h cre zar d y zeyine kmas bir apoptoz belirteci olup trombositlerde apoptozdan ziyade aktivasyonu d nd rmektedir. Di er taraftan, ekirdekli h crelerdeki apoptoz ve trombositlerdeki aktivasyon aras nda bir ok benzerlik bulunmaktad r. Bu al mada trombosit aktivasyonu ve apoptozu aras ndaki ili kiyi ara t rd k. Sa l kl 22 vericiden taze olarak al nan kandan izole edilen trombositler calcium ionophore A23187 bulunan ve bulunmayan t plerde inkube edildi. Trombosit aktivasyon belirteci olarak CD62P ve CD63, apoptozunun belirteci olarak anti-caspase-3 antikoru ve JC-1 katyonik boyas , h cre d y zeyindeki PS tespiti i in ise Annexin-V kullan ld . T m belirte ler A23187 ile inkubasyon ba lang c nda, 20. dakikada ve 5. saatte ak m sitometrisi ile al ld . nk basyonun 5. saatinde caspase 3 aktivasyonu ile PS ekternalizasyonu, ∆Ψm depolarizasyonu, CD63 aras nda ve ayr ca PS eksternalizasyonu ile CD62P aras nda anlaml korelasyon bulundu. Bu bulgular trombosit ...
TY - JOUR. T1 - Cyclooxygenase-2-mediated metabolism of arachidonic acid to 15-oxo-eicosatetraenoic acid by rat intestinal epithelial cells. AU - Seon, Hwa Lee. AU - Rangiah, Kannan. AU - Williams, Michelle V.. AU - Wehr, Angela Y.. AU - DuBois, Raymond N.. AU - Blair, Ian A.. PY - 2007/11. Y1 - 2007/11. N2 - Rat intestinal epithelial cells mat permanently express the cyclooxygenase-2 (COX-2) gene (RIES cells) were used to investigate COX-2-mediated arachidonic acid (AA) metabolism. A targeted chiral lipidomics approach was employed to quantify AA metabolites that were secreted by the cells into the culture media. When intact RIES cells were treated with calcium ionophore A-23187 (1 μM) for 1 h, 11-(R)-hydroxyeicosatetraenoic acid (HETE) was the most abundant metabolite, followed by prostaglandin (PG) E2, 15-(S)-HETE, 15-oxo-eicosatetraenoic acid (ETE), and 15-(R)-HETE. Incubation for a further 23 h after the calcium ionophore was removed resulted in a substantial increase in PGE2 ...
A Polymorphonuclear Granulocyte is a type of white blood cell that has granules (=small particles) with enzymes in their cytoplasm. They are released during infections, allergic reactions, and asthma. Neutrophils, eosinophils, and basophils are polymorphonuclear granulocytes. They are called polymorphonuclear because of the varying shapes of their nucleus (usually lobed into 3 segments.) As you…
The endoplasmic reticulum (ER) of a typical interphase 3T3 fibroblast consists of a compact perinuclear arrangement of cisternae and lamellae which can be observed by immunofluorescence with anti-endoplasmin. During mitosis the reticulum dissociates into small fragments from which it appears to re-assemble in the daughter cells. When interphase 3T3 cells are exposed to calcium ionophores, but not other ionophores, there is a similar dissociation of the ER into small uniform fragments, which are dispersed throughout the cytoplasm. Electron microscopy shows that the fragments consist of small vesicular structures and that essentially all of the rough ER except the nuclear envelope is dissociated. The dissociation of the ER by calcium ionophore is a relatively specific process since other organelles and supramolecular assemblies remain unaffected. When cells with dissociated ER are returned to normal medium, there is a rapid reassembly of the fragments into the continuous reticulum. In a proportion ...
FOWLER J. E. Seminars in Developmental Biology: Simple Systems for the Analysis of Important Developmental Problems. 6, 347-58, 1995 被引用文献1件 ...
The aim of this study was to determine the fate of foreign DNA molecules bound to porcine sperm that had been capacitated and acrosome reacted in vitro using calcium ionophore and then used in the in vitro fertilization ...
16. An investigator places an isolated neuron in a calcium-free medium, gives the neuron a suprathreshold stimulus and then performs an assay to test whether neurotransmitter is released into the medium. Which of the following outcomes would you predict? ...
BACKGROUND: Eosinophils from asthmatic patients are known to release greater amounts of leukotrienes than normal eosinophils when stimulated by the calcium ionophore A23187. The effect of platelet activating factor (PAF) in priming eosinophils was investigated. METHODS: Eosinophils were obtained from 18 asthmatic patients and 18 healthy donors. Cells separated by the Percoll gradients were incubated with PAF (C-18) for 30 minutes and then stimulated with the calcium ionophore A23187 (2.5 microM) for 15 minutes. The amount of leukotriene C4 (LTC4) in supernatants was measured using a combination of high pressure liquid chromatography and radioimmunoassay. RESULTS: The mean (SD) amount of LTC4 released by eosinophils from asthmatic patients upon stimulation with the calcium ionophore A23187 alone was 27.9 (9.9) ng/10(6) cells (n = 6). The amount of LTC4 released following stimulation with the calcium ionophore A23187 after pretreatment with PAF (1, 5, and 10 microM) was 57.2 (8.9), 75.1 (14.3), ...
Antibodies for proteins involved in calcium-mediated signaling using extracellular calcium source pathways, according to their Panther/Gene Ontology Classification
Fryd Food & Drink tapped QSLD Paris to create its new vodka-Vod-k Caramel and Truffle. The choice of ingredients was a crucial factor in its development, and the high quality inspired QSLD Paris in the creation of ...
Abstract: Interleukin-2 (IL-2) gene regulation was investigated in primary cultures of highly purified human peripheral blood CD28+T cells. Two discrete mechanisms for induction of T-cell proliferation could be distinguished by examining cell cycle progression and the expression of the IL-2 gene. Stimulation of cells by CD3 MoAb induced only transiently expressed, small amounts of IL-2 mRNA that was completely suppressed by cyclosporine. Costimulation of T cells with CD3 MoAb and either CD28 MoAb or PMA, but not calcium ionophore, induced a 50-100-fold increased in IL-2 gene expression and secretion. High levels of IL-2 gene expression could also be achieved by stimulation with calcium ionophore and PMA or CD28 MoAb and PMA, but not by CD28 MoAb plus calcium ionophore. IL-2 gene expression and T-cell proliferation induced by CD3 MoAb plus PMA or calcium ionophore plus PMA were completely suppressible by cyclosporine. In contrast, IL-2 gene expression and T-cell proliferation induced by CD28 MoAb ...
BioAssay record AID 131935 submitted by ChEMBL: Tested for its antiinflammatory activity in the A-23187 (calcium ionophore) ear edema model..
The effects of the calcium inonophore A 23187 on growing pollen tubes of Lilium longiflorumThunb. cv. Ace were investigated with the light and electron microscope. Tip growth is slowed down and...
A molecule that allows ions to cross lipid bilayers. There are two classes: carriers and channels. Carriers, like valinomycin, form cage like structures around specific ions, diffusing freely through the hydrophobic regions of the bilayer.…
Professional guide for Trifluoperazine. Includes: pharmacology, pharmacokinetics, contraindications, interactions, adverse reactions and more.
... is also known as Calcimycin, Calcium Ionophore, Antibiotic A23187 and Calcium Ionophore A23187. It is produced at ... "Characterization of the biosynthesis gene cluster for the pyrrole polyether antibiotic calcimycin (A23187) in Streptomyces ... a vendor's product page Calcimycin from Bioaustralis, a vendor's product page. ...
... calcimycin MeSH D03.438.221.346 - chlorzoxazone MeSH D03.438.221.370 - cialit MeSH D03.438.221.950 - zoxazolamine MeSH D03.438. ...
Transportan Family 2.B.11 The Calcimycin or A23187 Carrier-type Ionophore Family 2.B.12 The Salinomycin Family 2.B.13 The ...
Azide Biguanides Bupivacaine Calcimycin (A23187) Dodecyltriphenylphosphonium (C12TPP) Lasalocid (X537A) Long-chain fatty acids ...
Calcimycin, Calcium Ionophore) Abamectine Abietic acid Acetic acid Acetylcholine Actin Actinomycin D Adenine Adenosmeme ...
A23187 (Calcimycin, Calcium Ionophore). *Abamectin Abamectin. *Aigéad aibiteach Abietic acid. *Aigéad aicéiteach Acetic acid ...
Calcimycin and a number of similar molecules have been chemically synthesized (26-28). Calcimycin derivatives have also been ... C) HPLC analysis of calcimycin production in S. chartreusis NRRL 3882. I, calcimycin standard purchased from Sigma-Aldrich; II ... This trans complementation restored calcimycin production and thus proved that calN2 is required for calcimycin production (Fig ... Both genes are probably irrelevant to calcimycin production. It therefore seems likely that all the calcimycin biosynthetic ...
Calcimycin inhibits the growth of Gram-positive bacteria and some fungi. Calcimycin also inhibits the activity of ATPase and ... Calcimycin induces Ca2+-dependent cell death by increasing intracellular calcium concentration. ... Calcimycin (A-23187) is an antibiotic and a unique divalent cation ionophore (like calcium and magnesium). ... Calcimycin (A-23187) is an antibiotic and a unique divalent cation ionophore (like calcium and magnesium). Calcimycin induces ...
A23187 is also known as Calcimycin, Calcium Ionophore, Antibiotic A23187 and Calcium Ionophore A23187. It is produced at ... "Characterization of the biosynthesis gene cluster for the pyrrole polyether antibiotic calcimycin (A23187) in Streptomyces ... a vendors product page Calcimycin from Bioaustralis, a vendors product page. ...
Calcimycin / pharmacology * Colon / metabolism* * Colon / pathology * Colonic Neoplasms / metabolism* * Colonic Neoplasms / ...
Calcimycin / pharmacology * Calcium / physiology * Cell Adhesion Molecules / metabolism* * Cell Compartmentation * Cell ...
Calcimycin. An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports cations across ...
calcimycin. ZM 230,487. 6-[[3-fluoro-5-(4-methoxy-3,4,5,6-tetrahydro-2H-pyran-4-yl)phenoxy]methoyl]-1-ethylquinol-2-one. ... Additionally, bolinaquinone decreased potently the synthesis and release of leukotriene B4 (LTB4) in calcimycin (A23187)- ...
... calcimycin), suggesting that estrogens did not directly act on the secretory machinery. At the single cell level, estrogens ...
Calcimycin. An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports cations across ...
Calcimycin / pharmacology. Cells, Cultured. Chylomicrons / pharmacology*. Electrophoresis, Agar Gel. Endothelium, Vascular / ...
Calcimycin); 3G6A5W338E (Caffeine); 968JJ8C9DV (Sodium Azide); EC 2.7.11.31 (AMP-Activated Protein Kinases); F0X88YW0YK (AICA ...
Calcimycin (pharmacology) *Colforsin (pharmacology) *Cricetinae. *Cyclic AMP (metabolism, pharmacology) *Electrophoresis, ...
... calcimycin; si-AhR, short interfering RNA against the aryl hydrocarbon receptor; si-ARNT, short interfering RNA against the ...
Calcimycin mediates mycobacterial killing by inducing intracellular calcium-regulated autophagy in a P2RX7 dependent manner. ...
Rhythms could be reinitiated by a 10 min exposure to calcimycin (1 μg/ml; n = 2 of 2) or forskolin (10 μm; n = 8 of 8). ... We found that forskolin, calcimycin, and medium changes were all sufficient to reinitiate rhythms in glia. These stimuli may ...
... calcimycin MeSH D03.438.221.346 - chlorzoxazone MeSH D03.438.221.370 - cialit MeSH D03.438.221.950 - zoxazolamine MeSH D03.438. ...
Calcimycin Suppresses S100A4 Expression and Inhibits the Stimulatory Effect of Transforming Growth Factor β1 on Keloid ...
μM), with calcimycin (A23187, 1. μM), or with both indomethacin and A23187 at the same concentrations. Calcimycin (A23187) is a ... As expected, the calcium ionophore A23187 (calcimycin, 1uM) boosted the mean release of total cys-LTs by about 10-fold compared ... Calcimycin acts as a receptor-independent trigger of arachidonate release from membrane phospholipids; a high turnover of ... Calcium ionophore calcimycin (A23187), indomethacin, Trypan Blue solution (0.4%), and dimethylsulphoxide (DMSO) were from Sigma ...
Markram, H, Segal, M. Calcimycin potentiates responses of rat hippocampal neurons to N-methyl-D-aspartate. Brain Res. 1991. 540 ...
S100A4-induced cell motility and metastasis is restricted by the Wnt/beta-catenin pathway inhibitor calcimycin in colon cancer ...
Synonym: A23187 hemimagnesium salt, Antibiotic A 23187 hemimagnesium salt, Calcimycin hemimagnesium salt, Calimycin ...
Calcimycin Suppresses S100A4 Expression and Inhibits the Stimulatory Effect of Transforming Growth Factor β1 on Keloid ... Potential therapeutic targets include decapentaplegic homolog (Smad)3, high-mobility group box protein-1, and calcimycin. [81, ...
Calcimycin Suppresses S100A4 Expression and Inhibits the Stimulatory Effect of Transforming Growth Factor β1 on Keloid ...
A-23187 Free Acid (calcimycin; or Calcium Ionophore III). PK-CA707-59001 $99.00 ...
Calcimycin/pharmacology; Mutagenesis; Calcium-Binding Proteins/genetics; Tumor Suppressor Protein p53/genetics/*metabolism ...
Calcimycin/pharmacology. *Calreticulin. *Cell Line. *Chelating Agents/pharmacology. *Cloning, Molecular. *Cytoplasm/metabolism ...
Calcimycin/pharmacology; Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism; Tetrahydrofolate Dehydrogenase/metabolism; Tumor ...
Elevation of intracellular Ca2+ by calcimycin addition to neuronal cultures resulted in reduced bidirectional mitochondrial ...
... sulindac and calcimycin (Sack et al. J Natl Cancer Inst 2011; Stein et al. Neoplasia, 2011; Sack et al., Mol Biol Cell, 2011; ... sulindac and calcimycin (Sack et al., J Natl Cancer Inst, 2011; Stein et al., Neoplasia, 2011; Sack et al., Mol Biol Cell, 2011 ...
  • The pyrrole polyether antibiotic calcimycin (A23187) is a rare ionophore that is specific for divalent cations. (asm.org)
  • Calcimycin (A23187) is one of few natural ionophore antibiotics that specifically transport divalent cations such as calcium and magnesium ( 25 ). (asm.org)
  • A23187 is also known as Calcimycin, Calcium Ionophore, Antibiotic A23187 and Calcium Ionophore A23187. (wikipedia.org)
  • Additionally, bolinaquinone decreased potently the synthesis and release of leukotriene B 4 (LTB 4 ) in calcimycin ( A23187 )-stimulated human neutrophils as a consequence of the inhibition of 5-lipoxygenase activity, as well as PGE 2 and NO production on zymosan-stimulated mouse peritoneal macrophages. (aspetjournals.org)
  • Calcimycin also known as (A23187) is a calcium ionophore with antibiotic properties that kill gram positive bacteria and fungi. (agscientific.com)
  • Calcimycin (A-23187) is an antibiotic and a unique divalent cation ionophore (like calcium and magnesium). (medchemexpress.com)
  • However, these agents failed to modify the secretion elicited by high Ca 2+ in glands treated with the ionophore A-23187 (calcimycin), suggesting that estrogens did not directly act on the secretory machinery. (aspetjournals.org)
  • In the presence of calcimycin, a Ca 2+ ionophore, the inhibitory effect of D2 receptor agonists on production of cAMP was reduced. (sciencemag.org)
  • A-23187, also known as Calcimycin or Calcium Ionophore III, is a calcium ionophore that rapidly equilibrates intracellular and extracellular calcium concentrations. (biotium.com)
  • Always run a positive control with a buffer containing free ions of known concentration and an ionophore to open pores to those ions (for instance, for calcium indicators like Fluo-4 AM, this would include a buffer with added calcium combined with calcimycin, or for pH indicators, buffers of different pHs combined with nigericin). (thermofisher.com)
  • Calcimycin also inhibits the activity of ATPase and uncouples oxidative phosphorylation (OXPHOS) of mammalian cells. (medchemexpress.com)
  • When Fluo5N is introduced into the same kind of yeast cells we used in our discussion of the two-hybrid analysis , and these cells are then treated with calcimycin, what organelle would you expect to see fluoresce when the cells are examined by confocal microscopy? (biology-online.org)
  • Calcimycin induces Ca 2+ -dependent cell death by increasing intracellular calcium concentration. (medchemexpress.com)
  • Calcimycin (A-23187) mediates mycobacterial killing by inducing intracellular calcium-regulated autophagy in a P2RX7 dependent manner [4] . (medchemexpress.com)
  • Calcimycin incorporates into the cell membranes : first into plasma membrane and then very slowly into other intracellular membranes i.e. the membranes of mitochondria, nucleus, ER, Lysosomes, Golgi etc. (biology-online.org)
  • There are two additional natural pyrrole polyether antibiotics similar in structure to calcimycin: X-14885A from Streptomyces chartreusis (NRRL 12350) and cezomycin ( 8 , 19 , 35 ). (asm.org)
  • Cezomycin is also produced by Streptomyces chartreusis NRRL 3882 as a precursor for the much more valuable calcimycin ( 8 ). (asm.org)
  • Calcimycin, a toxin produced by the bacterium Streptomyces chartreusensis , acts as a mobile ion-carrier that allows Ca2+ ions to freely cross eukaryotic cell membranes, and indictors like Fluo5N give off fluorescence when bound to these ions. (biology-online.org)
  • Calcimycin inhibits the growth of Gram-positive bacteria and some fungi ( 20 ). (asm.org)
  • We propose a pathway for the biosynthesis of calcimycin and assign the genes to the biosynthesis steps. (asm.org)
  • Our findings set the stage for producing much desired calcimycin derivatives using genetic modification instead of chemical synthesis. (asm.org)
  • Firstly, I must mention we've heard nothing of the toxin nor the fluorophore in class, upon further research on the internet I've found that Calcimycin (aka 823187) does indeed bind and inhibit Mitochondria. (biology-online.org)
  • So, the main action of calcimycin will be through its incorporation in the plasma membrane. (biology-online.org)