Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.13.12.5 (aequorin)
1,451 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of three structural types of nipecotamides and their stereoisomers on collagen-induced aggregation and intraplatelet ionized calcium ([Ca2+]i) rise in human platelets were evaluated using aequorin as the [Ca2+]i indicator. The orders of potencies of racemic nipecotamides were different when collagen was the agonist compared with those obtained using ADP. It is suggested that in addition to their earlier hypothesized interactions with platelet anionic phospholipids of the plasma and organelle membranes, nipecotamides may, in addition, act at other receptor sites. In general, the inhibition of collagen-induced aggregation paralleled their inhibitory effects on the rise of [Ca2+]i. The compounds were stereoselective in inhibiting aggregation as well as [Ca2+]i rise. The meso diastereomers of I and II were more potent than the corresponding enantiomeric pairs. A single [Ca2+]i peak was noticed when the incubate contained 1.0 mM extracellular calcium [Ca2+]o. On the other hand a biphasic [Ca2+]i rise was noticed when the nominally Ca(2+)-free buffer contained 75 microM ethylene glycol tetraacetate (EGTA). The first peak corresponded with platelet shape change, suggesting Ca2+ discharge from internal stores, and the second, with aggregation. The second peak may reflect either Ca2+ flux across the plasma membrane or aequorin leak from internal cellular locations or from the canicular system. Inhibition of the rise in intraplatelet Ca2+ appears to be associated with the platelet aggregation-inhibitory actions of nipecotamides.
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PMID:Inhibition of agonist-induced rise in platelet Ca2+ by antithrombotic nipecotamides. 807 9

The results here are the first demonstration of a physiological agonist opening Ca2+ channels in bacteria. Bacteria in the gut ferment glucose and other substrates, producing alcohols, diols, ketones and acids, that play a key role in lactose intolerance, through the activation of Ca2+ and other ion channels in host cells and neighbouring bacteria. Here we show butane 2,3-diol (5-200mM; half maximum 25mM) activates Ca2+ transients in E. coli, monitored by aequorin. Ca2+-transient magnitude depended on external Ca2+ (0.1-10mM). meso-Butane 2,3-diol was approximately twice as potent as 2R,3R (-) and 2S,3S (+) butane 2,3-diol. There were no detectable effects on cytosolic free Ca2+ of butane 1,3-diol, butane 1,4-diol and ethylene glycol. The glycerol fermentation product propane 1,3-diol only induced significant Ca2+ transients in 10mM external Ca2. Ca2+ butane 2,3-diol Ca2+ transients were due to activation of Ca2+ influx, followed by activation of Ca2+ efflux. The effect of butane 2,3-diol was abolished by La3+, and markedly reduced as a function of growth phase. These results were consistent with butane 2,3-diol activating a novel La3+-sensitive Ca2+ channel. They have important implications for the role of butane 2,3-diol and Ca2+ in bacterial-host cell signalling.
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PMID:Fermentation product butane 2,3-diol induces Ca2+ transients in E. coli through activation of lanthanum-sensitive Ca2+ channels. 1684 48

Calcineurin B-like protein 9 (CBL9) plays important roles in response to ABA, K+ deprivation in plants. However, whether CBL9 modulates plant adaptation to low-temperature stress is elusive. In this study, we demonstrated that the cbl9 mutants increased freezing tolerance under both cold-acclimating and nonacclimating conditions in Arabidopsis. Cold-induced changes of cytosolic free calcium concentration ([Ca2+]cyt) were then monitored by aequorin-expressed Arabidopsis plants. The results showed that the cold-triggered increases in [Ca2+]cyt levels in cbl9 mutants were clearly higher than those in wild type (WT) plants, while cold-affected changes in free calcium concentration within cytosolic microdomains adjacent to the vacuolar membrane ([Ca2+]md) in cbl9 mutants were similar to those in WT plants. In addition, treatments of seedlings with Ca2+ chelator ethylene glycol-bis(2-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA) and Ca2+ channel blocker lanthanum chloride markedly inhibit changes of [Ca2+]cyt in cbl9 mutants, while the inhibition of calcium release by lithium chloride from intracellular pools demonstrated consistent suppression of [Ca2+]cyt in cbl9 mutants and WT plants. Together, these results indicate that CBL9 negatively modulates cold tolerance through decreasing [Ca2+]cyt in Arabidopsis.
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PMID:A calcium sensor calcineurin B-like 9 negatively regulates cold tolerance via calcium signaling in Arabidopsis thaliana. 3069 38