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)

Aplysia central neurons were injected with the calcium-sensitive photoprotein aequorin and stimulated with trains of identical depolarizing voltage-clamp pulses. The light emissions grew and the outward currents declined in successive pulses. Tetraethylammonium (TEA) enhanced the light emissions to single depolarizing pulses and suppressed the outward current. The remaining net inward current is carried primarily by calcium ions and does not facilitate. The aequorin emissions were larger at all amplitudes of depolarizing pulses that elicited emissions, and the facilitation of emissions in a train of pulses was reduced. The effect of TEA on outward current was nearly maximal when sodium ions were partially replaced with 0.1 M TEA, while the aequorin emissions were further enhanced by increasing the TEA concentration to 0.459 M. TEA enhanced the aequorin emissions at all voltages. These observations suggest that the action of TEA on aequorin emissions is not strictly a consequence of its better known outward current blocking action. The effects of TEA could be partly due to the lowered sodium concentration of these solutions. Replacement of sodium by Tris, sucrose or mannose, however, all produced no enhancement of emissions. Tetramethylammonium (TMA) replacement of sodium had effects similar to those of TEA. Thus TEA and TMA appear to have a specific effect. Part of the enhancement of light emissions by TEA is due to the removal of a series resistance error in the voltage clamp, and this may also account partly for the reduced facilitation of aequorin emissions in TEA. The remainder of the action of TEA on aequorin emissions evidently reflects a specific but previously unrecognized action on the cellular metabolism of calcium ions or on the voltage-dependent calcium channels.
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PMID:Effect of TEA on light emission from aequorin-injected aplysia central neurons. 45 96

Bombesin, a peptide mitogen for a variety of cell types, acts as a typical Ca2+-mobilizing hormone in Swiss 3T3 fibroblasts. At its mitogenic concentrations (1-25 nM), bombesin stimulates polyphosphoinositide turnover, i.e. breakdown of phosphatidylinositol 4,5-bisphosphate and a concomitant increase in inositol phosphates in a time- and dose-dependent manner. In particular, bombesin induces an initial transient increase in inositol 1,4,5-trisphosphate concentration, followed by an increase in the concentration of inositol 1,3,4-trisphosphate. Also, within 30 s of bombesin addition, the mass of 1,2-diacylglycerol nearly doubles and remains at this level for up to 60 min. Intracellular [Ca2+] measurements with a photoprotein, aequorin, demonstrate that bombesin stimulates a transient rise in cytosolic free Ca2+ concentration. A mobilization of Ca2+ from an intracellular pool is observed as a dose-dependent, transient increase in 45Ca2+ efflux from prelabeled cells, both in the presence and absence of extracellular Ca2+. Bombesin also induces a sustained increase in Ca2+ influx rate and stimulates 3-O-methyl-D-glucose transport across the plasma membrane. These composite results indicate that the mitogenic effect of bombesin is mediated through an activation of the Ca2+ messenger system.
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PMID:The effects of bombesin on polyphosphoinositide and calcium metabolism in Swiss 3T3 cells. 302 2

Salicylic acid beta-glucoside (SAG) is a storage form of a defense signal against pathogens, releasing free salicylic acid (SA), to meet the requirements in plants. Since excess SA induces locally restricted cell death following oxidative burst and Ca2+ influx in plants, the effects of SAG on cell viability, Ca2+ influx, and generation of superoxide (O2*-) were examined in suspension-cultured tobacco BY-2 cells expressing aequorin. Among SA-related chemicals tested, only SAG induced the slow and long-lasting O2*- generation, although SAG was less active in acute O2*- generation, Ca2+ influx and induction of cell death. The prolonging action of SAG is likely due to gradual release of SA and the data suggested that a peroxidase-dependent reaction is involved. Notably, pretreatment with low-dose SA (50 micromu) enhanced the response to SAG by 2.5-fold. There are four possible secondary messengers in early SA signaling detectable in the BY-2 culture, namely O2*-, H2O2, Ca2+ and protein kinase (PK). If these messengers are involved in the low-dose SA-dependent priming for SAG response, they should be inducible by low-dose SA. Among the four SA-inducible signaling events, PK activation was excluded from the low-dose SA action since a much higher SA dose (> 0.4 mmu) was required for PK activation.
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PMID:Salicylic acid glucoside acts as a slow inducer of oxidative burst in tobacco suspension culture. 1554 Jun 2