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Using a pharmacological approach, we provide evidence that agonist-induced increases in [Ca2+] i and ERK activity require (1) IP3 receptor-mediated mobilization of Ca2+ from the endoplasmic reticulum, (2) influx of extracellular Ca2+ through store-operated channels, (3) closure of KATP channels, and (4) Ca2+ entry via L-type voltage-operated Ca2+ channels.
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Manganese-enhanced MRI (MEMRI) has been considered a surrogate marker of Ca+2 influx into activated cells and tracer of neuronal active circuits.
In addition, parallel to H+ efflux, we described for the first time a simultaneous Ca+2 influx and anion efflux modulated by HA (Figures 4 and 5).
Calcium dynamics is influenced by voltage through the first term in the right-hand sides of (1c) and (1d), (-alpha_{mathrm{Ca}} I_{mathrm{Ca}}), which represents (mathrm{Ca}^{2+}) influx from the extracellular space through voltage-gated (mathrm{Ca}^{2+}) channels.
In contrast, Mg2+ influx pathways are more complex.
Fig. 1 Glutamate specifically triggers Ca2+ influx in rice roots.
This reduction of Mg2+ influx by amiloride indicates a 1: 1 stoichiometry of the Na+Mg2+ antiport.
Fig. 4 OsNPF7.2 influenced NO3− influx, NO3− concentration and total nitrogen content among transgenic lines.
Mg2+ influx could be partially inhibited by the Ca2+ channel blockers Ni2+, Co2+, La3+, and Gd2+.
K+ efflux decreases Ca2+ influx, which consequently influences ASMCs proliferation and migration.
Membrane interaction and subsequent Ca2+ influx were the mechanisms that triggered inflammation.
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