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Voltage-gated Ca2 + channels (VGCCs) mediate calcium entry into neuronal cells in response to membrane depolarisation and play an essential role in a variety of physiological processes.
Since a number of agents that affect the ability of TRPC3 to mediate calcium entry at the plasma membrane are also integral to the Golgi complex, e.g. DAG, PLCγ and PLD, an intriguing possibility is that these agents may affect channel function at both locations.
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G-protein and PTK can also activate PKC, which mediates calcium entry into the sperm cytosol from intracellular stores.
A novel inhibitor of receptor-mediated calcium entry (RMCE) is described.
Both of these effects mediate postsynaptic calcium entry, which is believed to be a critical activator of the biochemical steps necessary for increases in synaptic strength (Madison et al., 1991; Bliss and Collingridge, 1993; Blackstone and Sheng, 2002; Cavazzini et al., 2005).
TRPC6, encoding a member of the transient receptor potential (TRP) superfamily of ion channels, is a calcium-permeable cation channel, which mediates capacitive calcium entry into the cell.
Genes homologous to ionotropic glutamate receptors of animals are present in the genome of Arabidopsis [15], [16] and encode proteins that likely mediate sodium or calcium entry into cells [17].
However this does not rule out the possibility that prostaglandins, arachidonic acid or components of the prostaglandin-receptor mediated response stimulates calcium entry via TRPC3 channels.
TRPC4 may play a role as a store-operated cation channel, mediating calcium ion entry into the cell in times of SR calcium depletion (Dietrich et al., 2007).
RESULTS: In this study, we investigated the role of Ca2+ release-activated Ca2+ (CRAC) channels and the Ca2+ influx they mediate, called store-operated calcium entry (SOCE), in antitumour immunity.
Importantly, calcium entry mediated by the L-type calcium channel activator was inhibited in the presence of an L-type calcium channel inhibitor (Fig. 1e).
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