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Our simulations suggest that the burst is terminated when enough Ca2+ has entered through T-type channels to activate Ca2+-activated K+ channels, which overwhelm the Ca2+ current and terminate the burst.
Here, we took a bottom-up protein design approach and rationally engineered ion channels to activate in response to thermal stimuli.
The channels then open and cause a rebound excitation, which brings the membrane to threshold for Na+ channels to activate.
Furthermore, it seems plausible that ischemia-induced depolarization may cause inactivation of voltage-gated K+ channels that normally dominate presynaptic spike repolarization [56] [58], thus allowing more BK channels to activate and dominate the repolarization [48], [59].
describe the formation of a plasma membrane signaling complex that enables Ca2+ microdomains near Orai1 channels to activate nuclear gene expression through the transcription factor NFAT.
To circumvent these concerns, we designed experiments to compare the ability of V012C-Orai1 channels to activate NFAT, first in dispersed mode and then after re-localization to ER-PM junctions in the same cells.
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H2O2 will enter through this channel to activate the enzyme, forming compound I.
The top layer, used for control, has all the channels needed to activate valves.
At the same time, depolarization of the membrane potential could increase excitability of the axon by bringing it closer to the potential where large numbers of Na+ channels begin to activate.
In recent years some studies have begun to apply dual-channel FES to activate both the dorsiflexors and plantarflexors [ 29, 30].
It has been proposed that PADs may temporarily locate to intracellular calcium channels that can provide local calcium concentrations in the millimolar range upon channel opening, sufficient to activate PAD activity.
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