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In the presence of a membrane potential, this protonation site is subjected to an electrostatic force, and this force can be balanced by the hydrophobic mismatch force established by the presence of the conserved amphipathic helix H8.
Through interaction with the negative-inside membrane potential, this extra positive charge from the proton is subjected to an inward force (i.e. towards to the cytosolic side) and thus may stabilize the CIn conformation.
In contrast, although SHSY5Y cells expressing G2019S LRRK2 also showed decreased mitochondrial membrane potential, this was suggested to be associated with increased mitochondrial fragmentation linked with higher levels of DLP1 in the mitochondria (28).
However, relative values for different mutant 5-HT3 receptors are the same, and as cellular events are triggered by changes in membrane potential, this may be a more accurate indication of the ligand potency in vivo (19).
Of note, data in Fig. 2D show an age-dependent increase in mitochondrial membrane potential: This condition is always associated with a decreased efflux of H2O2 from mitochondria, and thus, it strengthens the notion that NOX activity is the major source of H2O2 in astrocytes and that it increases with age.
Because little is known about the effects of LPI as a possible vascular signalling mediator on endothelial membrane potential, this study was designed to investigate the effects of LPI on intracellular Ca2+ concentration, membrane potential, and to explore the underlying ion conductance in endothelial cells.
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It is speculated here that, due to lack of energy to maintain this potential, neurons lose their membrane potential at this time.
Here, the effect of the synaptic connections has been modeled as a jump in the state variable, the membrane potential in this case, when a neuron of the population receives a synaptic input.
In the former case the unstable fixed point acts as an excitation threshold: if the value of the membrane potential exceeds this point, it will spike once and then decay back to the stable equilibrium.
The compound acts on the bacterial cell cytoplasmic membrane by disruption of S. aureus's cell membrane potential, and this leads to the release of the cellular contents.
Although the maximum proportion of channels in the open state was decreased as the relative abundance of hERG1b was increased (figure 5C) the driving force on these channels were much greater due to the more depolarized membrane potential at this earlier phase resulting in the increased IKr amplitude.
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CEO of Professional Science Editing for Scientists @ prosciediting.com