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Abundant axonal mRNA transcripts encode mitochondrial proteins, and a recent in vitro study found that selective inhibition of axonal protein synthesis has been shown to reduce axonal mitochondrial membrane potential perhaps contributing to a reduced axonal membrane potential (Hillefors et al., 2007; Aschrafi et al., 2008).
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The mitochondrial membrane potential increased, perhaps due to the increase in mitochondrial mass (Supplementary Figures S5A and B), and the ATP level was slightly decreased.
To determine whether these changes in [Ca2+]i were related to membrane potential, and therefore perhaps to actions on K+ channels, we next repeated these experiments, but pre-constricting with 30 mmol/L K+ and l-NAME (instead of U46619), in order to partially dampen the driving force for K+ efflux thus preventing hyperpolarization through opening of K+ channels.
These effects of membrane potential on RyR and perhaps IP3R have been rather neglected because within the ER/SR such regulation is unlikely to be significant, but it may be very important when IP3R or RyR are expressed in the PM.
Perhaps any membrane potential that is present, is insufficient to support the function of a TIM23 translocase.
Iron is slowly oxidized, due to which, perhaps the mitochondrial membrane potential decreases.
We originally hypothesized that this would lead to greater mitochondrial membrane potential due to the increase in electron transport activity and perhaps also a higher cellular ATP.
The data suggest that the enhanced ROS release from primed macrophages may perhaps be due to effects of the drug on mitochondrial membrane potential rather than cellular signaling and macrophage priming.
Furthermore, we cannot discharge that, perhaps, the swimming exercise alters the cholinergic transmission and the resting membrane potential of intestinal smooth muscle cell, which could be the responsible for the contractile response attenuation.
HKIII is regulated by hypoxia and exerts protective effects against oxidative stress, perhaps by increasing ATP levels, reducing oxidant-induced ROS production, preserving mitochondrial membrane potential, and increasing mitochondrial biogenesis.
Furthermore, HKIII exerts protective effects against oxidative stress, perhaps by increasing ATP levels, reducing oxidant-induced ROS production, preserving mitochondrial membrane potential, and increasing mitochondrial biogenesis.
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