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Coenzyme Q10 (CoQ10), an essential cofactor of the electron transport chain, acts by maintaining the mitochondrial membrane potential, supporting adenosine triphosphate (ATP) synthesis and inhibiting ROS generation, thus protecting neuronal cells against oxidative stress in neurodegenerative diseases.
Coenzyme Q10 (CoQ10), an essential cofactor of the electron transport chain, acts by maintaining the mitochondrial membrane potential, supporting ATP synthesis and inhibiting reactive oxygen species (ROS) generation for protecting neuronal cells against oxidative stress in neurodegenerative diseases [ 20– 20].
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Without measurements of O2 uptake it is nearly impossible to tell whether membrane potential is supported by fermentation or by oxphos.
There are two ways to generate Δψm – via the respiratory chain and via reversal of the ATP synthase (e.g. [ 39]) and without measurements of O2 uptake it is nearly impossible to tell whether membrane potential is supported by fermentation or by OXPHOS.
Indeed, a closer examination into both the specific signaling proteins and how the cell's membrane potential changes has supported the hypothesis that RGCs share recent ancestry with rhabdomeric photoreceptors.
The herein observed anti-oxidant, anti-ROS and NOs generation potentials and, maintenance of mitochondrial membrane potential find substantial support from the reported anti-oxidant potential of flavonoids [ 33- 35].
In addition, the mitochondria membrane potential assay was further supported that the EAF of T. conoides inducing apoptosis in HepG2 cells.
The dominant K+ conductance of glial cells mediates spatial K+ buffering and is important for the very negative membrane potential of these cells, thereby supporting electrogenic membrane transporters.
In the present study, several possible mechanisms of dP32 function in mitochondria and synaptic transmission were considered and investigated, most notably possible roles in supporting mitochondrial membrane potential, ATP production, and presynaptic calcium signaling.
This suggests that energy-limited cells switch to more energy-efficient mechanisms for membrane potential generation and this was supported by the upregulation of the proton-translocating NADH menaquinone dehydrogenase complex I.
Our working hypothesis is that volume control is a complex process that requires a number of ion channels and transporters to both maintain an appropriate membrane potential and electrochemical gradient to support volume control.
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