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Besides the transcriptional control of mitochondrial genes steroid hormones may influence mitochondrial function by non genomic interactions that may control mitochondrial cation fluxes (reviewed in [45]).
For example, miR-146-mediated control of cytokine-receptor-signaling events may regulate beta-cell sensitivity to inflammatory factors, and miR-133a targeting of UCP-2 may control mitochondrial output of ROS.
These results are consistent with the idea that the Akt-GSK3β signaling pathway may control mitochondrial movement in neurons by modulating acetylation of microtubules via the regulation of HDAC6.
Our study provides new evidence critical for the ongoing journey in discovering mtDNA methylation and exploring its role in metabolic regulation [ 18– 20, 36] and suggests an insulin signaling-epigenetic-genetic axis that may control mitochondrial regulation.
Therefore, metformin-stimulated phosphorylation of CREB at Ser-133, which activates the promoter of PGC-1α and increases PGC-α mRNA and protein expression [ 25, 26], can also be viewed as part of the mechanism through which metformin may control mitochondrial biogenesis in tumor cells.
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Recently, it has been found that mTOR can directly control mitochondrial function, which raises the possibility that targeting mTOR may regulate the apoptotic pathway.
MISC-1 seems therefore to specifically control mitochondrial morphology.
Here, we have evaluated the effect of PGC-1α expression in the dopaminergic system to assess how this regulator of mitochondrial function may control neuronal function and survival.
Accept change, and we may control it".
Intragenic L1s may control hundreds of genes.
These two genes are associated with the autosomal recessive forms of parkinsonism and may act in the same pathway, controlling mitochondrial homeostasis [ 2– 4].
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