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Examination of Na+/K+-ATPase activity, which has been implicated in ion transport in many crustaceans, revealed that induction of high Na+/K+-ATPase activity varies among the posterior gills in response to salinities.
Analysis of LC3-II immunoreactivity, which is an indicator of autophagosome formation, further revealed that induction of macroautophagy was involved in the aggregate-clearing effects of 17-AAG.
ChIP-qPCR revealed that induction of gene expression was associated with a gain in gene activating histone H3 methylation and acetylation in Pou5f1 and Gfra1 promoters, whereas CpG DNA methylation was not affected.
Further transcriptional analysis under hypoxic conditions in vitro revealed that induction of the DosR regulon is transient, with expression of nearly half of the genes returning to baseline by 24 hours.
Analysis of the facultative Calnexin clients NHK and α1-antitrypsin (α1AT) revealed that induction of Malectin expression to simulate conditions of ER stress resulted in persistent association between the ER lectin and the model cargo glycoproteins, interfered with processing of cargo-linked oligosaccharides and reduced cargo secretion.
This study revealed that induction of r-protein expression provoked two major kinds of stress response.
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Adjusting model parameters to recapitulate epithelial scattering reveals that induction of cell migration is the major driver of epithelial scattering.
A recent study reveals that induction of acute kidney injury by high doses of folic acid is associated with increased expression of NF-κB members, RelA and NF-κB2 [ 99].
Live imaging in the chick neural tube reveals that induction of apico-basal divisions in neural progenitor cells results in neuronal differentiation of the apical daughter, while the basal daughter remains a progenitor with high Notch activity.
The data obtained in the present study reveal that induction of synovitis by TNF is accompanied by activation of p38MAPKα and ERK signalling in synovial macrophages and fibroblasts in vivo.
In fact provocative experiments utilizing inducers of autophagy reveal that induction and activation of autophagy processing can cleanse intracytosolic toxic molecules or different disease-associated intracytosolic aggregate-prone proteins such as mutant Huntington and A53T α-synuclein [41] [43].
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