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In this study, we postulated that acute mechanical strain of the arterial wall induces changes in syndecan-4 expression that in turn may modulate cellular events, which promote neointima formation.
We therefore propose a model in which the ECDs of LRP1b and LRP4 may modulate cellular signaling by scavenging and neutralizing extracellular ligands, thereby preserving signaling thresholds that are critical for proper embryonic development.
These findings suggest the presence of significant differences between EPOR-mediated signaling in hematopoietic cells compared to tumor cells and that the level of EPOR expression in tumor cells may modulate cellular responses to exogenous EPO.
These polymorphisms may alter transcriptional activity and thus VDR abundance and may modulate cellular responsiveness to 1,25(OH)2D.
We then used this model system to reveal key differences in the response of sensitive and resistant cell lines to HDACi that impact cell cycle progression and may modulate cellular sensitivity to the pro-apoptotic effects of these drugs in DLBCL.
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However, our study suggests that mammals may also modulate cellular H2S levels by regulating SQRDL-dependent destruction.
The hypothesis of differential action depending on target location opens a new field for the study of cytokines, showing that soluble or intracellular cytokines may differentially modulate cellular responses in both physiological and pathophysiological conditions.
Therefore, by inhibiting glutathione reductase an enzyme that plays critical roles in cellular oxidative balance, Carmustine treatment may modulate the cellular oxidative status.
Collectively, these results demonstrate major alterations in programs controlling cell proliferation and signal transduction, together with pathways regulating specific cellular stress, cell death, cell cycle and metabolic responses that may modulate the cellular phenotypes associated with TIA1 overexpression.
Nanoparticles (NP) absorbed in the body will come in contact with blood proteins and form NP/protein complexes termed protein coronas, which may modulate NP cellular uptake.
This preferential remethylation of specific loci suggests the involvement of factors which may modulate the cellular methylation efficiency after replication.
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may stimulate cellular
may inhibit cellular
may impact cellular
may involve cellular
may have cellular
may modulate fracture
may modulate TGF-β
may cause cellular
may modulate cancer-related
may modulate affective
may modulate carbohydrate
may diminish cellular
may affect cellular
may sequester cellular
may trigger cellular
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