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We hypothesized that the abnormal expression of NOTCH ligands in MB cells could trigger an alteration of the NOTCH cascade.
It would be of interest to check whether epiplasmin RNAi affects or not exocytosis since both actin and epiplasmin experiments trigger an alteration localized at the cell surface.
It is also well established that renal and cardiac function are closely related to fluid control and maladjustment in one of the organs may trigger an alteration in the other [ 46].
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During the first hours, RNAi of either Epi 2 or Epi 41 triggers an alteration of cell shape, the loss of their slenderness: cells round up except at the anterior pole, giving rise to pear shaped cells, a phenomenon also described for some actin RNAi experiments [ 14].
An attractive possibility would be that Rac1 nuclear accumulation is triggered by an alteration in either oxygen or carbon dioxide levels upon cell sedimentation, however the function of Rac1 in the nucleus remains to be elucidated.
This is triggered by an alteration of the secretion of the adipokines adiponectin, leptin, retinol binding protein 4 (RBP4) and resistin as well as inflammatory markers such as interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP).
At the concentrations where ascorbate (1mM) and MnPs (1 or 5 µM) alone did not trigger any alteration in cell viability, combined treatment suppressed cell viability up to 95%.
Reactive oxygen species (ROS) trigger a biomolecular alteration that causes functional and structural changes.
Cellular tracking analysis revealed that meningococci expressing pilC1 under the control of its endogenous promoter caused a severe reduction of cellular motility upon infection, whereas infection with Nme expressing pilC2 under the control of the same promoter failed to trigger a significant alteration in ME180 motility throughout the experiment (Figure 4, B and D).
Thus, levels in adults were not high enough to trigger a significant alteration of the uroporphyrinogen decarboxylase activity.
Therefore, through the phosphorylation and inhibition of FBW7, the KRAS-MAPK axis may mainly rescue c-Myc expression to trigger a major alteration in the transcription profile towards malignancy and cell growth advantage.
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