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The results show that anosmin-1 induced phosphorylation of FAK within 30 min, which peaked at around 2 h.
DDC induced the phosphorylation of p38 MAPK and Akt at 15 min, which peaked at 60 min and was sustained for up to 240 min.
However, cells from AT patients had a slower and lower γ-H2AX induction (p < 0.05 at 15, 30, and 60 min) which peaked two hours after irradiation.
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As expected, in rats which acquired a preference for lever C under the S-/C+ condition, cocaine induced a rapid increase in locomotion which peaked 1 min post-injection and then returned gradually to baseline within the 10-min inter-trial interval (Fig. 3a).
A rhotekin-based pull-down assay showed approximately 3-fold activation of RhoA 5 min after treatment by sublytic concentration of S. suis culture supernatant, which peaked at 10 min and was found to have returned to resting levels at 30 min (Fig. 2A).
The greatest reductions were seen 60 to 120 min after lights on, in contrast to induction, which peaked 15 to 60 min after lights on.
The same study found an axial shortening after metaphase which peaked 8 12 min after anaphase onset, so the absolute decondensation level may depend upon when the time during mitosis at which the chromosome was labelled and measured.
IL-1β induced rapid phosphorylation of p38 and ERK, which peaked 30 min post stimulation.
In shRNA control cells, C3a caused a transient ERK1/2 phosphorylation, which peaked at 5 min but disappeared by 10 min. Knockdown of β-arrestin-1, β-arrestin-2 or both enhanced the early response to C3a and rendered the cells responsive for ERK1/2 phosphorylation at later time points (10 30 min).
In this context, PIM2 triggered significant p65 NF-κB translocation from the cytosol to the nucleus which peaked at 15 60 min and then decreased at 120 min of treatment (Figure 6E and data not shown).
Peak levels of MAPK and Akt phosphorylation were reached at 20 min in all mesothelioma cell lines, with the exception of H2596 cells, which peaked at 60 min.
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