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Resistance and susceptibility do not depend only upon qualitative differences in the activated defense genes, but also on differences in the timing and magnitude of their expression [ 8].
The model described above was used to study differences in the activated EGFR-mediated conversion of Erk into its active diphosphorylated form (active Erk or Erk-PP) associated with the differing nature of contacts seen in low (0.09 mM) and near physiological (2 mM) calcium environments.
Thus the spectrum of TGF-β-induced Smad3 binding in the different cell lines reflects preexisting local differences in the activated chromatin landscape.
To investigate with greater precision the spatial differences in the activated clusters between the groups for specific contrasts, we calculated probabilistic functional maps using the aligned surface maps previously produced.
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This slight difference may be explained by a difference in the activating activity of 1,25(OH)2D3 and forskolin at different doses, although it is also possible that forskolin activated only a part of the signaling pathways activated by 1,25(OH)2D3.
The differences in the pathways activated downstream of these ligands is of paramount importance to the types of genes which are upregulated in response to these stimuli.
The contrasting observations in these papers could be due to differences in the activating stimuli (TNFα versus anti-CD3 and anti-CD28), differences between murine and human cells, or differences in responses between CD4+ and total T cells.
As for the steady-state activation, there is a wide difference in the fully activated current amplitude at −60 mV, which is not only determined by the I f conductance but also by the I f reversal potential as a determinant of the driving force.
No other associations or tests of sex differences in regions activated during the moderate > warmth condition were statistically significant.
Thus, the involvement of ERK in early or late events occurring in the different neuronal compartments is not a consequence of different kinetics of ERK activation in the different subcellular compartments, but is likely due to differences in the molecular targets activated by ERK in distinct cell compartments.
However, 7 days after cerulein-induced pancreatitis, no differences in the levels of activated p53 or p21 were observed in pancreata from G3 mTerc−/− mice compared to mTerc+/+ mice (Figure 5).
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