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Moreover, the activation of several oncogenic pathways failed to alleviate the fitness defect induced by aneuploidy.
In summary, the addition of cytokine combinations engaging a wide range of STAT signaling pathways failed to fully restore T-cell function in the EOC ascites environment.
While CO activated p38 MAPK, ERK1/2 and Akt and perhaps more importantly delayed LPS-induced JNK activation, inhibitors of these kinase pathways failed to substantially block CO suppression as measured by effects on IL-1β.
However, pharmacological antagonists of both pathways failed to prevent HO-1 up-regulation following PKCε activation.
However, inhibitors of the ERK and JNK pathways failed to block the effect of cis-UCA on cell viability.
However, every therapeutic challenge using the inhibitors for these pathways failed to cure diabetic complications including DN, indicating the inappropriate therapeutic strategy and needs for an alternative approach.
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We conclude that all four pathways fail to protect the mutually beneficial UK EU biotechnology relationship and that alternative pathways need to be explored.
Despite having the ability to destroy polarity and tight junction assembly, these oncogenic pathways fail to induce a mesenchymal, migratory phenotype [71].
Considering that K+ channels are involved in cell cycle progression, abundant expression of K+ channels is expected to cause loss of proliferative control if endogenous pathways fail to block excessively expressed K+ channels.
If it is true that stroke pathways fail to improve outcome at discharge and may even be associated with an adverse effect upon outcome, it is interesting to speculate why this might be so.
Two Nef mutants, which were unable to activate MAP kinases and NF- κB pathway, failed to activate TAK1.
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