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We then demonstrated that CB2 was involved in cannabinoid-induced PC-3 cell death, in that blocking its activation with a specific antagonist (SR2) almost totally prevented cell death after incubation of cells with MET and JWH-015.
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They include strategies to interfere with FGFR3 synthesis, block its activation, inhibit its tyrosine kinase activity, promote its degradation, and antagonize its downstream signals.
And studies with differentiating lens cells suggest that this pathway is not a circular one, as blocking MTOR activation with rapamycin has no measurable effect on the activity of MAPK/JNK.
While adding recombinant CSF-1 reduced macrophage expression of MHC II following LPS activation, blocking it with a soluble recombinant CSF-1R allowed a marked activation of these cells.
Conversely, blocking Akt activation with the PI3K inhibitor LY294002 effectively suppressed the protective effect of Sal B against ATO-induced cell apoptosis.
Our data demonstrate that blocking Erk activation with a small molecule inhibitor prior to PE stress blocks the previously observed increase in myostatin expression.
In a number of tumor cell lines carrying HD domain mutations, blocking proteolytic activation with GSIs triggers cell-cycle arrest and variable degrees of apoptosis [40], [41].
However, blocking CaMK activation with KN-93 (2 µM) had no effect on CRF-induced CREB phosphorylation (Figure 4A), although this concentration of KN-93 blocks depolarization-induced CREB phosphorylation [36].
In addition, we found that blocking PI3K/AKT activation with LY294002 eliminated LDR-induced ERK activation.
With this culture system it was possible to map the molecular components of the autophagy-inducing signaling pathway by blocking their activation with inhibitors.
In addition, surface biotinylation assays revealed that blocking Rac1 activation with the Rac1-DN caused a decrease in GABAAR surface levels.
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