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These results indicate that the −2000 to +1 region of the DUSP1 gene was already acetylated before DEX treatment.
As shown in Fig. 6A, the levels of AcH3/H3 in p300 RNAi cells were similar to those of control RNAi cells before DEX treatment.
In comparison to ChIP done with control IgG antibodies, we found that AcH3/H3 and AcH4/H4 levels were already enriched before DEX treatment in all genomic regions tested (Fig. S2).
We found that the region from −2000 to +1 (TSS) of DUSP1 was already sensitive to DNase I before DEX treatment (compared to DNA not digested by DNase I, Fig. 3A).
These results suggest that p300 is involved in DEX-induced histone H3 hyperacetylation surrounding the DUSP1 GRE, though it does not participate in acetylation of H3 before DEX treatment.
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Line 6 GVG:: gai seedlings appeared to be 'leaky', expressing gai even before the Dex-induction, and showing a slower growth rate.
To assess the functional relevance of this observation, we tested the killing activity of blood NK cells against K562, a NKG2D ligand-expressing target (Fig. 4C), before and after Dex therapy in the two cohorts of patients i.e. those who normalized their NKG2D expression levels and those who did not (Fig. 5C).
As observed before, addition of DEX to these endothelial cells reduced IL-8 transcript levels to 75% of that observed in untreated, time-matched control cells.
This study was designed to identify the signaling pathways involved in intrahepatic overexpression of IL-10 induced by pretreatement by Dex before CPB.
The mean number of anti-VEGF injections before the first DEX implant was similar in the monotherapy group (3.2) and the combination therapy group (3.4).
For the investigation of GR-dependent mechanisms, P1 NSCs were incubated with 200 nM Mifepristone for 30 min before exposure to Dex.
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