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Lomenick, B. et al. Target identification using drug affinity responsive target stability (DARTS).
After phosphorylation, STAT3 homodimerizes and translocates into the nucleus where it binds to promoter elements of responsive target genes to regulate their transcriptions26.
This methylation event robustly suppresses p53-mediated transcription activation of highly responsive target genes but has little influence on weak targets.
The datasets and in silico method(s) to identify and predict responsive target genes can be used to more efficiently design experiments to study Caco-2/intestinal epithelial-relevant biological processes.
Furthermore, since multiple other circulating factors have been shown to affect CNS function in old mice, there seems to be little doubt that the CNS is a surprisingly responsive target for blood-borne factors.
There was no evidence of KBU2046 binding to either CDC37 or HSP90β by biophysical methods, inclusive of isothermal titration calorimetry, fluorescence-based thermal shift assay, biolayer interferiometry, or by dynamic light scattering, nor by the biochemical method of drug affinity responsive target stability (DARTS) assay (Supplementary Fig. 14).
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We also overexpressed OsADF3 in Arabidopsis to provide further evidence of the OsADF3 function in enhancing drought/osmotic stress tolerance of transgenic Arabidopsis by modulating several downstream abiotic stress-responsive target genes related to drought responses.
Using western blot analysis, we observed that Britannin decreased the phosphorylated AKT and induced the nuclear accumulation of FOXO1 and also up regulation of FOXO-responsive target BIM in both pancreatic cancer cell lines.
Increased HH activity (evidenced by accumulation of HH-ligand-producing cells and HH-responsive target cells) strongly correlated with portal inflammation, ballooning, and fibrosis stage (each P < 0.0001), supporting a relationship between HH-pathway activation and liver damage.
In this study, we characterized the estrogenic activity of subglutinol A (1). Subglutinol A blocked the 17β-estradiol-induced activation of reporter plasmids and endogenous estrogen-responsive target genes in a dose-dependent manner and efficiently destabilized ER proteins as shown using the estrogen receptor antagonist ICI 182,780.
Furthermore, it has been shown to be one of the earliest OCT4-responsive target genes [17] and was significantly upregulated in our OCT4 knockdown experiments.
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