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The effect of modification on the binding was tested for three different types of DNA junction.
Potential SP1 binding was tested for 4 candidate target genes containing one or two best 20% SP1 and TFAP2A binding sites by Chromatin Immuno Precipitation (ChIP) assay, as indicated by Jaspar PWMs.
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Promoters selected from those in the genome that did not exhibit Rbf1 binding were tested for frequency of these motifs; E2F, DREF, and RAM motifs were considerably less enriched on these promoters than on those bound by Rbf1 (Table S4), indicating that these sequences may play a role in recruiting of Rbf1, or coregulation of the associated promoters.
Enrichment of genomic regions for protein binding was tested against a set of input DNA control (p-value ≤0.01).
To confirm that E2F1 operates by a transcriptional mechanism, an E2F1 mutant (E2F1E132) lacking the DNA binding domain was tested for its ability to induce the phosphorylation of S6K.
The pΔ(A25 -GFP construct feA25 -GFPdeletion of the constructSp1 binding sites, was tested featuringence upon expression.
Therefore, microtubule-binding affinity was tested for the three different tau constructs as an additional factor that could potentially affect tau-induced toxicity.
In order to validate whether this difference in release rate is truly due to the specific protein ligand binding, the system was tested for response to nonspecific binding proteins, and no discernible release was observed.
The Androgen binding protein (Abp) marker was tested for PCR subspecies-specific alleles as in [ 32, 33].
The competitive binding data for each ligand was tested for both one and two -site binding.
To precisely map the SRBF1 binding site, a 10-nucleotide sqt1 deletion series was tested for binding.
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