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The assembly kinetics, followed by ThT binding, were compared to that where full-length Ure2p fibrils and fibrils sharing no primary structure similarity with the prion domain of Ure2p e.g. α-synuclein fibrils are used to seed the assembly of soluble Ure2p.
Simulation results for stationary insulin receptor activation and insulin binding were compared to experimental data sets [ 57].
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The radiotracer binding data were compared to results obtained with TUNEL staining and clonogenic survival.
Using Encode ChIP-Seq data, the transcription factor binding sites were compared to the DHS sites, which showed highly overlapping percentage.
When tumors harboring TP53 mutations affecting the p53 L2/L3 DNA-binding domains were compared to those with wild-type TP53 or TP53 mutations outside the L2/L3 domains, this correlation was further strengthened (p = 0.0136).
Interestingly, this association for DSS became non-significant when tumors harbouring TP53 mutations affecting the p53 L2/L3 DNA-binding domains were compared to those with wild-type or TP53 mutations outside the L2/L3 domains (p = 0.095).
To further understand the basis of cladosporin selectivity, the amino acid residues of the ATP-binding pocket were compared to those in Krs1 of other species.
Odds ratio and statistical significance were calculated using Fisher's exact test, where motif counts in Foxp3-binding sites were compared to flanking 200nt regions to estimate the empirical enrichment over chance.
In order to determine whether IMMADs might be bound by RNA-binding proteins, IMMAD sequences were compared to RNA-binding protein recognition sequences reported in the literature.
The obtained HSA binding of known drug molecules were compared to the Immobilizd Artificial Membrane binding data (CHI IAM) obtained by our previously described HPLC‐based method.
In addition, both TFII-I binding sites and replication origins were compared to K562 modifiers.
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