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However, our competition binding study did not show any binding of SA and 3,10DDA and binding only at extreme concentrations (10−4 M) of 10H2DA, indicating that an interaction with ERs is not mediated via the ligand binding pocket.
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Our results are more consistent with an ER agonist property of digoxin, though some in vitro ER binding studies do not support this notion [ 23, 24].
For example, a large scale Y2H analysis of PDZ domains suggested that many PDZ domains do not rely on a free C-terminal region for binding, however the study did not identify the internal binding motifs [ 65].
The C allele creates an additional Sp1-type (CCAC C box) promoter site, and although it was initially suggested to increase expression of the gene [ 9], a subsequent study did not observe binding to the human transcription factor Sp-1 [ 16].
Furthermore, FST315 and FST288 have been shown to bind to other TGF-beta superfamily member proteins, such as BMP-6 and MBP-7 (Sidis et al. 2006), and current study did not examine the binding of FST-type proteins to other TGB-beta superfamily member proteins.
This study did not consider drug binding kinetics or dose dependencies, as well as potential adverse effects on the other parts on the heart.
However, this study did not experimentally validate the function of binding events.
This study did not show significant differences in the diencephalon/midbrain SERT binding in patients with idiopathic CD compared to controls.
This study did not identify any substitutions in DENV-2 VLPs that disrupted the binding of this MAb.
The remaining RNA-binding proteins newly identified in this study do not have domains known to bind nucleic acids.
Therefore the STAT1 binding motif obtained in the present study does not take into account putative low affinity sites.
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