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This study was designed to test the PPARγ binding potency of several major FRs, including FM550 and PBDEs along with their metabolites using a ligand-binding competitor assay.
Objectives: Our goal was to determine the PPARγ ligand binding potency of several major flame retardants, including polybrominated diphenyl ethers (PBDEs), halogenated phenols and bisphenols, and their metabolites.
The primary goals of the present study were to a) characterize the binding potency of several major FRs, such as PBDEs (and their metabolites), using a human protein ligand binding assay; b) test the PPARγ binding activity of indoor dust extracts; and c) examine the effect of in vitro bioactivation on the PPARγ binding potency of dust extracts.
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Several different in vitro assays have described the determination of the binding potency of environmental pollutants to TTR, either based on radiolabeled ligand competitive binding (RLBA) or on the use of non-radiolabeled ligand competitive binding (BA, SPR, ANSA, and FLU-TTR).
The in vitro binding potency of these new analogs toward S1PR1 was determined.
In this approach, an affinity fingerprint is the pattern of the in vitro binding potency of a single compound to a reference panel of eight diverse proteins.
The observed ~64-fold enhancement of affinity underscores the binding potency of ATRX1,244 1,285, and suggests an auto-inhibitory role of the ATRX1,244 1,285-flanking sequence.
To test this possibility we compared VNTR domain sizes with DC-SIGN binding potency of the corresponding milks.
Therefore, it is important to determine whether the PPARγ binding potency of contaminants changes with metabolism.
Thus, our data indicate that PPARγ binding potency of dust samples increases after metabolism.
The binding potency of house dust samples and their bioactivated extracts was also examined.
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