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Furthermore, SPR data revealed the conservation of antigenicity; if, on one hand, anti-BthTX-I/BPB loses affinity for immobilized BthTX-I, the same anti-BthTX-I/BPB gains affinity for immobilized BthTX-II.
These authors suggested that the MID domains of certain eukaryotic AGOs (that is, those involved in miRNA-mediated gene regulation) contain a second nucleotide-binding site in addition to the 5′-phosphate-binding pocket, which gains affinity for mGpppG cap analogues (or eventually for other ligands) only in the presence of the guide-strand RNA (and vice versa).
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In conclusion of this section, it is important to underline that the recruitment of nonhomologous crystallin genes occurred by independent changes in their promoters and enhancers, resulting in their gaining affinity for transcription factors that are members of the conserved developmental network used for eye and lens development in all species that have been studied.
This mutation was shown to be crucial for the gained affinity for one of the modules.
Affinity maturation resulted in an approximate 200-fold gain in affinity for sIL-6R compared to the parental Nanobody.
In case of ALX-0061, approximately a 200-fold gain in affinity for sIL-6R compared to the parental Nanobody was achieved through affinity maturation.
Conceptually, the same penalty is avoided when an element of the paratope is preconformed from germline, as is the case with LCDR2 in CH58-UA, and when the large gain in affinity for antigen (KD) through maturation is predominantly attributable to a decreased off-rate (kd).
Two of the 11 mutations acquired during somatic hypermutation contribute two new salt bridges to V2 residues, and their role in the observed gain in affinity for mature CH58 (from 11.0 μM to 4.6 nM) appears to be predominantly through decreasing off-rates (600-fold decrease in off-rate, and 4-fold increase in on-rate).
However, isolated phage clones displaying Fab cannot necessarily be used for efficient bacterial production of engineered Fab proteins, often due to deleterious defects in their proper folding abilities derived in compensation for the gain of high affinity for a particular antigen.
In the stationary phase, bundles of NFs are closely apposed, phosphorylated NFs that gained higher binding affinity for each other [ 17, 19].
Growth could be attributed to a mutated endogenous Hxt36 transporter, which has lost the ability to transport D-glucose, while gaining a higher affinity for D-xylose.
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