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Unfortunately, we have been unable to resolve the binding mode of compounds 14e and 14f by co-crystal structure determination to verify this hypothesis.
Techniques like surface plasmon resonance could possibly show differing values for on- and off-rates for the mutants, but would still not be able to resolve the binding modes within a wild-type population.
By analyzing interactions with a range of Tpz1 truncation proteins, we were able to resolve the binding sites for Pot1, Ccq1, and Poz1 to residues 155 213, 422 490, and 479 508, respectively.
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On the basis of previous in-chip EMSAs as well as previously characterized Vc2 binding rates, the expected interconversion rate between bound and unbound RNA is slower than the rate of electromigration, indicating that the EMSAs will resolve the binding-induced conformation change into two distinct bands.
By resolving the binding energy of the excess electron in real time with femtosecond resolution, we captured the ultrafast dynamics of the electron in the presolvated ("wet") and hydrated states and obtained, as a function of cluster size, the subsequent relaxation times.
One of the limitations of RIP-CHIP is that full-length mRNAs are extracted during immunoprecipitation, which does not allow resolving the binding site with single nucleotide resolution.
To address this question and to further resolve the specific DNA binding constant (Ksp), we utilized a competitive specific/nonspecific finite lattice DNA binding model originally described by Record and co-workers and implemented for EMS data by Senear and co-workers.
That we can resolve the G protein binding specificities at the base of each of these clades, but not at deeper nodes, suggests an early diversification of G protein binding specificities, coupled with relative stasis of protein interactions once the major opsin clades were established.
Importantly, GeF-seq could resolve the closely positioned binding sites that appear as one peak in the ChAP-seq method, as shown in Fig. 3A.
To resolve energetically the binding and the catalytic events, several of these duplexes are constructed with non-hydrolyzable lesion analogs that mimic the natural 8-oxo-dG substrate and the abasic-like intermediates.
PAI-1 may be an important component in the detachment of MEs, since PAI-1 is able to attenuate the cell matrix interaction by resolving the uPAR/Vn binding.
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