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In this approach, we estimate the birth rate α at which a new binding site may appear at a given position (per year), and a death rate β, at which an existing site is lost per year.
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Overall, from these preliminary studies on the potential Opc binding sites for α-actinin, it would appear that α-actinin binding site may reside close to the antibody B306 binding site.
As a result, blocking one binding site may also affect the function of the other binding site.
A lost binding site may have been replaced with a new, species-specific binding site - i.e. binding site turnover.
Placing a fluorophore too close to the binding site may disrupt binding, and fluorophores too far away from the binding site may not result in fluorescence changes.
Hence, the unexpectedly low number of predicted STAT-3 binding sites may not be due to our choice of parameters in MATCH, but appear to arise from a combination of the pattern matching algorithm and the STAT-3 binding site description.
Thus, although sequence-directed differences in propensity for nucleosome occupancy appear important for distinguishing transcriptionally responsive from memory effect genes, other factors, including sequences downstream of Abf1 binding sites, may also contribute to this effect.
The increase in binding affinity at lower pH was greater for the Ubx optimal binding site than for other DNA binding sites, indicating that subtle sequence alterations in DNA binding sites may influence pH-dependent behavior.
The lower affinity binding sites may represent a novel TxR or an alternative affinity state for the previously characterized high-affinity binding site.
Therefore, true binding sites may have SNPs less frequently than the non-binding sites.
Unoccupied 'perfect' STAT1 binding sites may include cell type specific binding sites and suggest a required but not sufficient function of the nucleotide sequence for DNA-protein binding.
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