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These binding events could act simply by preventing the binding of other factors such as DNA methyltransferases or by actively recruiting factors such as Tet enzymes.
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Considering peaks that were called in both replicates, 41, 683 ER binding events and 48, 898 CTCF binding events could be identified in the ZR75-1 cells.
Although energetically coupling between the two binding events could not be resolved (analysis not shown), it is likely that it does exist because the second binding event is 1 order of magnitude tighter than nonspecific binding.
Considering peaks that were called in both replicates, 55, 176 CTCF binding events could be identified across the genome.
Accordingly, optimal detection of binding events could be based upon use of HSP72 as analyte and peptide as ligand.
They suggested that disordered regions are particularly important for flexible binding and could act as flexible linkers between globular protein domains.
These observations indicated that cohesin/CTCF binding sites could act as contact insulators that prevent chromosomal interactions across them, not only at domain borders but also within domains.
The G-quadruplex structure after binding to hemin could act as a horseradish peroxidase (HRP -mimicking DNAzyme and catalyzed tHRP -mimickingf 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic aciDNAzymeS) by H2O2.
Visuomotor binding could act through a conceptually similar yet independently implemented mechanism.
Tighter binding could act to decrease the steady state concentration of presumably aggregation-prone or protease sensitive Im7 folding intermediates, thus increasing the Im7 level in the cell.
Additionally, further attentional and executive mechanisms including top-down inhibitory processes are also likely to play a role in ASA: as well as binding 'target' auditory events, such mechanisms could act by suppressing interference from irrelevant 'background' sound.
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