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In this study, we sought to determine whether the yeast endocytic dynamin Vps1 was able to bind to actin and whether binding was required for all or just a subset of Vps1 functions in membrane trafficking.
From this preliminary SAR studies, it was speculated that the D-Ala-D-Ala binding was required for this series of compounds since the corresponding des-leucine derivative is inactive.
We previously demonstrated using HCT116 p53+/+ and p53-transfected SaOS2 cells that the ERα or ERβ could bind only the FLT1-T promoter construct in the presence of p53 suggesting that p53 binding was required for ER binding [17].
In addition, NF-κB binding was required for cyclin D1 transcription.
In summary, our data on the G-domain mutants showed that ATP binding was required for PM association of EHD2 and for the formation of 60 75S complexes.
Systematical analysis of the catalytic core with site-directed mutagenesis indicated that neither enzymatic activity nor RNA binding was required for negative regulation of antiviral signaling by LGP2.
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Furthermore, neurabin binds to actin [76] and this binding is required for its localization in dendritic spines [39].
However, while ORC binding is required for replication licensing, ORC also binds to regions where initiation does not take place.
MLL2 binding is required for changes in chromosome architecture around developmental genes and establishes promoter-enhancer looping interactions in a cell-cycle-dependent manner.
Wilson and al. [48] suggested that CTCF binding is required for MyoD-induced IGF-2 gene activity in muscle.
Combined, these data confirm that synphilin-1 is a lipid binding protein and suggest that lipid binding is required for inclusion formation.
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