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Examination of residues involved in ligand recognition supports a general model of ligand binding, but x-ray crystal structures of ErbB3 and ErbB4 with bound ligands are needed to address whether the ErbB3/ErbB4 ligands bind similarly to their receptors and how subtle differences in ligand binding lead to differences in receptor signaling.
These results show the promising potential of urushiol derivatives as potent HDAC2 binding lead compounds.
Our guiding hypothesis was that weak binding lead peptides could be readily identified from a screen of a small chemical library of unstructured short random peptide sequences.
Internal energies also favour binding of H4K20me2/3 ligands, whereas disfavour binding of H3K4me3 and H3K9me3 ligands proposing that the conformational changes upon binding lead to internal strains in JMJD2A tudor- H3K4me3/H3K9me3 complexes [19], [20].
Conformational changes of the guanine riboswitch aptamer domain induced by guanine binding lead to transcriptional regulation of genes involved in guanine biosynthesis.
Point mutations in latent TGFβ1 that inhibit integrin binding lead to developmental defects that phenocopy those in Tgfb1−/− mice (Yang et al., 2007).
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While RANKL binding leads to osteoclastogenesis activation, osteoblasts also express OPG, a decoy receptor of RANKL, leading to negatively controlled osteoclast development and further bone resorption.
The data demonstrate that GRHL2 physically binds at gene promoters of EDC and other GRHL2 target genes, and such binding leads to alter gene promoter activity.
But the binding leads the cell to react as if normal p53 is defective and should be destroyed.
This binding leads to the activation of complement and the disruption of the viral envelope.
This antisense binding leads to a decrease in the corresponding protein levels.
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