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Genome-wide binding studies have identified that PcG proteins are associated with members of the TGFbeta signaling pathway and show PcG dissociation from the genes that were derepressed following differentiation [21], [25].
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Although the molecular basis of the DNA-binding specificity of FoxO transcription factors is poorly understood, high-affinity DNA-binding studies have identified a consensus FoxO-recognized element (FRE) as (G/C) (T/A AA(C/T AA [ 6- 8].
Since mutagenesis studies have identified drug binding sites, we had a closer look at phalloidin binding sites.
Electron microscopy studies have identified the binding site of the additional antennae complexes along the PsaL/PsaH-PsaK side (Kargul et al., 2005; Kouril et al., 2005).
Other recent studies have identified putative neurosteroid binding sites on GABAA receptors.
Collectively these studies have identified S100 calcium binding protein beta (S100ß), neuron specific enolase (NSE), neurofilament protein (NFL), myelin basic protein (MBP), glial fibrillary acidic protein (GFAP), the microtubule- associated tau proteins, monocyte chemotactic protein 1 (MCP-1), and interleukins 6 and 8 (IL-6 and IL-8) as potential markers of spinal cord damage [6], [11].
However, recent studies have identified GPCR ligand binding and signaling profiles that do not conform to this theoretical framework.
These studies have identified TLR ligand-binding sites.
Multiple studies have identified various RNA-binding proteins as regulators of miRNA biogenesis.
Recent structural studies have identified possible peptide-binding sites in both the lectin and arm domains of CRT (Chouquet et al., 2011; Pocanschi et al., 2011).
Bioinformatic analysis and site-directed mutagenesis studies have identified a calmodulin-binding domain on the N terminus of Orai1, between residues 68 and 90 [ 21].
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