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The two approaches, ChIP-seq and ChIP-chip, yield strongly overlapping results revealing that HLH-1 preferentially binds to promoter regions of genes enriched for E-box sequences (CANNTG), known binding sites for this well-studied class of transcription factors.
We have used our anti AP2-exp antibodies to explore the binding sites for this AP2 member using ChIP-seq.
Using the Boolean conditions of each state transition generated from a given characteristic equation defining one state level (Eq. S4), we can determine possible functions and interactions between binding sites for this state level.
Remarkably, the 100 best low resolution docking solutions for Mal lie at the TLR4 dimer interface indicating that dimer formation creates two specific symmetry related binding sites for this molecule.
Since Promoter 1 is aggregation-specific, it will be of interest to determine if this promoter, that presents several possible binding sites for this transcription factor, is also dependent on CbfA for activation.
Because we found the same mechanism of resistance in multiple strains representing several field populations, we conclude that target site alteration is the most likely means that field populations evolve resistance to Cry2 proteins in Helicoverpa spp. Our work also confirms the presence in the insect midgut of specific binding sites for this class of proteins.
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Peaks 39 and 40 both appear in the promoter region of MSMEG4643, possibly indicating multiple GlnR binding sites for the regulation of this gene; rate limiting qPCR showed enrichment of this and the other 7 binding sites (Additional file 5: Figure S2).
Whereas for the fast protein on ternary mixtures we observe creation and destruction of macroion/PIP2 "binding sites", for the slower protein this lipid-protein "complex" stays intact for the entire trajectory.
The binding sites for the transcription factors found within this AICAR-responsive region of the promoter are shown in Fig. 1.
In an interesting parallel, however, the hsa-mir-148a has been proposed to bind HLA-C 3′UTR, and a polymorphism in the binding site for this miRNA, which increase the binding strength, has been associated with poor HIV-1 infection control (see the following section).
Enantiomeric 3- 3-hydroxyphenyl pyrrolidine analogues were also prepared in order to test the chirality preference of the orthosteric binding site for this scaffold.
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