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This scheme includes two major components, one of which only involves STAT1 regulation, and the other one includes both STAT1 and its collaborating factor AP1. From ChIP-seq data, we have observed STAT1-enriched binding sites around the transcription start sites of JUN and FOS genes, two transcription factors that target AP-1 binding sites.
Interestingly, we could identify a clear overrepresentation of putative SREBP binding sites around the transcriptional start site in the T3-regulated group compared to the control group.
In fact, numerous ChIP-seq data for TFBS from the ENCODE project reveal a distribution of binding sites around the transcription start site, into the introns [ 56, 64].
The presence of highly enriched SUMO-2/3 binding sites around the promoter regions during viral reactivation suggest that SUMO-2/3 might be directly or indirectly targeting a large group of transcription factors during KSHV reactivation.
The slope in the z-score distribution of the AT-rich factors like GATA-3, Ets-1 and TCF-1 is the manifestation of the under-representation of their binding sites around the functional window.
Targeted ChIP-qPCR of CREB binding sites around the known cAMP-inducible genes Pck1 and Ppargc1a in both metabolic states confirmed the constitutive binding pattern observed in our ChIP-seq experiment.
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There is some indication of increased conservation of the binding site (around positions 52, 68, and 92).
In many previous studies [ 8, 22- 24], relatively large neighborhoods surrounding the ERα binding site (around 500~1000bp) were scanned for consensus sequences of TFBSs.
The conformational transformation may depend on the functional group and binding pose of the ligand, giving the binding pocket greater flexibility and accordingly allowing for an induced fit of the enzyme-ligand binding site around the newly introduced ligand.
For the members of Ftsk-HerA superfamily, the phage phi29 packaging motor, each subunit moves along DNA during viral DNA packaging and the sequential translocation in each subunit of the hexameric protein lead to the rotation of DNA binding site around the protein ring, a process described as the evolution movement.
In the present study, we found three PPARγ-binding sites around the TSS of ADIPOQ that were hypomethylated during differentiation to FatCs (Fig. 6A; Fig. S6C).
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