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To explore potential contributions of c-FOS and MITF to mast cell-specific binding of the shared TFs, ChIP-Seq experiments were performed for both c-FOS and MITF in primary mast cells.
This analysis showed that genes more strongly upregulated in mast cells than predicted by differential binding of the shared factors commonly contained several binding peaks for the mast cell-specific TFs.
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Removal of MAF1 by knockdown then leads to recruitment of TFIIIB through enhanced binding of TBP; the shared surface of TBP then directs both Pol II and Pol III binding through association with TFIIB and TFIIIB, respectively.
As previously demonstrated for H. armigera, Cry2Ab binding sites in H. punctigera were shown to be shared by Cry2Ae, which explains why an alteration of the shared binding site would lead to cross-resistance between the two Cry2A toxins.
The genomic distribution of ESR1 binding sites was similar regardless of the shared number of datasets (Additional file 1: Table S3).
Genomic sequences of the shared binding regions associated with expressed genes were analyzed for presence of an E-box consensus site on the sense or antisense strand (5'-CANNTG-3'), which would indicate a potential Twist1 binding site.
However, other mechanisms translating fine differences in antigen binding of antibodies sharing the same CDR into profound differences in their biological properties have not been established.
This observation therefore suggested that, just as for those regions bound in both cell types, direct DNA binding via established consensus motifs plays an important role for the binding of shared TFs to cell type-specific regions.
The resulting data show a strikingly similar binding pattern of MP, BRM and SYD at the shared target loci, which is unlikely to be coincidental.
Interestingly, we found that three arginine residues in this motif involved in binding of PIP2 are shared also by plant members of the PXPH-PLD subfamily (Fig. 4B).
Importantly, our observation that differential binding of shared factors is predictive of differential gene expression is consistent with the notion that cell type-specific binding of shared TFs makes meaningful contributions to differential gene expression.
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