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In view of the ubiquity of genetics in many research disciplines, with bioinformatics as its infrastructure, genes are bound to play a role in identity work.
It is possible that non-Ig genes are bound and deaminated by AID in Ramos.
The promoters of these genes are bound by Myc protein [13].
These results are consistent with the hypothesis that, at specific sites, ZNF274 recruits KAP1, which recruits SETDB1, which results in trimethylation of histone H3 on lysine 9. We have previously shown that homeobox genes are bound by H3K27me3 whereas the 3' regions of zinc finger genes are bound by H3K9me3 [3], [10] [10].
Interestingly, most of these genes are bound in ESCs by two or more pluripotency and/or reprogramming factors and are mostly not bound by the polycomb group (see Figure S6 and supplementary File S3).
On the other hand, ChIP-chip analysis shows that 45 out of 158 induced dependent genes and 2 out of 24 repressed dependent genes are bound by Atf1/Pcr1 at the promoter.
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Then, we investigated how many of these 53 genes were bound by AG using a publicly available AG ChIP-seq dataset40.
Over 90% of genes harboring H3K27me3 marks in WT cells had reduced H3K27me3 in Mtf2−/− CD71+Ter119-/lo pro-erythroblasts and nearly half (48.9%) of these genes were bound by Mtf2 at this stage of development (Fig. 3h).
This was substantially higher than what would be expected considering that only 6% (141/2365) of all deregulated genes was bound by Ring1b.
And ∼34.2% of the Atf1-specific genes was bound by Atf1/Pcr1, which was more than 2-fold of the level by chance (p-value<0.01).
We found that ∼27.3% of the Atf1/Pcr1-dependent genes was bound by Atf1/Pcr1, which was 1.65-fold of the level by chance (16.6%, p-value<0.01) (Figure 5B).
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