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To determine if this was also the case for the binding targets we identified by ChIP-chip, we examined the level of mitochondrial gene expression in microarray data.
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In order to confirm binding of ELK1/4 to NKX2-5∆HD off-targets, we identified ELK1 and ELK4 target peaks in HL-1 cells using DamID.
Using genome-wide analysis of MBD4 binding sites, we identified new targets potentially co-regulated by MBD4 and DNA methylation.
From the Argonaute (Ago) protein family associated with small RNA identification and binding, and target cleavage, we identified Ago-1, Ago-2, and Ago-3, PIWI, and Aubergine, all based on homologues from B. mori (Fig. 5; Additional file 7: Table S6).
We refined this list by focusing on target genes whose expression was inversely correlated with the miRNA expression (i.e. potentially downregulated), and using a Targetscan context + score of < −0.30 for at least one binding site, we identified five predicted gene targets for miR-29b and four for miR-223 (Table 4).
We further validated a subset of Myc binding targets identified in our ChIP-chip experiments and their associated histone mark profiles by employing direct ChIP assays with c-Myc, N-Myc, AcH3K9 and H3K4me3 antibodies, with all those tested being validated.
Further analysis showed that there is only a low overlap (~3%) between the knockout targets and the binding targets identified by chromatin immunoprecipitation (ChIP -chip [ 6].
A plethora of potential binding targets has been identified, including cytoskeletal components such as actin and myosin, and proteins linked to acquired neurodegenerative diseases such as synuclein, tau and β-amyloid [4], [17], [18].
Hence we only showed the applicability of our method to the binding target of Ste12 identified by ChIP-seq.
Here, we identified 1469 Myc direct binding target genes in HeLa cells and human foreskin fibroblasts using human core promoter microarrays.
First, we identified p53 binding to DNA targets using a ChIP on chip method.
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