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To determine whether EBP1 is a bona fide E2F target, we first conducted ChIP experiments using chromatin isolated from asynchroous cultures of primary human epidermal keratinocytes.
We conducted ChIP analysis on 3 Su TPE) candidate proteins, Hdac1, Su var)3-9 and Hp1c and a control, the Su var) protein, Hp1a, which is not involved in TPE ([38] and this study).
To further confirm that the four cis-elements found in the proximal promoter of PP2A-Aα were functional in vivo, we conducted ChIP assays using mouse αTN4-1 cells [34].
To begin understanding the histone code that defines the identity of an oligodendrocyte and characterizes the changes occurring during the differentiation process, we conducted ChIP assay with antibodies specific for activating and repressive histone modifications and compared the chromatin landscape at the Mbp and Mag loci of primary OPCs differentiating into oligodendrocytes.
MC conducted ChIP experiments and bioinformatic identification of VDREs in the promoter regions of genes.
As an alternative approach to quantify KAP1 enrichment specifically within MERVL elements, we conducted ChIP using a KAP1-specific antibody.
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We conducted ChIP-chip experiments on four TFs, CREB, E2F1, MAX, and YY1 in 1% of the human genome.
To test whether this co-localization is indeed present in ESC, we also conducted ChIP-seq analysis with a validated CTCF BAC-GFP tagged cell line (Fig. S1).
As an independent biological validation, we conducted ChIP-seq experiments on one histone mark, dimethylation of lysine 4 at histone H3 (H3K4Me2).
We conducted ChIP-Chip experiment using tiling array for 4 TFs: CREB, E2F1, MAX and YY1 in the ENCODE regions (see Methods and Supplementary data).
We then conducted ChIP-qPCR for these loci in the TrAP transgenic plants.
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