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NANOG, OCT4 and SOX2 bind the intron 1 region of Xist and binding of these factors has been implicated in direct repression of Xist (Navarro et al. 2008).
BMP-6 treatment significantly reduced the binding of these factors to miPPR-21 by decreasing the expression of δEF1 and c-Fos/c-Jun.
esBAF binding is enriched at sites bound by the general pluripotency regulators OCT4, SOX2, and NANOG, consistent with previous work demonstrating that BRG1 facilitates the binding of these factors to their target sites12.
Initiation thus requires that the DNA structure facilitates the binding of these factors as well as the appropriate DNA melting.
To elucidate the binding of these factors to the respective promoters, we performed chromatin immune-precipitations.
The authors showed that the binding of these factors is correlated with retinoic-acid-induced gene expression profiles [ 9].
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One ambitious and fruitful experiment determined the binding sites of these factors genome-wide, uncovering a cellular logic of gene recognition.
In mouse ES cells Loh et al. performed RNAi-based knockdowns for Oct4 and Nanog and compared the differential expression pattern with potential binding sites of these factors, using a ChIP-PET approach [15].
Profiling DNA binding sites of these factors at a high resolution is an important step in understanding their functions and regulation networks.
To obtain a better picture of the chromatin binding landscape of these factors, we utilized a clustering approach using seqMINER [ 32], which compares the presence of multiple factors at a given chromosomal location within a 600-bp window and clusters together those binding sites that share a similar pattern of factor localization.
Genome-wide profiling by ChIP-Seq has made it possible to map genomic binding sites of these factors and to distinguish direct vs. indirect regulators of PPARγ expression during adipogenesis in an unbiased way.
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