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We suggest that these binding profiles may be strongly influenced by chromatin accessibility and provide evidence of a link between Ubx/Hth binding and chromatin state at genes regulated by Polycomb silencing.
The current study aims at describing the links between gene expression and DNA methylation subtypes of UC as well as investigating the RF binding and chromatin state associations of UC DMRs.
The ENCODE consortium has studied transcription factor binding and chromatin state in a large number of cell lines, but three "Tier-1" cell lines were studied especially thoroughly in human: GM12878, a lymphoblastoid cell line, H1-hESC, human embryonic stem cells, and K562, an immortalized myelogenous leukemic cell line.
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Furthermore, the relation between VDR binding and chromatin states has never been explored.
In addition to establishing the differential binding landscape of RFs with respect to UC DMRs, we highlight the connection between RF binding and chromatin states in both a cell-type specific and independent context.
To investigate the genome-wide association among gene expression, EWS-FLI1 binding, and chromatin states, we stratified all genes by their RNA levels and by the distance from the transcription start site (TSS) to the nearest EWS-FLI1 binding peaks, which were mapped previously (Bilke et al., 2013), and we plotted average ChIP-seq intensities for each histone mark around the TSS.
Reprogramming to induced pluripotent stem cells (iPSCs) proceeds in a stepwise manner with reprogramming factor binding, transcription, and chromatin states changing during transitions.
Establishment and maintenance of epigenetic control (gene silencing) has several aspects, which include promoter region hypermethylation, methyl-binding proteins, DNA methyltransferases (DNMTs), histone deacetylases (HDAC), and chromatin state.
The identification of human-specific changes in gene expression, epigenetic modifications, trans-factor binding, and overall chromatin state is an essential complement to the study of cis-regulatory elements with human-specific activities.
Protein binding and open chromatin state are commonly associated with propensity for SM breakpoints.
Protein binding and open chromatin state are associated with nearby SM breakpoints in many cancer datasets.
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