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. 2019 Nov 19;10(11):941. doi: 10.3390/genes10110941

Table 1.

Comparative analysis of Chromatin Immune Precipitation followed by whole genome sequencing (ChIP-seq) binding sites of Ring1 and YY1 binding RYBP, RNF2/RING1B, PCGF6, and RAR on retinoic acid (RA) pathway members, upregulated in the Rybp-/- ES cells.

Gene Name Transcriptome
(Rybp+/+/Rybp-/-)
Raw Counts
Fold Change RYBP ChIP-seq (GSM1041375) RING1B ChIP-seq (GSM1041372) PCGF6 ChIP-seq (GSE84905) RAR ChIP-seq (GSM482749)
Adh1 0/0.7 Inf - - - -
Adh4 0/5.65 Inf - - - +
Rarb 0/2.12 Inf - + - +
Rxrg 0/1.41 Inf - + + +
Crabp1 36.8/218.5 5.94 + + - -
Rdh14 4.2/13.4 3.166 - - - -
Rxra 29.7/38.2 1.285 - + - +

Raw reads from genome-wide transcriptomics from wild type (Rybp+/+) and Rybp-/- embryonic stem (ES) cells reported by Ujhelly et al., 2015 [126]. ChIP-seq data for the binding targets of RYBP, RNF2/RING1B, PCGF6, and RAR (see Methods) were analyzed for upregulated RA pathway members in the Rybp-/- ES cells. ‘+’ represents identified ChIP binding targets and ‘–‘ represents no binding. RYBP, RING1 and YY1 binding protein. ES, embryonic stem. PCGF6, Polycomb group ring finger 6.