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H2A.Z.1 mono-ubiquitylation antagonizes BRD2 to maintain poised chromatin in ESCs [RNA-seq]
PubMed Full text in PMC Similar studies SRA Run Selector
H2A.Z.1 mono-ubiquitylation antagonizes BRD2 to maintain poised chromatin in ESCs
PubMed Full text in PMC Similar studies
H2A.Z.1 mono-ubiquitylation antagonizes BRD2 to maintain poised chromatin in ESCs [ChIP-seq]
H2AZ extended acidic patch is necessary for formation specialized chromatin states in ESCs
H2AZ extended acidic patch is necessary for formation specialized chromatin states in ESCs [RNA-Seq]
H2AZ extended acidic patch is necessary for formation specialized chromatin states in ESCs [ChIP-Seq]
H2A.Z Facilitates Access of Active and Repressive Complexes to Chromatin in Embryonic Stem Cell Self-renewal and Differentiation
Parallel PRC2/cPRC1 and vPRC1 pathways silence lineage-specific genes and maintain self-renewal in mouse embryonic stem cells
RNA expression profiling in G-CCE cells with a knock down of MMTR or overexpression of the full length, N-terminal or C-terminal of MMTR
PubMed Full text in PMC Similar studies Analyze with GEO2R
Chip-chip from WT and Polycomb Component Knock Out Mouse ES cells for H2AZ, H3K27me3, EZH2 and Ring1B.
H2A.Z landscapes and dual modifications in pluripotent and multipotent stem cells underlie complex genome regulatory functions
Histone H2A mono-ubiquitination is a crucial step to mediate PRC1 dependent repression of developmental genes to maintain ES cell identity.
ChIP-on-chip analysis of Ring1B, Ring1A, H2AK119u1 and H3K27me3 in mouse ES cells
Expression data from Ring1A(-/-);Ring1B(fl/fl);R26::CreERT2 ES cells expressing either of mock, WT or mutant Ring1B construct before or after OHT treatment
Wdr5
Transcriptome of Wdr5 and (or) p53 double knockout ESCs and embryoid bodies
Genome profiling of MAX binding in mouse embryonic bodies using SFEBq differentiation methods
Genome profiling of WDR5 and H3K4me3 binding in mouse embryonic stem cells
Chromatin accessibility profiling of mouse embryonic stem cells and embryonic bodies using SFEBq differentiation methods upon Wdr5 and P53 deletion with or without WT or mutant hWDR5 rescue
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