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RLF and ZFP292 regulate bivalent genes through CoREST complex [RNA-seq]

ABSTRACT: This dataset includes ChIP-seq and RNA-seq data derived from mouse embryonic stem cells (mESCs) to investigate the roles of RLF and ZFP292 in transcriptional regulation and chromatin organization.

ORGANISM(S): Mus musculus

PROVIDER: GSE297950 | GEO | 2026/03/17

REPOSITORIES: GEO

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RLF and ZFP292 regulate bivalent genes through CoREST complex [ChIP-seq]

Project description:This dataset includes ChIP-seq and RNA-seq data derived from mouse embryonic stem cells (mESCs) to investigate the roles of RLF and ZFP292 in transcriptional regulation and chromatin organization.

2026-03-17 | GSE297949 | GEO

RLF and ZFP292 regulate bivalent genes through CoREST complex [RNA-seq]

Project description:RLF and ZFP292 regulate bivalent genes through CoREST complex [RNA-seq]

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RLF and ZFP292 regulate bivalent genes through CoREST complex [ChIP-seq]

Project description:RLF and ZFP292 regulate bivalent genes through CoREST complex [ChIP-seq]

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IP-MS analysis of RLF/ZFP292-FLAG

Project description:We performed immunoprecipitation followed by LC-MS/MS (IP-MS) in mouse embryonic stem cells in which endogenous RLF or ZFP292 was tagged with FLAG. This approach enabled the identification of proteins associated with RLF/ZFP292. The dataset provides a resource to investigate the composition of RLF/ZFP292-associated chromatin regulatory complexes.

2026-03-21 | PXD075910 | Pride

IP-MS analysis of RLF/ZFP292/ZFP654-FLAG

Project description:We performed immunoprecipitation followed by LC-MS/MS (IP-MS) in mouse embryonic stem cells in which endogenous RLF, ZFP292 or ZFP654 was tagged with FLAG. This approach enabled the identification of proteins associated with RLF/ZFP292/ZFP654. The dataset provides a resource to investigate the composition of RLF/ZFP292.ZFP654-associated chromatin regulatory complexes.

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CoREST is an integral component of the CoREST- human histone deacetylase complex.

Project description:Here we describe the components of a histone deacetylase (HDAC) complex that we term the CoREST-HDAC complex. CoREST-HDAC is composed of polypeptides distinct from previously characterized HDAC1/2-containing complexes such as the mSin3 and nucleosome remodeling and deacetylating (NRD, also named NURD, NuRD) complex. Interestingly, we do not observe RbAp46 and RbAp48 in this complex, although these proteins have been observed in all previously identified complexes and are thought to be part of an HDAC1/2 core. We identify the transcriptional corepressor CoREST and a protein with homology to polyamine oxidases as components of CoREST-HDAC. The HDAC1/2-interacting region of CoREST is mapped to a 179-aa region containing a SANT domain, a domain found in other HDAC1/2-interacting proteins such as NCoR, MTA1, and MTA2. Furthermore, we demonstrate that the corepressor function of CoREST depends on this region. Although CoREST initially was cloned as a corepressor to REST (RE1 silencing transcription factor/neural restrictive silencing factor), we find no evidence for the existence of the eight-zinc finger REST transcription factor as an interacting partner in this complex; however, we do find evidence for association of the putative oncogene ZNF 217 that contains eight zinc fingers.

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

Project description:To investigate if Rif1 depletion compromised the accurate genomic targeting of the PRC1.6 complex, we performed ChIP-seq analyses of Rif1, Pcgf6, RNF2, and the H2AK119ub in the control and Rif1-depleted mESCs.

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Kdm2b maintains murine embryonic stem cell status by recruiting PRC1 complex to CpG islands of lineage genes [ChIP-Seq]

Project description:Polycomb group (PcG) proteins play important roles in repressing lineage-specific genes and maintaining the undifferentiated state of mouse embryonic stem cells (mESCs). However, the mechanisms by which PcG proteins are recruited to their targets are largely unknown. Here, we show that the histone demethylase Kdm2b is highly expressed in mESCs and regulated by the pluripotent factors Oct4/Sox2 directly. Depletion of Kdm2b in mESCs causes de-repression of lineage-specific genes and induces early differentiation. The function of Kdm2b depends on its CXXC-ZF domain, which mediates Kdm2b’s genome-wide binding to CpG islands (CGIs). Kdm2b interacts with the core components of the Polycomb repressive complex 1 (PRC1) and recruits the complex to the CGIs of early lineage-specific genes. Thus, our study not only reveals a novel Oct4/Sox2-Kdm2b-PRC1-CGI regulatory axis and its function in maintaining undifferentiated state of mESCs, but also demonstrates a critical function of Kdm2b in recruiting PRC1 to the CGIs of lineage-specific genes to repress their expression. In this dataset, we include the ChIP-seq data of Kdm2b, Ezh2 and Ring1b in both control and Kdm2b knock down mouse embryonbic stem cells.

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Tbx3 controls Dppa3 levels to regulate exit from pluripotency towards mesodermal lineage

Project description:Tbx3, a member of the T-box family, plays important roles in development, stem cells, nuclear reprogramming and cancer. Loss of Tbx3 induces differentiation in mouse embryonic stem cells (mESCs). However, we show that mESCs exist in an alternate stable pluripotent state in the absence of Tbx3. In-depth transcriptome analysis of this mESC state reveals Dppa3 as a direct downstream target of Tbx3. Also Tbx3 facilitates the cell fate transition from pluripotent cells to mesoderm progenitors by directly repressing Wnt pathway members required for differentiation. Wnt signaling regulates differentiation of mESCs into mesoderm progenitors and helps maintain a naïve pluripotent state. We show that Tbx3, a downstream target of Wnt signaling, fine-tunes these divergent roles of Wnt signaling in mESCs. In conclusion, we identify a signaling-TF axis that controls the exit of mESCs from a self-renewing pluripotent state towards mesoderm differentiation. ChIPSeq and RNASeq (population and single cell) was performed on the indicated cell lines. Replicates are indicated as needed. The mm9 genome assembly was used. For single cell mRNA-Seq preparation, SSEA1+DAPI- mESCs were sorted and collected.

2015-07-21 | E-GEOD-60066 | biostudies-arrayexpress

Targeting the GFI1/1B-CoREST Complex in Acute Myeloid Leukemia.

Project description:One of the hallmarks of acute myeloid leukemia (AML) is a block in cellular differentiation. Recent studies have shown that small molecules targeting Lysine Specific Demethylase 1A (KDM1A) may force the malignant cells to terminally differentiate. KDM1A is a core component of the chromatin binding CoREST complex. Together with histone deacetylases CoREST regulates gene expression by histone 3 demethylation and deacetylation. The transcription factors GFI1 and GFI1B (for growth factor independence) are major interaction partners of KDM1A and recruit the CoREST complex to chromatin in myeloid cells. Recent studies show that the small molecules that target KDM1A disrupt the GFI1/1B-CoREST interaction and that this is key to inducing terminal differentiation of leukemia cells.

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