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Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

ABSTRACT: This experiment was designed to determine the extent of gene misregulation in mESCs containing catalytically dead Ring1B in comparison to mESCs lacking Ring1B.

ORGANISM(S): Mus musculus

PROVIDER: GSE69824 | GEO | 2015/09/20

SECONDARY ACCESSION(S): PRJNA286873

REPOSITORIES: GEO

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Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

Project description:This experiment was designed to determine the extent of gene misregulation in mESCs containing catalytically dead Ring1B in comparison to mESCs lacking Ring1B. Polyadenylated mRNA was prepared from wildtype mESCs (WT), mESCs deficient for Ring1B (KO) and mESCs cells containing catalytically dead Ring1B (I53A). Each sample is represented by 3 biological replicate hybridisations.

2015-09-20 | E-GEOD-69824 | biostudies-arrayexpress

Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

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Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

Project description:ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub). Two biological replicates were performed for Ring1B and H3K27me3 ChIPs in WT and Ring1B I53A/I53A mouse ESCs. Input chromatin was sequenced for each replicate as a control for ChIP enrichment.

2015-09-20 | E-GEOD-69955 | biostudies-arrayexpress

Kruppel-like factor 2 is important for endoderm-related gene regulation with Ring1b-mediated mechanism in mESCs

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2021-02-01 | GSE165873 | GEO

Transcriptome profile of oocytes expressing a catalytically inactive knock-in allele of Ago2

Project description:The RNase III enzyme DICER generates both microRNAs (miRNAs) and endogenous short interfering RNAs (endo-siRNAs). Dicer deletion in mouse oocytes leads to female infertility due to defects during meiosis I. Because miRNA function is suppressed in mouse oocytes, it has been proposed that endo-siRNAs may have a role during female meiosis. By utilizing a catalytically inactive knock-in allele of AGO2 specifically in oocytes, we disrupt the function of siRNAs and analyze the transcriptome of these oocytes in comparison with Ago2 null, and Dicer null oocytes. Germinal vesicle-intact, full-grown oocytes were collected from eCG-primed females expressing a catalytically inactive knock-in allele of Ago2 (Ago2 ADH) specifically in oocytes. Oocytes were also collected from Ago2 null and Ago2 fl/fl oocytes, as well as Dicer wild-type and null mice. Oocytes were freed of attached cumulus cells by pipetting. Twenty oocytes collected from 3 different mice were used for high-throughput RNA sequencing. Three replicates for all genotypes except Ago2 null (two). The mouse background strain is "mostly" C57BL6, i.e., it is a cross between 3 different transgenic mice of different strains.

2015-01-20 | E-GEOD-57514 | biostudies-arrayexpress

Mus musculus

Project description:Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

| PRJNA286873 | ENA

Hey3Met2 human ovarian cancer cells overexpressing wild type or catalytically-dead mutant RNASET2

Project description:Hey3Met2 cells were stably transfected with plasmids encoding either wild-type RNASET2 or a catalytically dead form (whose cDNA has been previously mutagenized in the two CAS catalytic sites) or with the empty vector as a control. The control of ovarian tumorigenesis by RNASET2 occurs through modification of the cellular microenvironment and involvement of immunocompetent cells, thus providing evidence for specific modulations of cellular responses induced by RNASET2 that might underlay ovarian tumorigenesis. In order to get more inside on the effect of RNASET2 on the modulation of other genes, a whole genome expression has been run on Hey3Met2 cell transfected with wildtype or mutated RNASET2. Hey3Met2 human ovarian cancer cells were transfected with espression vectors encoding either wild type or catalitycally dead mutant RNASET2. Clones transfected with the empty vectors were used as negative controls. Three independent clones were used for the each type of transfected plasmid.

2011-06-01 | E-GEOD-28478 | biostudies-arrayexpress

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Project description:Polycomb repressive complex PRC1 is essential for gene regulation in numerous cell fate decisions. We show that RING1B (RING2, RNF2) and canonical PRC1 (cPRC1) genes are amplified and overexpressed in breast cancer (BC). Moreover, cPRC1 complexes functionally associate with genes regulated by cell type specific key transcription factors such as estrogen receptor (ER) in ER+ tumor cells and BRD4 in triple negative BC cells. cPRC1 is recruited to active enhancers in a manner independent of PRC2 and RING1B enzymatic activity. RING1B regulates enhancer activity and gene transcription not only by promoting the expression of BC oncogenes but also by regulating chromatin accessibility for oncogenic transcription factors. RING1B recruitment, and thus PRC1 association, to active enhancers occurs in multiple cancers.

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RING1B calibrated ChIP-seq (cChIPseq) datasets for control mESCs and an Scc1-AID auxin-inducible degron.

Project description:RING1B calibrated ChIP-seq (cChIPseq) datasets for control mESCs and an Scc1-AID auxin-inducible degron.

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Transcriptome of miR-290-295 KO mESCs

Project description:In order to identify direct microRNA targets in mouse embryonic stem cells (mESCs), we knocked out microRNA effector genes, profiled their transcriptomes and integrated the data with additional published OMICs data sets. To validate the analysis, we generated miR-290-295 KO mutant cell lines, assessed the transcriptome profile and compared the observed misregulation to the predictions of the analysis.

2022-07-15 | GSE179450 | GEO

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