Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Menin and H3K4me3 ChIP_Seq in mouse decidua

ABSTRACT: To detect the direct target genes of Menin and H3K4me3 in decidual stromal cells, decidual stromal cells are collected and subjected to ChIP-Seq. After aligned to mouse mm10 by STAR, peaks are called by MACS2. We found that Menin and H3K4me3 was significantly enriched at the transcription start site (TSS) of expressed genes (RPKM>1). A direct comparison of Menin and H3K4me3 ChIP-seq peaks at gene promoters showed a significantly strong positive correlation (R2=0.5888291). The promoters of 6,800 genes bound by Menin (92% of all genes with promoter bound by Menin) were also H3K4me3 modified.

ORGANISM(S): Mus musculus

PROVIDER: GSE182539 | GEO | 2022/01/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

H3K4me3 ChIP_Seq in mouse decidua

Project description:To detect the direct target genes of H3K4me3 in decidual stromal cells, decidual stromal cells are collected and subjected to ChIP-Seq. After aligned to mouse mm10 by STAR, peaks are called by MACS2. We found that H3K4me3 was significantly enriched at the transcription start site (TSS) of expressed genes (RPKM>1). A direct comparison of Menin and H3K4me3 ChIP-seq peaks at gene promoters showed a significantly strong positive correlation (R2=0.5888291). The promoters of 6,800 genes bound by Menin (92% of all genes with promoter bound by Menin) were also H3K4me3 modified.

2022-01-20 | GSE191327 | GEO

Menin and H3K4me3 ChIP_Seq in mouse decidua

Project description:Menin and H3K4me3 ChIP_Seq in mouse decidua

| PRJNA756692 | ENA

H3K4me3 ChIP_Seq in mouse decidua

Project description:H3K4me3 ChIP_Seq in mouse decidua

| PRJNA790987 | ENA

Histone H3K4me3 signal breadth reveals constitutive and hypoxia stress responsive endometrial functions linked to endometriosis

Project description:We report sequening of chromatin immunoprecipitated DNA (ChIP-Seq) of histone H3 at lysine 4 (H3K4me3) normoxic and hypoxia treated endometrial stromal fibroblasts (ESF) and hypoxia treated differentiated decidual stromal cells (DSC),

2022-01-01 | GSE167946 | GEO

Targeting Menin disrupts the KMT2A/B and polycomb balance to paradoxically activate bivalent genes [CUT&TAG]

Project description:Precise control of activating H3K4me3 and repressive H3K27me3 histone modifications at bivalent promoters is essential for normal development and is frequently corrupted in cancer. By coupling a cell surface readout of bivalent MHC class I gene expression with whole genome CRISPR/Cas9 screens, we identify specific roles for MTF2-PRC2.1, PCGF1-PRC1.1 and Menin- KMT2A/B complexes in maintaining bivalency. Unexpectedly, genetic loss or pharmacological inhibition of Menin phenocopies the effects of polycomb disruption, resulting in derepression of bivalent genes in both cancer cells and pluripotent stem cells. Whilst Menin and KMT2A/B contribute to H3K4me3 at active genes, a separate Menin-independent function of KMT2A/B maintains H3K4me3 and opposes polycomb-mediated repression at bivalent genes. Release of KMT2A from active genes following Menin targeting alters the balance of polycomb and KMT2A at bivalent genes, facilitating gene activation. This functional partitioning of Menin-KMT2A/B complex components reveals novel therapeutic opportunities that can be leveraged through inhibition of Menin.

2023-01-13 | GSE222516 | GEO

Gene expression profiling of mouse uterine decidua isolated on morning of day 8 of pregnancy

Project description:Placenta development involves complex molecular and cellular interactions between the maternal endometrium and the developing embryo, however, it is not clear what are the precise mechanisms regulating this maternal-fetal crosstalk. Using genetic and cell biological approaches, we have demonstrated that Ras-related C3 botulinum toxin substrate 1 (Rac1), a maternal factor expressed in decidual cells and is markedly elevated in mouse decidua on days 7 and 8 of gestation, regulates the secretory pathways that mediate stromal-endothelial and stromal-trophoblast crosstalk within a narrow temporal window during placenta development. Our study revealed that ablation of Rac1 did not affect the formation of the decidua but led to fetal loss in mid gestation accompanied by extensive hemorrhage. To gain insights into the molecular pathways affected by the loss of Rac1, we performed gene expression profiling which revealed that RAC1 signaling regulates the expression of genes involved in angiogenesis and vesicle trafficking. Consequently, the Rac1-null decidual cells exhibited impaired secretory functions that led to poor vascularization of the uterus and abnormal trophoblast expansion and placentation.

2017-02-09 | GSE70446 | GEO

RNA sequencing of macrophages and monocytes from first-trimester human decidua basalis (decB), decidua parietalis (decP), and placenta

Project description:Aim of the study was to characterize decidual macrohage populations and to verify the isolation protocol by showing the distinction between macrophages and monocytes

2023-01-11 | GSE196917 | GEO

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (ChIP-Seq)

Project description:Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. To study the role of menin-dependent H3K4me3, we performed in vitro differentiation of wild-type as well as menin-null mouse embryonic stem cells (mESCs) into pancreatic islet-like endocrine cells (PILECs). Gene expression analysis and genome-wide H3K4me3 ChIP-Seq profiling in wild-type and menin-null mESCs and PILECs revealed menin-dependent H3K4me3 at the imprinted Dlk1-Meg3 locus in mESCs, and all four Hox loci in differentiated PILECs. Specific and significant loss of H3K4me3 and gene expression was observed for genes within the imprinted Dlk1-Meg3 locus in menin-null mESCs and the Hox loci in menin-null PILECs. Given that the reduced expression of genes within the DLK1-MEG3 locus and the HOX loci is associated with MEN1-like sporadic tumors, our data suggests a possible role for menin-dependent H3K4me3 at these genes in the initiation and progression of sporadic pancreatic endocrine tumors. Furthermore, our investigation also demonstrates that menin-null mESCs can be differentiated in vitro into islet-like endocrine cells, underscoring the utility of menin-null mESC-derived specialized cell types for genome-wide high-throughput studies. Genome-wide mapping of H3K4me3 and microarray gene expression profiling in TC-1 wild-type (WT) mESCs, menin-null (Men1-ko) mESCs (3.2N), pancreatic islet-like endocrine cells (PILECs) derived from WT mESCs, and PILECs derived from Men1-ko mESCs.

2012-06-01 | E-GEOD-37774 | biostudies-arrayexpress

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (mRNA)

2012-05-31 | E-GEOD-37775 | biostudies-arrayexpress

Targeting Menin disrupts the KMT2A/B and polycomb balance to paradoxically activate bivalent genes [ChIP-seq]

Project description:Precise dynamic control of activating H3K4me3 and repressive H3K27me3 histone modifications at bivalent gene promoters is essential for normal development and frequently corrupted in cancer. Using whole genome CRISPR/Cas9 screens we identify specific roles for MTF2-PRC2.1 and PCGF1-PRC1.1 polycomb complexes, and MLL1/2-COMPASS-like complex components in maintaining bivalency. Contrary to expectations, loss of Menin or inhibition of the Menin-MLL1/2 interaction, induces activation of bivalent genes via loss of polycomb-mediated repression and defines distinct roles for MLL1/2 and Menin in gene regulation. Whilst Menin and MLL1/2 contribute to maintenance H3K4me3 at active genes, a separate Menin-independent function of MLL1/2 opposes polycomb mediated repression at bivalent genes. MLL1/2 are essential for basal transcription and, although dispensable for transcription factor driven activation, facilitate transcriptional consistency during dynamic changes in gene expression. This functional partitioning of COMPASS complex components reveals therapeutic opportunities to target oncogenic and immunosuppressive functions of PRC2 through pharmacological inhibition of Menin.

2023-01-13 | GSE181823 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data