EED inhibitor impedes dendritic cell inflammatory functions
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1154627 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30495862_1.fastq.gz | Fastqsanger.gz | |||
| SRR30495862_2.fastq.gz | Fastqsanger.gz | |||
| SRR30495863_1.fastq.gz | Fastqsanger.gz | |||
| SRR30495863_2.fastq.gz | Fastqsanger.gz | |||
| SRR30495864_1.fastq.gz | Fastqsanger.gz |
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Project description:Dendritic cells (DCs), the main antigen-presenting cells, are at the forefront of the immunity in response to autoimmune diseases. Epigenetic histone H3 lysine K27 trimethylation (H3K27me3) modification by embryonic ectoderm development (EED) is tightly associated with restrained transcriptional programs and has important functions in diverse biological processes and diseases, but its role in DC functionality remains elusive. In this study, we show that EED inhibitors block the activation especially migration of DCs, thus emphasizing EED as a pivotal regulator in DC homeostasis, which may be of great value for autoimmune disorders.
2025-04-09 | GSE276064 | GEO
Project description:Eed (embryonic ectoderm development) is a core component of the Polycomb Repressive Complex 2 (PRC2) which catalyzes the methylation of histone H3 lysine 27 (H3K27). Trimethylated H3K27 (H3K27me3) can act as a signal for PRC1 recruitment in the process of gene silencing and chromatin condensation. Previous studies with Eed KO ESCs revealed a failure to down-regulate a limited list of pluripotency factors in differentiating ESCs. Our aim was to analyze the consequences of Eed KO for ESC differentiation. To this end we first analyzed ESC differentiation in the absence of Eed and employed in silico data to assess pluripotency gene expression and H3K27me3 patterns. We linked these data to expression analyses of wildtype and Eed KO ESCs. We observed that in wildtype ESCs a subset of pluripotency genes including Oct4, Nanog, Sox2 and Oct4 target genes progressively gain H3K27me3 during differentiation. These genes remain expressed in differentiating Eed KO ESCs. This suggests that the deregulation of a limited set of pluripotency factors impedes ESC differentiation. Global analyses of H3K27me3 and Oct4 ChIP-seq data indicate that in ESCs the binding of Oct4 to promoter regions is not a general predictor for PRC2-mediated silencing during differentiation. However, motif analyses suggest a binding of Oct4 together with Sox2 and Nanog at promoters of genes that are PRC2-dependently silenced during differentiation. In summary, our data further characterize Eed function in ESCs by showing that Eed/PRC2 is essential for the onset of ESC differentiation. RNAs obtained from undifferentiated (d0) wild type and Eed KO ESCs and from day 3 (d3) and day 7 (d7) respective Ebs were subjected to Affymetrix Mouse Gene 1.0 ST Array. 24 samples in total.
2014-08-28 | E-GEOD-49305 | biostudies-arrayexpress
Project description:Polycomb Repressive Complexes 1 and 2 (PRC1 and 2) play a critical role in the epigenetic regulation of transcription during cellular differentiation, stem cell pluripotency, and neoplastic progression1-3. Here we show that the Polycomb group protein EED, a core component of PRC2, physically interacts with and functions as part of the PRC1 complex. Components of PRC1 and PRC2 compete for EED binding. EED functions to recruit PRC1 to H3K27me3 loci and enhances PRC1 mediated H2A ubiquitin E3 ligase activity. Taken together, we uncover the integral role of EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2. EED, uH2A, RING1A, RING1B, BMI1 and H3K27Me3 ChIP-seq in EED stable knockdown and control Scramble DU145 prostate cancer cell line
2014-01-23 | E-GEOD-42566 | biostudies-arrayexpress
Project description:Eed (embryonic ectoderm development) is a core component of the Polycomb Repressive Complex 2 (PRC2) which catalyzes the methylation of histone H3 lysine 27 (H3K27). Trimethylated H3K27 (H3K27me3) can act as a signal for PRC1 recruitment in the process of gene silencing and chromatin condensation. Previous studies with Eed KO ESCs revealed a failure to down-regulate a limited list of pluripotency factors in differentiating ESCs. Our aim was to analyze the consequences of Eed KO for ESC differentiation. To this end we first analyzed ESC differentiation in the absence of Eed and employed in silico data to assess pluripotency gene expression and H3K27me3 patterns. We linked these data to expression analyses of wildtype and Eed KO ESCs. We observed that in wildtype ESCs a subset of pluripotency genes including Oct4, Nanog, Sox2 and Oct4 target genes progressively gain H3K27me3 during differentiation. These genes remain expressed in differentiating Eed KO ESCs. This suggests that the deregulation of a limited set of pluripotency factors impedes ESC differentiation. Global analyses of H3K27me3 and Oct4 ChIP-seq data indicate that in ESCs the binding of Oct4 to promoter regions is not a general predictor for PRC2-mediated silencing during differentiation. However, motif analyses suggest a binding of Oct4 together with Sox2 and Nanog at promoters of genes that are PRC2-dependently silenced during differentiation. In summary, our data further characterize Eed function in ESCs by showing that Eed/PRC2 is essential for the onset of ESC differentiation.
2014-08-28 | GSE49305 | GEO
Project description:Polycomb Repressive Complexes 1 and 2 (PRC1 and 2) play a critical role in the epigenetic regulation of transcription during cellular differentiation, stem cell pluripotency, and neoplastic progression1-3. Here we show that the Polycomb group protein EED, a core component of PRC2, physically interacts with and functions as part of the PRC1 complex. Components of PRC1 and PRC2 compete for EED binding. EED functions to recruit PRC1 to H3K27me3 loci and enhances PRC1 mediated H2A ubiquitin E3 ligase activity. Taken together, we uncover the integral role of EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2.
2014-01-23 | GSE42566 | GEO
Project description:Multi-modal control of dendritic cell functions by nociceptors
| PRJNA899112 | ENA
Project description:Primary rib chondrocyte were isoloated from P0.5-day old wildtype and Col2-Cre:floxed EED conditional knockout mouse pups,and cultured overnight in 10%FCS containing DMEM. RNA was isolated and subjected to Affymetrix Mouse Gene ST 1.0 array. Primary rib chondrocyte were isoloated from P0.5-day old wildtype and Col2-Cre:floxed EED conditional knockout mouse pups,and cultured overnight in 10%FCS containing DMEM. RNA was isolated and subjected to Affymetrix Mouse Gene ST 1.0 array. Biological duplicate. Mice were in a mixed genetic background of C57/B6 and 129sv.
2015-11-01 | E-GEOD-66862 | biostudies-arrayexpress
Project description:Epigenetic modification by polycomb repressive complex (PRC) molecules appears to have a role in tumorigenesis and aggressiveness of neuroblastoma (NB). Embryonic Ectoderm Development (EED) is a member of PRC2 complex and binds the H3K27me3 mark deposited by EZH2, via propagation on adjacent nucleosomes. Here we studied the molecular roles of EED in MYCN-amplified neuroblastoma cells by using EED-knocked down shRNAs, EED-knocked out sgRNAs, and EED small molecule inhibitor EED226. EED suppression profoundly inhibited the NB cell proliferation and flat-and soft agar colony formation. Transcriptome analysis by microarray of the EED-KD NB cells indicated the de-repression of the cell cycle regulated and differentiation-related genes; GSEA analysis results suggested that cell cycle repressed gene sets were strongly upregulated. Further, epigenetic treatment by the combination of EED inhibitor EED226 and HDAC inhibitor valproic acid effectively suppressed NB cell proliferation and colony formation. The combinatory epigenetic treatment up-regulated the cell cycle regulation- and differentiation-related genes.
2022-09-03 | GSE183369 | GEO
Project description:Danio rerio eed, embryonic ectoderm development [Source:NCBI gene;Acc:550463], is expressed in 1 baseline experiment(s);
| ENSDARG00000099640 | ExpressionAtlas
Project description:Rattus norvegicus Eed, embryonic ectoderm development [Source:RGD Symbol;Acc:1309782], is differentially expressed in 20 experiment(s);
| ENSRNOG00000017509 | ExpressionAtlas