Similar Datasets
Project description:We report the genome wide occupancy of G9a in RH41 Alveolar Rhabdomyosarcoma cell line.
2019-01-29 | GSE118666 | GEO
Project description:Genome-wide binding of EHMT2 in RD18 ERMS cells
| PRJNA518103 | ENA
Project description:Genome-wide binding of EHMT2 in RH41 ARMS cells.
| PRJNA486384 | ENA
Project description:G9a (EHMT2) and the G9a-like protein GLP (EHMT1) form a stable G9a/GLP heterodimer in embryonic stem cells and function cooperatively to establish and maintain the abundant repressive H3K9me2 modification, in addition to modifying several non-histone proteins. The G9a-dependent H3K9me2 is implicated in lineage-specific gene silencing and covers large chromosomal domains. While the mechanism of H3K9me2maintenance by G9a/GLP is known, how new patterns of this modification are established is not well understood. With this in mind, we used FLAG affinity purification of G9a under two different stringency conditions (150 and 300 mM NaCl) coupled with mass spectrometry to identify proteins stably associated with G9a/GLP, which could serve as potential recruiters of the complex to unmodified chromatin.
2016-03-16 | PXD003466 | Pride
Project description:The Euchromatic Histone Methyl Transferase Protein 2 (EHMT2), also known as G9a, deposits transcriptionally repressive chromatin marks that play pivotal roles in the maturation and homeostasis of multiple organs.Recently, we have shown that Ehmt2 inactivation in the mouse pancreas alters growth and immune gene expression networks, antagonizing Kras-mediated pancreatic cancer initiation and promotion. Here, we elucidate the essential role of Ehmt2 in maintaining a transcriptional landscape that protects organs from inflammation. Comparative RNA-seq studies between normal postnatal and young adult pancreatic tissue from Ehmt2 conditional knockout animals (Ehmt2 fl/fl ) targeted to the exocrine pancreatic epithelial cells (Pdx1-Cre and P48 Cre/+ ), reveal alterations in gene expression networks in the whole organ related to injury-inflammationrepair, suggesting an increased predisposition to damage. Thus, we induced an inflammation repair response in the Ehmt2 fl/fl pancreas and used a data science-based approach to integrate RNA-seq-derived pathways and networks, deconvolution digital cytology, and spatial transcriptomics. We also analyzed the tissue response to damage at the morphological, biochemical, and molecular pathology levels. The Ehmt2 fl/fl pancreas displays an enhanced injury-inflammation-repair response, offering insights into fundamental molecular and cellular mechanisms involved in this process. More importantly, these data show that conditional Ehmt2 inactivation in exocrine cells reprograms the local environment to recruit mesenchymal and immunological cells needed to mount an increased inflammatory response. Mechanistically, this response is an enhanced injury-inflammationrepair reaction with a small contribution of specific Ehmt2-regulated transcripts. Thus, this new knowledge extends the mechanisms underlying the role of the Ehmt2-mediated pathway in suppressing pancreatic cancer initiation and modulating inflammatory pancreatic diseases.
2024-06-06 | GSE269256 | GEO
Project description:The Euchromatic Histone Methyl Transferase Protein 2 (EHMT2), also known as G9a, deposits transcriptionally repressive chromatin marks that play pivotal roles in the maturation and homeostasis of multiple organs.Recently, we have shown that Ehmt2 inactivation in the mouse pancreas alters growth and immune gene expression networks, antagonizing Kras-mediated pancreatic cancer initiation and promotion. Here, we elucidate the essential role of Ehmt2 in maintaining a transcriptional landscape that protects organs from inflammation. Comparative RNA-seq studies between normal postnatal and young adult pancreatic tissue from Ehmt2 conditional knockout animals (Ehmt2 fl/fl ) targeted to the exocrine pancreatic epithelial cells (Pdx1-Cre and P48 Cre/+ ), reveal alterations in gene expression networks in the whole organ related to injury-inflammationrepair, suggesting an increased predisposition to damage. Thus, we induced an inflammation repair response in the Ehmt2 fl/fl pancreas and used a data science-based approach to integrate RNA-seq-derived pathways and networks, deconvolution digital cytology, and spatial transcriptomics. We also analyzed the tissue response to damage at the morphological, biochemical, and molecular pathology levels. The Ehmt2 fl/fl pancreas displays an enhanced injury-inflammation-repair response, offering insights into fundamental molecular and cellular mechanisms involved in this process. More importantly, these data show that conditional Ehmt2 inactivation in exocrine cells reprograms the local environment to recruit mesenchymal and immunological cells needed to mount an increased inflammatory response. Mechanistically, this response is an enhanced injury-inflammationrepair reaction with a small contribution of specific Ehmt2-regulated transcripts. Thus, this new knowledge extends the mechanisms underlying the role of the Ehmt2- mediated pathway in suppressing pancreatic cancer initiation and modulating inflammatory pancreatic diseases.
2024-06-06 | GSE269251 | GEO
Project description:Epigenetic modifications modulate gene expression and, when deregulated, contribute to the development and progression of cancer. G9a (EHMT2) and EZH2 are two histone methyltransferases commonly upregulated in several cancer types, leading to the silencing of tumor suppressor genes. We performed high throughput sequencing of a breast cancer cell line (MDA-MB-231), an ovarian cancer cell line (CAOV3) and a melanoma cell line (D14) treated with a G9a inhibitor (UNC0642), EZH2 inhibitor (GSK126) and their combination.
2022-02-20 | GSE168763 | GEO
Project description:NSTS-11 cell line derived from a primary embryonal rhabdomyosarcoma was used for serial xenotransplantation in NSG mice in vivo. Subsequently, three cell lines, LTB1, LTB5, and LTB24, were derived from primary, secondary, and tertiary xenograft tumors, respectively. Gene expression profiling of all four cell lines was performed to identify changes in gene expression over the course of serial xenotransplantation, which was associated with a gradual increase of stemness of embryonal rhabdomyosarcoma cells. For each of the xenograft-derived cell lines, the parental NSTS-11 cell line served as a reference control.
2019-04-30 | E-MTAB-7664 | biostudies-arrayexpress
Project description:The experiment was designed to interpret transcription changes in embryos that are developmentally delayed due to different genetically induced deficiencies in the Ehmt2 gene encoding the H3K9 methyltransferase EHMT2. The deficiencies included zygotic homozygosity, maternal mutation, and parental (maternal, paternal, and biparental) haploinsufficiencies, and their respective controls. The age of the embryos was between 8.5 and 9.5 dpc to allow collecting somite-stage matched embryos and detect transcriptome changes shortly before the death of homozygous mutant embryos at 10.5 dpc. Analyzing the homozygous mutants in a novel four-way comparison we distinguished differentially expressed genes (DEGs) that are direct effects of the mutation from those that correspond to embryo development. We separated the developmental DEGs that occur regardless of EHMT2 between the 6-and 12-somite stages, and then identified those developmental DEGs that uniquely change in either the normal or the mutant development. Ehmt2 zygotic and maternal mutant embryos display an increased variance, suggesting that EHMT2 is responsible for narrowing the transcriptional noise after gastrulation. Some transposable element classes correlate with genotype, but others correlate with developmental stage. EHMT2 is required for suppressing long noncoding transcripts that initiate in transposable elements predominantly of the ERVK-class. The ERVK promoters of noncanonical imprinted genes in the embryo require EHMT2 for biallelic silencing and DNA methylation. The transcriptome of delayed parental haploinsufficient wild type embryos is normal, consistent with their good survival prospects. Our four-way comparison approach is generally applicable to functional dissection of essential transcriptional regulators during development.
2021-11-01 | GSE156538 | GEO
Project description:A series of conditional mouse models of embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma and spindle cell sarcoma were generated and validated for relavence to corresponding human cancers. Conditional mouse models of embryonal rhabdomyosarcoma, alveolar rhabdomyosarcoma and spindle cell sarcoma were created by activation or deletion of Pax3:Fkhr, p53, Ptch1 or Rb1 genes.
2011-02-17 | E-GEOD-22520 | biostudies-arrayexpress