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MiRNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

ABSTRACT: miRNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

PROVIDER: PRJNA782199 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16991534_1.fastq.gz	Fastqsanger.gz
	SRR16991534_2.fastq.gz	Fastqsanger.gz
	SRR16991535_1.fastq.gz	Fastqsanger.gz
	SRR16991535_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

miRNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

Project description:Purpose: The aim of this study is to compare brain transcriptome profile (RNA-seq) after G9a inhibition. Methods: Hippocampus profiles of 7-month-old SAMP8 Control and SAMP8 Treated mice groups were generated by deep sequencing, pooled using Ilumnia Hiseq. Results: G9a inhibition with UNC0642 induces a transcriptional profile that allows beneficial effects on cognitive performance. Differential expression analysis identified 697 differentially expressed genes (DEG) (fold change cutoff of ≥1.3, p-value<0.05). Of which 217 are reduced, and 480 are increased in SAMP8 UNC0642. Conclusions: Our study showed the first transcriptome analysis of whole brain after G9a inhibition, generated by RNA-seq technology, demonstrating transcriptomic changes.

2021-11-24 | GSE189248 | GEO

RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

2021-11-24 | GSE189249 | GEO

RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

Project description:RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

| PRJNA782200 | ENA

miRNA-seq and RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

Project description:miRNA-seq and RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

| PRJNA782198 | ENA

Pharmacological inhibition of G9a ameliorates pulmonary vascular remodeling in PAH

Project description:Background:Pulmonary arterial hypertension (PAH) is a severe condition characterized by progressive vascular remodeling of small pulmonary arteries (PAs) causing sustained elevation of PA pressure, right ventricular failure and death. Similar to cancer cells, PA smooth muscle cells (PASMCs), which play a key role in pulmonary vascular remodeling, have adopted multiple mechanisms to sustain their survival and proliferation in the presence of stress. The histone methyltransferase G9a has been shown to exert oncogenic effects and to serve as a buffer against an exaggerated transcriptional response. Therefore, we hypothesized that G9a up-regulation in PAH plays a pivotal role in pulmonary vascular remodeling by maintaining the abnormal phenotype of PAH-PASMCs. Methods: G9alevels were measured in PAs and isolated PASMCs of PAH patients and animal models. Selective G9a pharmacological inhibitors were used in human PAH-PASMCs and in rodent PAH models (i.e.Fawn-Hooded rats and Sugen/Hypoxia-exposed mice). Results: We present evidence of increased expression of G9a in PASMCs from PAH patients as well as in remodeled PAs from animal models. We found that pharmacological inhibition of G9a activity using BIX01294 and UNC0642significantly reduces the prosurvival and proproliferative potentials of cultured PAH-PASMCs. Using RNA sequencing, further exploration revealed that G9a promotes extracellular matrix production and affords protection against the negative effects of an overactive stress response. Finally, we found that therapeutic treatment with BIX01294 reduced pulmonary vascular remodeling and lowered mean PA pressure in Fawn-Hooded rats. Treatment of Sugen/hypoxia-challenged mice with BIX01294 also improved pulmonary hemodynamics and right ventricular function. Conclusions:These findings suggest that G9a inhibition may represent a new therapeutic approach in PAH.

2023-01-20 | GSE200821 | GEO

RNA-seq and miRNA-seq data from pharmacological inhibition of the G9a/GLP histone methyltransferase complex with UNC0642 in SAMP8 mice.

Project description:Growing evidence demonstrates the epigenetic modulation as a key event in Alzheimer's disease (AD) pathology. Furthermore, recent data suggests that the epigenetic regulation by the methyltransferase G9a is a crucial mechanism involved in learning and memory formation. Taking this into account, we hereby provide genomics data from pharmacological intervention with UNC0642, a potent and selective G9a/GLP in SAMP8 mice, a model of Alzheimer's disease (AD). We have generated novel RNA-seq and miRNA-seq data for three groups, healthy SAMR1, SAMP8 control and SAMP8 treated with UNC0642 (5 mg/Kg). Thus, the new data can be used to find miRNA regulation, and the mRNA's modified in AD under G9a/GLP inhibition.

| S-EPMC8257974 | biostudies-literature

Non-canonical function of histone methyltransferase G9a in the translational regulation of chronic inflammation

Project description:We report a novel translation-regulatory function of G9a, a histone methyltransferase and well-understood transcriptional repressor, in promoting hyperinflammation and lymphopenia; two hallmarks of endotoxin tolerance (ET)-associated chronic inflammatory complications. Using multiple approaches, we demonstrate that G9a interacts with multiple translation regulators during ET, particularly the N6-methyladenosine (m6A) RNA methyltransferase METTL3, to co-upregulate expression of certain m6A-modified mRNAs that encode immune-checkpoint and anti-inflammatory proteins. Mechanistically, G9a promotes m6A methyltransferase activity of METTL3 at translational/post-translational level by regulating its expression, its methylation, and its cytosolic localization during ET. Additionally, from a broader view extended from the G9a-METTL3-m6A translation regulatory axis, our translatome proteomics approach identified numerous “G9a-translated” proteins that unite the networks associated with inflammation dysregulation, T cell dysfunction, and systemic cytokine response. In sum, we identified a previously unrecognized function of G9a in protein-specific translation that can be leveraged to treat ET-related chronic inflammatory diseases.

2023-10-20 | PXD044382 | Pride

MYC interacts with the G9a histone methyltransferase to drive transcriptional repression and tumorigenesis

Project description:MYC is an oncogenic driver that regulates transcriptional activation and repression, yet molecular mechanisms of MYC transformation remain unclear. We demonstrate that MYC interacts with the G9a H3K9-methyltransferase complex to control transcriptional repression. Inhibiting G9a hinders MYC chromatin binding at MYC-repressed genes and de-represses gene expression to antagonize cellular transformation. By identifying the MYC Box II region as essential for MYC-G9a interaction, a long-standing missing link between MYC transformation and gene repression is unveiled. In breast cancer, anti-proliferative sensitivity to G9a pharmacological inhibition associates with MYC sensitivity and the basal subtype. Inhibiting G9a in vivo suppresses MYC-dependent basal breast tumor growth. Our findings reveal G9a as an epigenetic regulator of MYC-mediated transcriptional repression and a therapeutic vulnerability in MYC-driven cancers.

2018-10-08 | GSE115024 | GEO

Pharmacological inhibition of G9a ameliorates pulmonary vascular remodeling in PAH

Project description:Pharmacological inhibition of G9a ameliorates pulmonary vascular remodeling in PAH

| PRJNA826869 | ENA

Histone H3K9 Methyltransferase G9a Represses PPARγ Expression and Adipogenesis [Affymetrix expression data]

Project description:PPARγ promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is enriched on the entire PPARγ locus. H3K9me2 and G9a levels decrease during adipogenesis, which correlates inversely with induction of PPARγ. Removal of H3K9me2 by G9a deletion enhances chromatin opening and binding of adipogenic transcription factor C/EBP-beta to PPARγ promoter, which promotes PPARγ expression. Interestingly, G9a represses PPARγ expression in an HMT activity-dependent manner but facilitates Wnt10a expression independent of its enzymatic activity. Consistently, deletion of G9a or inhibiting G9a HMT activity promotes adipogenesis. Finally, deletion of G9a in mouse adipose tissues increases adipogenic gene expression and tissue weight. Thus, by inhibiting PPARγ expression and facilitating Wnt10a expression, G9a represses adipogenesis. Examination of gene expression changes in G9a KO brown preadipocytes

2013-02-01 | E-GEOD-41456 | biostudies-arrayexpress

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