Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]

ABSTRACT: PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]

PROVIDER: PRJNA643578 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12130209_1.fastq.gz	Fastqsanger.gz
	SRR12130209_2.fastq.gz	Fastqsanger.gz
	SRR12130210_1.fastq.gz	Fastqsanger.gz
	SRR12130210_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

PRMT7 regulated chromatin accesibility in myeloid cells [ATAC-Seq]

Project description:Under inflammatory conditions the extravasation of monocytes into tissues through trans-endothelial migration is a fundamental immunological process underlying innate inflammatory responses across multiple organ systems contributing to tissue injury and the progression of autoimmunity, cardiovascular disease and particularly chronic lung disease. Methylation of protein arginine residues via protein arginine methyltransferases (PRMTs) is a post-translational epigenetic modification implicated in inflammatory responses. How PRMTs, particularly PRMT7, epigenetically regulates monocyte-driven inflammatory response in disease remains unclear. Here, we perform ATAC-seq analysis on an MHS macrophage cell line in which PRMT7 has been disrupted by CRISPR/Cas9 to examine chromatin accessibility regulated by PRMT7.

2022-01-12 | GSE153666 | GEO

Transcriptome sequencing of skeletal muscle for PRMT7 knockout mouse

Project description:We report that whole body PRMT7-/- adult mice display a significant reduction in in muscle mass. RNA sequencing was performed to identify potential PRMT7 targets. We found that top canonical pathways affected by the loss of PRMT7 includes cell cycle and senescence. RNA was extracted from tibialis anterior muscles harvested from 3 WT and 3 PRMT7 null mice at 8months. RNA sequencing was performed to compare mRNA in skeletal muscles between WT and KO mice.

2016-07-03 | E-GEOD-75993 | biostudies-arrayexpress

PRMT7 substrates

Project description:Protein arginine methyltransferases (PRMTs) regulate diverse biological processes and are increasingly being recognized for their potential as drug targets. Here we report the discovery of a potent, selective and cell active chemical probe for PRMT7. SGC3027 is a cell permeable prodrug, which in cells, is converted to SGC8158, a potent, SAM-competitive PRMT7 inhibitor. Inhibition or knockout of cellular PRMT7 resulted in drastically reduced levels of monomethylation of HSP70 family members and other stress-associated proteins. Structural and biochemical analysis revealed that PRMT7-driven in vitro methylation of HSP70 at R469 requires an ATP-bound, open conformation of HSP70. In cells, SGC3027 inhibited methylation of both, constitutive and inducible forms of HSP70, and led to decreased tolerance for perturbations in proteostasis. These results demonstrate a role for PRMT7 in stress response. SGC3027 is the first chemical probe for PRMT7 and together with its inactive control SGC3027N, will be valuable chemical tools to further investigate the role of PRMT7 in human health and disease.

2022-02-23 | PXD012119 | Pride

Transcriptome sequencing of skeletal muscle for PRMT7 knockout mouse

2016-01-01 | GSE75993 | GEO

Effect of the depletion of RBP33 (Tb927.8.990) on chromatin accesibility in bloodstream Trypanosoma brucei [ATAC-seq]

Project description:Depletion of RBP33 by RNAi does not seem to have profound effects on chromatin accesibility

2022-11-03 | GSE186562 | GEO

RNA-seq in QGY-7703 cell line before and after PRMT7 knockdown

Project description:To explore the mechanism by which PRMT7 regulates HCC cell malignant phenotypes, we performed RNA-seq in QGY-7703 cells before and after PRMT7 knockdown to identify the affected signaling pathways. 296 differentially expressed genes were identified in PRMT7-downregulated cells (Figure 6A) and these genes were enriched in cancer-related pathways including MAPK signaling pathway, p53 signaling pathway, and FoxO signaling pathway (Figure 6B), as revealed by DAVID KEGG analysis.

2021-02-25 | GSE167432 | GEO

PRMT7 knockdown in Jurkat-Cas9 and Molt-4 T-ALL cell line

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with only few established prognostic biomarkers.In this study, we examined the expression of protein arginine methyltransferases across hematological malignancies and discovered high levels of PRMT7 mRNA in T-ALL, particularly in the mature subtypes of T-ALL. High PRMT7 was associated with decreased event-free and overall survival in two independent patient cohorts. Genetic deletion of PRMT7 by CRISPR-Cas9 significantly decreased the colony-forming capacity of the cells and negatively impacted cell viability. In the knockout cells, alterations were seen in the monomethyl arginine levels in proteins associated with RNA processing. These results suggest that PRMT7 plays an active role in T-ALL pathogenesis.

2021-10-22 | GSE186238 | GEO

CRISPR screens identify PRMT7 as a therapeutic target to enhance T cell-mediated killing in breast cancer

Project description:Genome-wide association studies (GWAS) have identified more than 220 loci associated with breast cancer susceptibility, yet identifying effector genes, their modes of action and prioritising therapeutic targets remains a significant challenge. To address this, we performed pooled CRISPR knockout and inhibition screens to identify genes at risk loci that influence cytotoxic T lymphocyte (CTL) killing of MCF7 breast cancer cells in co-culture. These screens uncovered 33 candidate modulating genes, of which we validated six by single gene editing in two cell lines. Deletion of IRF1, ATF7IP, and CASP8 conferred resistance to CTL killing, while disruption of CFLAR, CREBBP and PRMT7 enhanced sensitivity. Analysis of clinical data showed that PRMT7 expression is negatively correlated with CD8+ infiltration and survival in breast cancer patient cohorts. Pharmacological inhibition of PRMT7 sensitized breast cells to CTL killing in vitro, and Prmt7-deficient tumors exhibited reduced growth and increased CD8+ T cell infiltration in immunocompetent mice. Enhanced Prmt7-dependent tumor growth was not observed in immunodeficient mice, implicating Prmt7 in immune evasion. This study underscores the utility of CRISPR screens for high-throughput functional follow-up of GWAS findings and identifies PRMT7 inhibition as a promising therapeutic strategy.

2026-02-18 | GSE316985 | GEO

Deoxyshikonin-induced chromatin accesibility changes in porcine intestinal epithelial cells

Project description:The objectives of this study is to evaluate the chromatin accesibility changes after deoxyshikonin stimulation in porcine intestinal epithelial cells.

2023-04-09 | GSE228772 | GEO

Chromatin accesibility in mice T-ALL tumors

Project description:Long-range enhancers play an important role in the temporal and spatial control of gene expression and are deregulated in many cancers. Yet, the mechanisms that govern enhancer activity during development and oncogenesis remain poorly understood. In this study we analyze the chromatin accesibility of mice T-ALL tumors.

2018-12-21 | GSE124175 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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