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

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

PROVIDER: PRJNA643578 | ENA |

REPOSITORIES: ENA

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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

BANP opens chromatin and activates CpG island regulated genes [ATAC-Seq]

Project description:BANP opens chromatin and activates CpG island regulated genes [ATAC-Seq]

| PRJNA650492 | ENA

Chromatin interactions of the EVI1 oncogene in myeloid leukaemia (ATAC-Seq)

Project description:EVI1 expression is associated with poor prognosis in myeloid leukaemia. Aberrant expression can result from Chr.3q alterations, which cause juxtaposition of enhancers that induce EVI1 activation via long-range chromatin interactions. More often, however, EVI1 expression occurs unrelated to 3q alterations, and it is unclear if its expression underlies similar dependencies as 3q+ cells. As enhancers regulate promoters by physical interaction/chromatin looping, we explored if the EVI1 promoter in EVI1+3q- cells interacts with distally located chromatin and if these intereactions promote EVI1 expression. To monitor TF binding sites at interactions involving active chromatin, we performed ATAC-Seq.

2023-12-24 | GSE250133 | 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

Chromatin accessibility (ATAC-seq) of human acute leukemias and healthy donors

Project description:ATAC-seq of 79 primary samples obtained from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). Moreover, ATAC-seq of CD34+ HSPCs from 3 healthy donors are included. ATAC-seq was performed as described (Buenrostro et al., 2013) with a modification in the lysis buffer to reduce mitochondrial DNA contamination. Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011050 (dataset).

2023-08-31 | E-MTAB-13118 | biostudies-arrayexpress

Hormone-dependent control of developmental timing through regulation of chromatin accessibility

Project description:We identify a temporal cascade of ecdysone-inducible transcription factor gene expression during Drosophila wing development. This temporal cascade corresponds with dynamic changes in chromatin accesibility during wing development. We hypothesized that these temporally regulated transcription factors may coordinate these dynamic open chromatin changes. To test this, we investigate the ecdysone-inducible transcription factor, E93, which we determine is required for coordinating transitions in developmental stage by regulating chromatin accesibility of cis-regulatory elements.

2017-06-06 | GSE97956 | GEO

IKAROS and MENIN are Functionally Cooperative Therapeutic Targets in Acute Myeloid Leukemia [ATAC-seq]

Project description:Using ATAC-seq, we examined genome-wide chromatin accessibility in the MOLM13 and MV4;11 human MLL-fusion acute myeloid leukemia cell lines.

2022-03-10 | GSE168459 | GEO

Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [ATAC-seq]

Project description:Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [ATAC-seq]

| PRJNA612061 | ENA

Impact of MEF2C on chromatin accessibility of mouse BM pre-B and myeloid cells

Project description:We analyzed the chromatin accessibility of control and Mef2c deficient mouse BM pre-B and myeloid cells by ATAC-seq analysis.

2016-07-12 | GSE81508 | GEO

Frequent and Transient Acquisition of Pluripotency During Somatic Cell Trans-Differentiation with iPSCs Reprogramming Factors (ATAC-Seq)

Project description:Recent reports have proposed a new paradigm for obtaining mature somatic cell types from fibroblasts without going through a pluripotent state, by briefly expressing canonical iPSC reprogramming factors Oct4, Sox2, Klf4 and c-Myc (abbreviated as OSKM), in cells expanded in lineage differentiation promoting conditions. Here we apply genetic lineage tracing for endogenous Nanog, Oct4 and X chromosome reactivation during OSKM induced trans-differentiation, as these molecular events mark final stages for acquisition of induced pluripotency. Remarkably, the vast majority of reprogrammed cardiomyocytes or neural stem cells derived from mouse fibroblasts via OSKM mediated trans-differentiation were attained after transient acquisition of pluripotency, and followed by rapid differentiation. Our findings underscore a molecular and functional coupling between inducing pluripotency and obtaining “trans-differentiated” somatic cells via OSKM induction, and have implications on defining molecular trajectories assumed during different cell reprogramming methods. poly RNA-Seq and Chromatin accesibility (ATAC-seq) were measured during conversion of mouse embryonic fibroblasts to neural stem cells using OSKM trans-differentiation method, as well as in mouse emrbyonic fibroblasts, iPSCs and mouse ESCs.

2015-04-30 | E-GEOD-67298 | biostudies-arrayexpress

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