Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Manipulating the transcriptome and chromatin accessibility in T cells through CRISPR-induced alternative splicing of IKZF1 (ATACseq)

ABSTRACT: Manipulating the transcriptome and chromatin accessibility in T cells through CRISPR-induced alternative splicing of IKZF1 (ATACseq)

PROVIDER: PRJNA1074710 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27918039_1.fastq.gz	Fastqsanger.gz
	SRR27918039_2.fastq.gz	Fastqsanger.gz
	SRR27918040_1.fastq.gz	Fastqsanger.gz
	SRR27918040_2.fastq.gz	Fastqsanger.gz
	SRR27918041_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 68

Similar Datasets

Manipulating the transcriptome and chromatin accessibility in T cells through CRISPR-induced alternative splicing of IKZF1 (ATACseq)

Project description:Genome-wide association studies have identified statistically significant associations between genetic variants in or near the IKZF1 gene and several autoimmune disorders. IKZF1, encoding the transcription factor Ikaros, produces at least 10 distinct transcripts via alternative splicing. To explore the role of alternative splicing of IKZF1 in mature T cells, we generated a panel of Jurkat T-cell clones with various truncating mutations in IKZF1 exon 4, exon 6 or both. Differences among clones in gene expression, chromatin accessibility, and protein abundance were assessed by RNA-seq, ATAC-seq and immunoblotting. Clones with single targeting events in either exon 4 or 6 clustered separately from double-targeted clones on multiple parameters, but overall, clone responses were highly heterogeneous. Perturbation of IKZF1 splicing resulted in significant differences in expression and chromatin accessibility of other autoimmunity-associated genes and elicited compensatory expression changes in other IKZF family members. Our results suggest that even modest perturbations of IKZF1 splicing can have significant effects on gene expression and function in mature T cells.

2024-06-01 | GSE255337 | GEO

Manipulating the transcriptome and chromatin accessibility in T cells through CRISPR-induced alternative splicing of IKZF1 (RNAseq)

2024-06-01 | GSE252707 | GEO

Manipulating the transcriptome and chromatin accessibility in T cells through CRISPR-induced alternative splicing of IKZF1 (RNAseq)

Project description:Manipulating the transcriptome and chromatin accessibility in T cells through CRISPR-induced alternative splicing of IKZF1 (RNAseq)

| PRJNA1062296 | ENA

Single cell ATACseq of lung dendritic cells from hyperglycemic mice

Project description:We performed single cell ATACseq to measure chromatin accessibility in different subsets of lung dendritic cells hyperglycaemic mice. We used genetic model to achieve hyperglycaemia and compared wild type and Akita mice.

2023-06-29 | E-MTAB-11392 | biostudies-arrayexpress

How C/EBPa creates an elite cell state for reprogramming to pluripotency [ATACseq]

Project description:Mouse Bcell, upon ectopic expression of the transcription factor Cebpa for 18h, can be reprogrammed to iPS with extremely high efficiency. To understand the molecular control of this phenomena we performed multiple high throughtput functionnal genomic analysis. Chromatin accessibility by ATACseq in Bcell, Bcell+Cebpa18h, Bcell+Cebpa18h+OKSM1d, Bcell+Cebpa18h+OKSM2d, ES cells

2016-02-19 | E-GEOD-71214 | biostudies-arrayexpress

Efficacy of retinoids in IKZF1-mutated BCR-ABL1 acute lymphoblastic leukemia

Project description:Alterations of IKZF1, encoding the lymphoid transcription factor IKAROS, are a hallmark of high risk acute lymphoblastic leukemia (ALL), however the role of IKZF1 alterations in ALL pathogenesis is poorly understood. Here we show that in mouse models of BCR-ABL1 leukemia, Ikzf1 and Arf alterations synergistically promote the development of an aggressive lymphoid leukemia. Ikzf1 alterations were associated with acquisition of stem cell-like features, including self-renewal and increased bone marrow stromal adhesion. Rexinoid receptor agonists reversed this phenotype, in part by inducing expression of IKZF1, resulting in abrogation of adhesion and self-renewal, cell cycle arrest and attenuation of proliferation without direct cytotoxicity. Retinoids potentiated the activity of dasatinib in mouse and human BCR-ABL1 ALL, providing a new therapeutic option in IKZF1-mutated ALL. Significance: The outcome of therapy for high-risk acute lymphoblastic leukemia remains suboptimal despite contemporary chemotherapy and the advent of targeted therapeutic approaches. Recent genomic studies have identified deletions or mutations of IKZF1 as a hallmark of high-risk ALL, but an understanding of how IKZF1 alteration contribute to leukemia development are lacking. Here we show that IKZF1 alterations drive lymphoid lineage, a stem cell-like phenotype, abnormal bone marrow adhesion, and poor responsiveness to tyrosine kinase inhibitor (TKI) therapy. Using a high-content screen, we show that retinoids reverse this phenotype in part by inducing expression of wild type IKZF1, and increase responsiveness to TKIs. These findings provide new insight into the pathogenesis of high-risk ALL and potential new therapeutic approaches. Pre-B mRNA profiles of p185 MIG and IK6 cells, DMSO or drug treated, in 3 or 4 replicates, using Illumina HiSeq 2500.

2015-09-04 | E-GEOD-68391 | biostudies-arrayexpress

ATACseq of TNG-A derived mESCs comparing WT to Dax1, Nr5a2 and Dax1/Nr5a2 knock-out clones

Project description:ATACseq in WT, Dax1, Nr5a2 and Dax1/Nr5a2 knock-out clones of mESCs in order to determine the role of the Dax1/Nr5a2 complex on chromatin accessibility and the activity of cis-regulatory elements during differentiation.<br>This experiment is part of the study: "Mechanistic framework of lineage restriction in embryonic stem cells" by Olivieri et al.

2021-03-15 | E-MTAB-9453 | biostudies-arrayexpress

Tumor Suppressor IKZF1 Mediates Glucocorticoid Therapy Resistance in B Cell Precursor Acute Lymphoblastic Leukemia

Project description:Analysis of the effect of Prednisolone in mouse splenocytes with and without Ikzf1 at gene expression level. The hypothesis tested in the present study was that loss of Ikzf1 affects the induction and repression of the Glucocorticoid receptor target genes. Results provide important information of the differentially expressed genes regulated by Ikzf1 upon Prednisolone treatment, explaining the resistance towards Glucocorticoid-induced apoptosis in splenocytes harboring Ikzf1 loss. Total RNA was obtained from WT and Ikzf1+/- splenocytes subjected to 16 hours Prednsiolone treatment compared to untreated cells.

2015-02-04 | E-GEOD-65554 | biostudies-arrayexpress

ATACseq

Project description:ATACseq data for this study.

| EGAS00001007166 | EGA

Efficacy of retinoids in IKZF1-mutated BCR-ABL1 acute lymphoblastic leukemia

2015-09-04 | GSE68391 | GEO