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Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

ABSTRACT: Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

PROVIDER: PRJNA955112 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24299900.fastq.gz	Fastqsanger.gz
	SRR24299901.fastq.gz	Fastqsanger.gz
	SRR24299896.fastq.gz	Fastqsanger.gz
	SRR24299897.fastq.gz	Fastqsanger.gz
	SRR24299898.fastq.gz	Fastqsanger.gz

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Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

| PRJNA955103 | ENA

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

| PRJNA955106 | ENA

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

| PRJNA955107 | ENA

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-08-07 | GSE229592 | GEO

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:To investigate the role of IkE5 in Treg cell biology, we established IkE5-deficient Treg cells from Foxp3-Cre IkE5 floxed mice. We then performed gene expression profiling analysis using data obtained from bulk RNA-seq of wild-type and IkE5-deficient Treg cells.

2024-08-07 | GSE229591 | GEO

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:To investigate the role of IkE5 in Treg cell biology, we established IkE5-deficient Treg cells from Foxp3-Cre IkE5 floxed mice. We then performed Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for several transcription factors and epigenetic regulators as well as the histone modification H3K27ac in wild-type and IkE5-deficient Treg cells.

2024-08-07 | GSE229590 | GEO

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:To investigate the role of IkE5 in Treg cell biology, we established IkE5-deficient Treg cells from Foxp3-Cre IkE5 floxed mice. We then performed assay for transposase-accessible chromatin (ATAC)-seq to evaluate the chromatin accessibility in wild-type and IkE5-deficient Treg cells.

2024-08-07 | GSE229588 | GEO

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

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

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

2015-09-04 | GSE68391 | GEO