Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of splenic follicular B cells from wild-type and IKZF1 L132P mutant mice

ABSTRACT: RNA-seq of splenic follicular B cells from wild-type and IKZF1 L132P mutant mice

PROVIDER: PRJEB42263 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of splenic follicular B cells from wild-type and IKZF1 L132P mutant mice

Project description:Comparing the effect of the L132P variant in ZF1 of IKZF1 on the gene expression in sorted follicular B cells.

2021-01-29 | E-MTAB-9975 | biostudies-arrayexpress

Splenic Tfh that express SLAM reside in the follicular mantle zone

Project description:Splenic Tfh that express SLAM reside in the follicular mantle zone

2020-06-01 | GSE136303 | GEO

RNA-seq analysis of splenic follicular IgD low and IgD high, and marginal zone B cells

Project description:RNA sequencing was performed to determine the uniqueness of splenic follicular IgD low B cells compared to splenic follicular IgD high and marginal zone B cells.

2018-12-03 | GSE111911 | GEO

WT and Ikaros-deficient follicular B cells stimulated with anti-IgM

Project description:We have observed that follicular B cells from mice with a hypomorphic mutation (IkL/L) in the Ikzf1 gene (which encodes the Ikaros transcription factor) exhibit an increased proliferative response to anti-IgM stimulation (Kirstetter et al, Eur J Immunol, 32:720-30, 2002). We asked if Ikaros controls the transcriptional response that unfolds after activation, or if differences in the transcriptional landscape of resting B cells could explain the altered response. To this end, we have determined the transcriptome of unstimulated WT and IkL/L follicular B cells, as well as that of cells stimulated for 3h and 12h with anti-IgM. Samples from 2 independent experients were analyzed. Follicular splenic B cell were sorted from 6-week old WT or IkL/L mice, and stimulated for 3 or 12h with anti IgM, or cultured without anti-IgM for 3h (unstimulated samples) 2 independant experiments were performed

2016-01-26 | E-GEOD-75712 | biostudies-arrayexpress

Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [it325]

Project description:The characterisation of two zebrafish ikzf1 mutant lines missing the two C-terminal zinc fingers only and both part of the DNA binding domain plus the C-terminal zinc fingers respectively gives insight into the specific roles of these elements during zebrafish hematopoiesis

2022-10-08 | GSE214953 | GEO

Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [ikaros]

2022-10-08 | GSE214952 | 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

Stage- and cell type-specific requirements of ikzf1 during haematopoietic differentiation in zebrafish

Project description:The zinc finger transcription factor Ikaros1 (Ikzf1) is required for lymphoid development in mammals. It is characterized by the presence of four zinc fingers in its DNA binding domain and two zinc fingers in the C-terminal protein interaction module. Here, we describe the phenotypes of zebrafish homozygous for two distinct mutant ikzf1 alleles. The IT325 variant lacks the C-terminal two zinc fingers, whereas the fr105 variant retains only the first zinc finger of the DNA binding domain. Our results indicate that an intact ikzf1 gene is required for larval T cell development, whereas low levels of adult lymphoid development recover in the mutants. By contrast, the mutants exhibit a signature of increased myelopoiesis at larval and adult stages. Of note, both mutants stimulate erythroid differentiation in larvae, indicating that the C-terminal zinc fingers negatively regulate the extent of red blood cell production. An unexpected differential effect of the two mutants on adult erythropoiesis suggests a direct requirement of an intact DNA binding domain for entry of progenitors into the red blood cell lineage. Collectively, our results reinforce the biological differences between larval and adult haematopoiesis, indicate a stage-specific function of ikzf1 in regulating the hierarchical bifurcations of differentiation, and assign distinct functions to the DNA binding domain and the C-terminal zinc fingers.

2022-12-09 | GSE200756 | GEO

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

Splenic Tfh that express SLAM reside in the follicular mantle zone

Project description:Splenic Tfh that express SLAM reside in the follicular mantle zone

| PRJNA562144 | ENA