Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression in mouse splenic CD4+CD25+ (Treg) cells from Ikzf2-/-, Ikzf4-/- and double Ikzf2-/-Ikzf4-/- (dKO) mice

ABSTRACT: CD4+CD25+ cells were sorted from the spleen of 6-7 week old mice WT, Ikzf4-/- and dKO mice (group 1) were processed separately from a a second group (group2) containing Ikzf2-/- and their WT controls. Group 1 originates from an ultra clean sterile bioBubble, while group 2 originates from a specific pathogne free facility. In each group 3 samples were analyzed for each genotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE162023 | GEO | 2023/10/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

ChIP-seq HELIOS (Ikzf2)

Project description:ChIP-seq HELIOS (Ikzf2)

| PRJNA627719 | ENA

Dual IKZF2 and CK1α degrader targets acute myeloid leukemia cells

Project description:Acute myeloid leukemia (AML) is a hematologic malignancy for which several epigenetic regulators have been identified as therapeutic targets. Here we report the development of cereblon-dependent degraders of IKZF2 and casein kinase 1 alpha (CK1α) termed DEG-35 and DEG-77. We utilized a structure-guided approach to develop DEG-35 as a nanomolar degrader of IKZF2, a hematopoietic specific transcription factor that contributes to myeloid leukemogenesis. DEG-35 possesses additional substrate specificity for the therapeutically relevant target CK1α which was identified through unbiased proteomics and a PRISM screen assay. Degradation of IKZF2 and CK1α blocks cell growth and induces myeloid differentiation in AML cell lines through CK1α–p53- and IKZF2-dependent pathways. Target degradation by DEG-35 or the analog DEG-77 delays leukemia progression in murine and human AML mice models. Overall, we provide a strategy for multi-targeted degradation of IKZF2/CK1α to enhance efficacy against AML that may be expanded to additional targets and indications.

2023-03-08 | PXD039474 | Pride

Gene expression profiling of CTCL cell line Hut78 via IKZF2 knockdown by RNA-seq

Project description:IKZF2 is an important nuclear matrix protein and plays a pivotal role in T cell development and differentiation, while its expression and function in Cutaneous T cell lymphoma (CTCL) remain ambiguous. Our study aimed to investigate the expression pattern, biological function of IKZF2 in a large clinical cohort. IKZF2 is specifically over-expressed in malignant T cells with MF tumor-stage. In order to explore the function of IKZF2 in the pathogenesis of CTCL, transcriptome sequencing was performed among Hut78 cells transfected with shRNAs targeting IKZF2 (shIKZF2) and scrambled shRNA(sh0) to investigate genes regulated by IKZF2 in CTCL cells .

2022-02-28 | GSE179433 | GEO

Single cell transcriptional profiles of control and Ikzf2-transfected mouse cochlear cells

Project description:In order to determine the transcriptional effect of Ikzf2 overexpression in mammalian auditory hair cells, mouse cochleae were transfected with either a control GFP or a Ikzf2 virus between postnatal day 1 and 3 (P1-3) and then harvested for single cell gene expression profiling at postnatal day 8 (P8) on the 10X Genomics Single Cell 3' v2 platform.

2018-11-28 | GSE120462 | GEO

IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program II

Project description:We report that IKZF2 is required for maintaining chromatin accessibility in leukemic stem cells in myeloid leukemia. RNA seq and ATAC-seq were performed to investigate the changes in chromatin accessibility of differentially expressed genes in leukemic stem cells when IKZF2 was absent. We found that IKZF2 maintains open accessibility in self-renewal transcription factor motifs such as HOXA9 sites whereas motifs of differentiation transcription factors including C/EBPs are kept closed.

2018-09-29 | GSE120623 | GEO

IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program I

2017-12-21 | GSE108367 | GEO

Design and development of IKZF2 and CK1α dual degraders

Project description:Lenalidomide achieves its therapeutic efficacy by recruiting and removing proteins of therapeutic interest through the E3 ligase substrate adapter cereblon. Here, we report the rational design and characterization of 81 cereblon ligands for their ability to degrade the transcription factor Helios (IKZF2) and casein kinase 1 alpha (CK1α) in acute myeloid leukemia MOLM-13 cells. Using a structure-based approach, we identified a key naphthamide scaffold that depleted both intended targets. Structure-activity relationship studies for degradation of the desired targets over other targets (IKZF1, GSPT1) afforded an initial lead compound, termed DEG-35. A subsequent scaffold replacement campaign informed by degradation profiles against a panel of substrates identified DEG-77, which selectively degrades IKZF2 and CK1α, and possesses suitable pharmacokinetic properties, solubility, and selectivity for in vivo studies. Finally, we show that DEG-77 has antiproliferative activity in diffuse large B cell lymphoma (DLBCL) cell line OCI-LY3 and ovarian cancer cell line A2780, indicating that these dual degraders and their targets may have efficacy against additional cancer types.

2024-01-04 | PXD045327 | Pride

Ikzf2/helios mutant cochlear RNA-seq analysis

Project description:Ikzf2/helios mutant cochlear RNA-seq analysis

| PRJNA479955 | ENA

Genes regulated by DEG-35, a dual degrader of IKZF2 and CK1A in AML cells

Project description:To investigate the genes regulated in MOLM-13 cells treated with DMSO or DEG-35, a dual degrader of IKZF2 and CK1A in AML cells

2023-01-16 | GSE220707 | GEO

Helios KO Tregs

Project description:Transcriptome of splenic Treg cells (CD4+CD25+) from 7-week old WT and Ikzf2-/- mice (RNA-seq)

2023-10-24 | GSE180159 | GEO