Similar Datasets
Project description:Abarrent transcriptional regulation is one of hallmarks of leukemia. GFI1 is a transcriptional regulator with context-dependent roles in hematopoiesis and leukemogenesis. Reduced or loss of GFI1 expression has been reported in myeloid malignancies, while high GFI1 expression has been observed in AML1-ETO-positive acute myeloid leukemia (AML) and acute lymphoid leukemia, but without clear roles defined for GFI1 in APL pathogenesis. We here performed ChIP-seq analysis using antibodies against GFI1 and identified genome-wide binding site of GFI1 in NB4 cells.
2020-08-26 | GSE154269 | GEO
Project description:Genome-wide binding of GFI1 in NB4 cells
| PRJNA643696 | ENA
Project description:Identify genome-wide binding sites of GFI1 in NB4 cells
| PRJNA645697 | ENA
Project description:Gfi1 is a transcription factor broadly participate in differentiation of immune cells and loss of Gfi1 could result in severe neutrophil deficiency. To gain insight into the consequences of lack of Gfi1 on a genome-wide level, we conducted genome-wide transcriptome profiling in Wide-type (WT) and Gfi1–/– Raw264.7 macrophage cells using Affymetrix Mouse 3’ IVT microarrays
2020-06-20 | GSE152868 | GEO
Project description:Innate type-2 lymphoid cells (ILC2s) function in immune responses against helminth parasites and are implicated in allergic inflammation and asthma. ILC2s are activated by the epithelial-derived cytokines IL-33 and IL-25 and are major sources of the type-2 cytokines IL-5 and IL-13. We show that the transcription factor Gfi1 promotes the generation of ILC2s and controls their responsiveness during Nippostrongylus brasiliensis infection as well as IL-33- or IL-25-instigated inflammation. Gfi1 directly activates Il1rl1, which encodes the IL-33 receptor. IL- 33 signaling upregulates Gfi1, thereby constituting a positive feedback loop that enables rapid and robust expansion of ILC2s in response to IL-33 signaling. Loss of Gfi1 in activated ILC2s results in an unusual effector state involving derepression of the IL-17 inflammatory program and co-expression of IL-13 with IL-17. ChIPseq reveals key Gfi1 targeted genes that are activated or repressed to maintain ILC2 identity. We propose that Gfi1 functions as a shared determinant within innate and adaptive immune cells to specify type-2 responses, while actively repressing the IL-17 effector state. ILC2s (~3 x 10^7 cells) were sorted from the MLN of IL-25-treated mice. Chromatin fragments bound by Gfi1 were subject to ChIP using Gfi1 antibodies and followed by high-throughput sequencing.
2013-09-13 | E-GEOD-50806 | biostudies-arrayexpress
Project description:ChIP-Seq Analysis of H3K9Ac in pairs of mouse and human samples carrying either the Gfi136S or the GFi136N variants. The objective of the study was to identify the changes in H3K9 acetylation at gene promoters that occur in samples expressing the 36N variant of the Gfi1 gene. 3 pairs of bone-marrow AML samples were obtained from mice where 1 mouse in each pair was homozygous for Gfi136S and 1 heterozygous for Gfi136N, or homozygous for 36N in one case. 2 pairs of AML samples were obtained from human patients were 1 patient was homozygous for Gfi1 36S and one was heterozygous for Gfi1 36N. H3 and H3K9Ac ChIP-Seq was carried out on each sample.
2016-08-01 | E-GEOD-71254 | biostudies-arrayexpress
Project description:The zinc finger transcription factor growth-factor-independent-1 (Gfi1) has been involved in various cellular differentiation processes. Gfi1 acts as a transcriptional repressor and splicing control factor upon binding to cognate binding sites in regulatory elements of its target genes. Here, we report that Gfi1-deficient mice develop autoimmunity. Gfi1-deficient peripheral B-cells show a hyperproliferative phenotype, leading to expansion of plasma cells, increased levels of nuclear autoantibodies, and immunoglobulin deposition in brain and kidneys. Dysregulation of multiple transcription factors and cell-cycle control elements may contribute to B-cell dependent autoimmunity. Gfi1 thus emerges as a novel master-regulator restricting autoimmunity. Experiment Overall Design: Splenic B220+CD19+ CD138- B cells of 4 week old Gfi1+/+ and Gfi1-/- mice were isolated and RNA was extracted from one sample per group and microarray analysis was performed.
2008-10-25 | E-GEOD-12545 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to identify sites in genomic DNA that are occupied by GFI1 and the NurD complex, represented by its member the chromodomain helicase CHD4 or by a complex of GFI1 and CHD4 in myeloid precursors cells and to determined the effect on gene expression. Methods: Granulocytic-monocytic precursors (GMPs) as well as pre neutrophils and mature neutrophils were sorted by flow cytometry from murine bone marrow and sujected to RNA-seq and Chromatin-immuno-precipitation and sequencing (ChIP-Seq) and ATAC-seq procedures. Ch-IP seq experiments were done with antibodies against GFI1, CHD4 or different histone H3 modifications as indicated. Results: GFI1 and GFI1/CHD4 complexes occupies both promoter and enhancers of genes that are down or upregulated during the formation of preNeu and matNeu cells from GMPs Conclusions: Myeloid precursors required GFI1 to tether the NuRD complex to a specific set of target genes that are either transcriptionally active or poised to enable their transcriptional regulation during neutrophil differentiation by chromatin remodeling
2021-10-13 | GSE173533 | GEO
Project description:GFI1 is a transcriptional repressor protein that plays an essential role in HSCs development, lymphoid and myeloid differentiation and Acute Myeloid Leukaemic (AML) pathogenesis. Low expression levels of GFI1 is associated with a poor prognosis in AML development. In addition, a single nucleotide polymorphism (SNP) variant of GFI1 results in the generation of GFI1 protein with asparagine (N) instead of serine (S) at the 36th amino acid position, known as GFI136N. Expression of the GFI1-36N allele leads as well to poor prognosis and promotes AML development. In this study, we demonstrated with the help of RNAseq transcriptomic analysis that the presence of GFI1-36N is associated with increased frequency of chromosomal aberrations and mutational burden in murine and human AML cells. In particular, GFI1-36N modulates DNA repair pathways, O6-methylguanine-DNA-methyltransferase (MGMT)-mediated repair and homologous recombination repair (HR). Mechanistically, GFI1-36N exhibits impaired binding to Ndrg1 promoter element compared to GFI1-36S (wild type), causing decreased NDRG1 levels, consequently leading to suppression of MGMT expression, imprinted at the transcriptome and proteome, thus leaving the AML cells vulnerable to DNA damaging agents. Furthermore, we showed that a low expression level of GFI1 in leukemic cells is associated with high OXPHOS and enhanced glutamine metabolism. However, we hypothesise that the observed metabolic phenotype is mediated through FOXO1 protein. RNAseq transcriptomic analysis revealed higher Foxo1 mRNA expression levels with lower GFI1 expression, providing the first hint of Foxo1 as a potential target gene of GFI1 protein. The mRNA and protein levels of high Foxo1 with reduced GFI1 expression was confirmed by RT-PCR and western blot, respectively. In addition, CHIPseq and ATACseq analysis further proved that Foxo1 is a potential target gene of GFI1. In summary, we show that GFI1 plays a role during DNA repair and metabolism and thus provides critical insights into a novel therapeutic option for AML patients carrying the GFI1-36N variant or having a low expression level of GFI1.
2023-12-01 | GSE195955 | GEO
Project description:To determine the potential targets of FTO and identify treatment significance of FTO inhibition in AML, we conducted transcriptome wide RNA seq with NB4 cells upon DMSO and FTO inhibitors (FB23 and FB23-2) treatment.
2019-04-29 | GSE103495 | GEO