GEO DataSets

(Submitter supplied) Ikaros functions as a master regulator of lymphocyte differentiation and a tumor suppressor. Ikaros binds DNA and regulates gene expression by chromatin remodeling. Mechanisms of Ikaros-mediated tumor suppression are unknown. Here we examined genome-wide occupancy of Ikaros and histone deacetylase 1 (HDAC1) and Histone midificaition markers in human leukemia, and found that the Ikaros and HDAC1 showed similar binding partern and HDAC1–DNA interactions are associated with the presence of bivalent chromatin, and the recruitment of HDAC1 by Ikaros is associated with bivalent chromatin at Ikaros target genes.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL11154 GPL9115

10 Samples

Download data: COD

(Submitter supplied) High-risk B-cell acute lymphoblastic leukemia (B-ALL) is an aggressive disease, often characterized by resistance to chemotherapy. A frequent feature of high-risk B-ALL is loss of function of the Ikaros tumor suppressor. In leukemia, Ikaros’ function is impaired by oncogenic Casein Kinase II (CK2), which is overexpressed in B-ALL. Phosphorylation by CK2 reduces Ikaros binding to the promoter of its target gene, particularly Bcl-xL. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24676

11 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL15143 GPL11154 GPL9115

13 Samples

Download data: COD, PAIR

(Submitter supplied) Identify the expression intensity for all genes in Nalm6 cells and all the genes are divided into 4 equal groups with group 1 containing the 25% of genes that were expressed at the highest levels, and group 4 containing the 25% of genes that were expressed at the lowest levels.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL15143

3 Samples

Download data: PAIR

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

16 Samples

Download data: TXT

(Submitter supplied) To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

2 Samples

Download data: TXT

(Submitter supplied) To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

2 Samples

Download data: TXT

(Submitter supplied) To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

12 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

28 Samples

Download data: BED, BEDGRAPH, BIGWIG

(Submitter supplied) Using patient-derived Ph+ pre-B ALL cells that harbor deletions of the IKZF1 DNA binding domain (Ik6), we performed ATAC-sequencing in cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

2 Samples

Download data: BEDGRAPH

(Submitter supplied) RNA-seq was performed in human Ph+ pre-B ALL cells that harbor a deletion of the Ikaros DNA binding domain (Ik6) after doxycycline induction of exogenous expression of wild-type Ikaros (Ik1) or control empty vector over 0, 12, 24 and 48 hours. Biological replicates (n=2) using independent cultures and inductions were performed.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

16 Samples

Download data: TXT

(Submitter supplied) ChIP-seq was performed in patient-derived BCR-ABL1+ (Ph+) pre-B ALL cells that harbor heterozygote deletions of the IKZF1 DNA binding domain (Ik6), using cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

10 Samples

Download data: BED, BIGWIG

(Submitter supplied) IKAROS is an important tumor suppressor in human pre-B ALL and is mutated or deleted in a high percentage of human BCR-ABL1+ (Ph+) pre-B ALL. We here report the genome-wide binding of IKAROS in two independent patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells that express wild type full-length IKAROS.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

8 Samples

Download data: BEDGRAPH, TXT

(Submitter supplied) Deletions within the human IKZF1 gene, which encodes Ikaros, a zinc finger transcription factor critical for lymphopoiesis, appear to be the most prominent recurring lesion in human BCR-ABL1+ (Ph+) B-ALL. Furthermore, IKZF1 mutations correlate with poor prognosis of progenitor B-ALL, further strengthening the notion that IKZF1 is a critical tumor suppressor gene in human B-lineage malignancies. To better understand the relationship between Ikzf1 mutations, BCR-ABL, and B-lineage leukemia, we examined the effect of two newly generated Ikzf1 germline mutation on BCR-ABL-induced proliferation and leukemogenesis in vitro and in vivo. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: BIGWIG, TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL17021 GPL9250

46 Samples

Download data: BIGWIG, BW

(Submitter supplied) Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL17021 GPL9250

38 Samples

Download data: BW

(Submitter supplied) Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL17021

8 Samples

Download data: BIGWIG

(Submitter supplied) The transcription factor Ikaros represses Notch signaling. Since Ikaros and Notch treanscriptional mediator RBPJ both recognize sequences that contain the same core TGGGAA motif, it was hypothesized that Ikaros represses Notch signaling by targeting Notch response elements and competing with RBPJ for their binding. Here we used the mouse T-cell leukemia cell line T29 to compare the genomic binding profiles of Ikaros and RBPJ by ChIP-seq.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11002

6 Samples

Download data: WIG

(Submitter supplied) We used an immature mouse T cell line engineered to express a biotinylated form of the cleaved form of Notch1 (ICN1). ICN1-bound sites were precipitated with streptavidin-coated beads and subjected to ChIP-sequencing.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11002

2 Samples

Download data: WIG

(Submitter supplied) The mouse Ikaros-deficient thymic lymphoma cell line T29 was treated with a gamma-secretase inhibitor or vehicle (DMSO) for 36h and subjected to transcriptome analysis.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

4 Samples

Download data: CEL