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IKAROS re-expression modulates transcriptional networks in IKZF1-mutant Ph+ B-ALL [CUT&RUN]

ABSTRACT: With the goal to investigate tumor suppressor mechanisms regulated by IKAROS (IKZF1) in PH chromosome–positive B-cell acute lymphoblastic leukemia (B-ALL) harboring IKZF1 mutations. This dataset includes bulk RNA-seq profiles from human MXP5 and PDX2 cell lines, which were engineered to express doxycycline-inducible wild-type IKAROS (IK1) or an empty vector control. RNA was collected 24 hours post-induction to capture early transcriptional responses to IK1 re-expression. These data are part of a larger multi-omics study integrating RNA-seq, ChIP-seq, CUT&RUN, ATAC-seq, and HiChIP to define IKAROS-regulated transcriptional and chromatin networks in IKZF1-deficient Ph⁺ B-ALL.

ORGANISM(S): Homo sapiens

PROVIDER: GSE310959 | GEO | 2026/02/20

REPOSITORIES: GEO

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IKAROS re-expression modulates transcriptional networks in IKZF1-mutant Ph+ B-ALL [HiChIP]

Project description:With the goal to investigate tumor suppressor mechanisms regulated by IKAROS (IKZF1) in PH chromosome–positive B-cell acute lymphoblastic leukemia (B-ALL) harboring IKZF1 mutations. This dataset includes bulk RNA-seq profiles from human MXP5 and PDX2 cell lines, which were engineered to express doxycycline-inducible wild-type IKAROS (IK1) or an empty vector control. RNA was collected 24 hours post-induction to capture early transcriptional responses to IK1 re-expression. These data are part of a larger multi-omics study integrating RNA-seq, ChIP-seq, CUT&RUN, ATAC-seq, and HiChIP to define IKAROS-regulated transcriptional and chromatin networks in IKZF1-deficient Ph⁺ B-ALL.

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IKAROS re-expression modulates transcriptional networks in IKZF1-mutant Ph+ B-ALL [RNA-Seq]

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Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ChIP-seq]

Project description: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.

2017-02-06 | GSE90656 | GEO

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ATAC-Seq]

Project description: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.

2017-02-06 | GSE90666 | GEO

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [RNA-seq]

Project description: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.

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Stage-specific control of early B cell development by the transcription factor Ikaros

Project description:Ikaros is an essential regulator of lymphopoiesis. Here, we studied the B-cell-specific function of Ikaros by conditional Ikzf1 inactivation in pro-B cells. B-cell development was arrested at an aberrant ‘pro-B’ cell stage characterized by increased cell adhesion and loss of pre-B cell receptor signaling. Ikaros was found to activate genes coding for pre-BCR signal transducers and to repress genes involved in the downregulation of pre-BCR signaling and upregulation of the integrin signaling pathway. Unexpectedly, derepression of Aiolos expression could not compensate for the loss of Ikaros in pro-B cells. Ikaros differentially controlled active chromatin at promoters and enhancers of repressed and activated target genes. Notably, Ikaros binding and target gene expression was dynamically regulated at distinct stages of early B-lymphopoiesis. 16 RNA-Seq samples in pre-proB cells (4 replicates, for each 2 controls and 2 experimental samples); 4 RNA-Seq samples in pro-B cells in Rag2-/- backgrounds (Ikzf1 deleted versus non deleted, 2 replicates each); 4 RNA-Seq samples in c-Kit high pro-B cells (Ikzf1 deleted versus non deleted, 2 replicates each); 4 RNA-Seq samples in pro-B cells (Ikzf1 deleted versus non deleted, 2 replicates each); 2 RNA-Seq samples pre-B cells wild type; 8 chromatin ChIP-Seq samples (4x H3K9ac, 4x H3K4me3, Ikzf1 deleted/non deleted, two replicates each).; 4 Transcription factor ChIP-Seq samples in pro-B cells; 1 Transcription factor ChIP-Seq samples in DP-T cells; 1 Transcription factor ChIP-Seq samples in pre-pro-B cells; 2 Mi-2b Chip-Seq samples (Ikzf1 deleted versus non deleted); 1 ChIP-Seq input track for pro-B cells; 1 ChIP-Seq input track for DP-T cells

2014-02-09 | E-GEOD-53595 | biostudies-arrayexpress

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Project description:We used microarrays to analyze gene expression changes in the Ikaros null ILC87 T cell tumor line after re-expression of Ikaros. ILC87 cells were transduced to stably express the 4-hydroxytamoxifen-inducible (4OHT) Ikaros1-ER fusion protein. ILC87-Ik1-ER cells were treated with mock (EtOH) or 4OHT for 1 day and the global gene expression changes were assessed by microarray analysis.

2015-11-03 | E-GEOD-72801 | biostudies-arrayexpress

Mapping of Ikaros and RBPJ binding sites in the mouse T cell leukemia cell line T29

Project description: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. The T29 cell line is derived from a Ikaros-deficient T-cell leukemia (Dumortier et al, MCB 26, 209-220, 2006) and exhibits strong Notch activation. We performed two chip-seq experiments with an anti-RBPJ antibody to map RBPJ binding sites. To map Ikaros binding sites, we engineered a T29-derived cell line that expresses a fusion protein between Ikaros and the ligand binding domain of the estrogen receptor (Ik1-ER) which is activated by addition of 4-hydroxy-tamoxifen (4OHT). We used an anti-Ikaros antibody to map the sites bound by Ik1-ER after treatment of the cells with 4OHT. Sequencing were performed with the Illumina GAII sequencer as as single end 36 base pair reads.

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