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Changes in Ikaros binding and histone-modifications upon oncogenic β-catenin activation [ChIP-Seq]

ABSTRACT: We find that, in contrast to most cancer types, beta-catenin activation in preB-ALL cells supresses proliferation and leads to cell death. Proteomic analyses indicate that unlike in solid tumors beta-catenin interacts with Ikaros factors (IKZF1 and IKZF3) in pre-B cells. In order to examine the interaction between IKZF1/IKZF3 and beta-catenin we performed ChIPseq to assay chromatin state and TF binding in CTNNB1-GOF and IKZF1/3-LOF conditions.

ORGANISM(S): Mus musculus

PROVIDER: GSE196745 | GEO | 2025/08/08

REPOSITORIES: GEO

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Gene expression changes in B-ALL upon oncogenic β-catenin activation [RNA-Seq]

Project description:We find that, in contrast to most cancer types, beta-catenin activation in preB-ALL cells supresses proliferation and leads to cell death. Proteomic analyses indicate that unlike in solid tumors beta-catenin interacts with Ikaros factors (IKZF1 and IKZF3) in pre-B cells. We performed RNA-seq in order to examine changes in expression upon beta-catenin activation in the presence and absence of Ikaros factors.

2025-08-08 | GSE196767 | GEO

Analysis of EMCN+ bone marrow cells in Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt mice

Project description:Endothelial-derived Wnt/Ctnnb1-signaling is an important angiocrine regulator. Ctnnb1 gain-of-function (GOF) in sinusoidal endothelial cells was generated via Stab2-iCreF3tg/wt Ctnnb1(Ex3)fl/wt mice to analyze the effects of endothelial β-catenin signaling on bone marrow function. We used microarrays to detail the global programme of gene expression in bone marrow EMCN+ cells with β-catenin (Ctnnb1) gain-of-function compared to Wildtype.

2021-10-13 | GSE180477 | GEO

Analysis of liver sinusoidal endothelial cells (LSECs) with β-catenin (Ctnnb1) activation

Project description:Endothelial-derived Wnt/Ctnnb1-signaling is an important angiocrine regulator. Ctnnb1 gain-of-function (GOF) in liver sinusoidal endothelial cells was generated by crossing Clec4g-iCre (Wohlfeil SA et al, 2019, Cancer Research) with Ctnnb1(Ex3) fl/fl mice (Harada N et al, 1999, EMBO J) to analyze the effects of endothelial β-catenin signaling on LSEC differentiation and liver function We used microarrays to detail the global programme of gene expression in liver sinusoidal endothelial cells with β-catenin (Ctnnb1) gain-of-function compared to control animals.

2021-11-18 | GSE175777 | GEO

Ikaros and Aiolos directly regulate AP-1 transcriptional complexes and are essential for natural killer cell development [CUT&Run]

Project description:Ikaros family transcription factors regulate lymphocyte biology and are targets of the immunomodulatory imide drugs (IMiDs) for hematological malignancies. Ikaros (Ikzf1/IKZF1) is the most broadly expressed family member in lymphocytes, yet its role in innate lymphopoiesis is unknown. Here we used gene inactivation to reveal that NK cell-expression of Ikaros is essential for normal NK lymphopoiesis. Mechanistically, IKZF1 directly repressed Cish and Socs2, known negative regulators of IL-15R resulting in impaired IL-15 signaling in Ikzf1-null NK cells. Bcl2l11/BIM levels and apoptosis were increased in Ikzf1-null NK cells which in part accounted for the NK lymphopenia since both apoptosis and NK cell frequency were restored to normal levels when Ikzf1 and Bcl2l11 were co-deleted. Ikzf1-null NK cells presented extensive transcriptional alterations with a striking reduction in expression of genes encoding AP-1 transcriptional complexes (Fos/Jun members) and a compensatory increase in Ikzf2 and Ikzf3. Both IKZF1 and IKZF3 directly bound AP-1 family members and deletion of both Ikzf1 and Ikzf3 in NK cells resulted in a further reduction in Jun/Fos expression and a complete loss of peripheral NK cells in mice. Consistently, IKZF1 bound Jun/Fos genes at the same locations in activated B cells identifying a novel and conserved role for IKZF1 in Jun/Fos regulation. Collectively we show the Ikaros-family are novel regulators of apoptosis, cytokine responsiveness and AP-1 transcriptional activity required for NK cell development and function.

2023-11-08 | GSE247281 | GEO

Ikaros and Aiolos directly regulate AP-1 transcriptional complexes and are essential for natural killer cell development [ChIP-seq]

2023-11-08 | GSE247280 | GEO

Ikaros and Aiolos directly regulate AP-1 transcriptional complexes and are essential for natural killer cell development [RNA-seq]

2023-11-08 | GSE247282 | GEO

Ikaros and Aiolos directly regulate AP-1 transcriptional complexes and are essential for natural killer cell development [ATAC-seq]

2023-11-08 | GSE247279 | GEO

PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites

Project description:PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in Pbk–/– preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by Ikzf1, Ikzf3, Znf131 and Zbtb11. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction.

2025-07-21 | PXD057894 | Pride

PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites

2025-07-21 | PXD057898 | Pride

TMPRSS2-ERG and gain-of-function p53 mutants co-dictate pyrimidine synthesis and prostate cancer fitness [RNA-seq-2018 ERG-p53 project]

Project description:TMPRSS2-ERG fusion is the most common genetic alteration in prostate cancer (PCa) and TP53 is the most frequently mutated gene in human cancers. However, their precise roles in PCa pathogenesis remain elusive. Here we showed that TMPRSS2-ERG fusion co-occurred with TP53 deletion/mutation in PCa patient specimens. ERG overexpression and Trp53 knockout/R172H mutant knockin induced pyrimidine synthesis gene (PSG) expression and prostate tumorigenesis in mice. Gain-of-function p53 mutants bound to the CTNNB1 promoter and upregulated β-Catenin. Overexpressed ERG and β-Catenin co-occupied PSG loci and mediated PSG expression, and high PSG expression associated with increased β-Catenin level and poor overall survival of PCa patients. β-Catenin inhibition by proteolysis-targeting chimeras (PROTACs) of its co-activator CBP and partner proteins LEF1/TCFs blocked ERG/p53-mutant PCa growth. Our study identifies CTNNB1 as a transcriptional target of p53 GOF-mutants, and reveals a druggable dependency on β-Catenin and pyrimidine synthesis in p53-mutated cancers with or without TMPRSS2-ERG fusion.

2023-06-27 | GSE184624 | GEO

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