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IRF2BP2 promotes neuroblastoma progression

ABSTRACT: IRF2BP2 promotes neuroblastoma progression

PROVIDER: PRJNA990742 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25115635_1.fastq.gz	Fastqsanger.gz
	SRR25115635_2.fastq.gz	Fastqsanger.gz
	SRR25115636_1.fastq.gz	Fastqsanger.gz
	SRR25115636_2.fastq.gz	Fastqsanger.gz
	SRR25115637_1.fastq.gz	Fastqsanger.gz

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IRF2BP2 promotes neuroblastoma progression

Project description:We report a previously unrecognized role of IRF2BP2 in neuroblastoma. To explore IRF2BP2-dependent gene regulation, RNA-seq analysis was conducted and the differently expressed genes were revealed in the IRF2BP2-knockdown SK-N-BE(2) cells in comparison to control group. We find that IRF2BP2 contributes to maintenance ADRN signature of neuroblastoma cell.

2024-06-24 | GSE236390 | GEO

Occupancy profiling of IRF2BP2, MYCN, AP-1 and SOX11 by CUT&Tag from Neuroblastoma cells

Project description:MYCN and SOX11 are master transcription factors (TFs) in neuroblastoma by directly occupying each other's and their own super-enhancers (SEs). Additionally, Master TFs cooperatively co-occupy the same SE components, which promotes the expression of IRF2BP2 involved in cell survival. We also observed the significant enrichment of the AP-1 family at the binding sites of IRF2BP2. In the present study, CUT&Tag (Cleavage Under Targets and Tagmentation) analysis was performed to explore the target of IRF2BP2, MYCN, AP-1 and SOX11 in NB cells.

2024-06-24 | GSE246065 | GEO

IRF2BP2 Modulates Chromatin Accessibility in Neuroblastoma

Project description:IRF2BP2 Modulates Chromatin Accessibility in Neuroblastoma

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Super-enhancer-associated TTC8 promotes neuroblastoma progression

Project description:Super-enhancer-associated TTC8 promotes neuroblastoma progression

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IRF2BP2 Modulates Chromatin Accessibility in Neuroblastoma

Project description:Chromatin accessibility of SK-N-BE(2) cells without or with IRF2BP2 depletion were profiled using transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) to identify potential regulatory elements.

2024-06-24 | GSE246063 | GEO

SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7

Project description:SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7

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Transcriptional regulation of adipocyte lipolysis by IRF2BP2 [CUT&RUN]

Project description:Adipocyte lipolysis controls systemic energy levels and metabolic homeostasis. Lipolysis is regulated by post-translational modifications of key lipolytic enzymes. However, less is known about the transcriptional mechanisms that regulate lipolysis. Here, we identify the transcriptional factor interferon regulatory factor-2 binding protein 2 (IRF2BP2) as a repressor of adipocyte lipolysis. Deletion of IRF2BP2 in primary human adipocytes increases lipolysis without affecting glucose uptake, whereas IRF2BP2 overexpression decreases lipolysis. RNA-seq and ChIP-seq analyses reveal that IRF2BP2 directly represses several lipolysis-related genes, including LIPE (HSL, hormone sensitive lipase), which encodes the rate-limiting enzyme in lipolysis. Adipocyte-selective deletion of Irf2bp2 in mice increases Lipe expression and free fatty acid levels, resulting in elevated adipose tissue inflammation and glucose intolerance. Altogether, these findings demonstrate that IRF2BP2 restrains adipocyte lipolysis and opens new avenues to target lipolysis for the treatment of metabolic disease.

2024-11-14 | GSE281494 | GEO

Transcriptional regulation of adipocyte lipolysis by IRF2BP2 [ChIP-seq]

2024-11-14 | GSE281495 | GEO

IRF2BP2 counteracts the ATF7/JDP2 heterodimer to prevent inflammatory overactivation in AML cells

Project description:Acute myeloid leukemia (AML) is a hematological malignancy characterized by the abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator that has been implicated in AML pathogenesis, although its precise role in this disease is not fully understood. In this study, we demonstrate that in AML cells IRF2BP2 interacts with the transcriptional heterodimer ATF7/JDP2, which is involved to activate inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene activating function. Loss of IRF2BP2 leads to the overactivation of inflammatory pathways, resulting in immediate cell death. Our findings suggest that a delicate balance of activating and repressive transcriptional mechanisms establishes a pro-oncogenic inflammatory set-up in AML cells, and that manipulation of the ATF7/JDP2-IRF2BP2 regulatory axis may offer a potential vulnerability for AML treatment. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.

2024-05-16 | PXD041817 | Pride

IRF2BP2 counteracts the ATF7/JDP2 heterodimer to prevent inflammatory overactivation in AML cells [ChIP-seq]

Project description:Acute myeloid leukemia (AML) is a hematological malignancy characterized by abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of cell-intrinsic inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator implicated in AML pathogenesis, although its precise role in this disease is not fully understood. In this study, we demonstrate that IRF2BP2 interacts with the AP-1 heterodimer ATF7/JDP2, which is involved in activating inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene-activating function. Loss of IRF2BP2 leads to overactivation of inflammatory pathways, resulting in strongly reduced proliferation. Our research indicates that a precise equilibrium between activating and repressive transcriptional mechanisms creates a pro-oncogenic inflammatory environment in AML cells. The ATF7/JDP2-IRF2BP2 regulatory axis is likely a key regulator of this process and may, therefore, represent a promising therapeutic vulnerability for AML. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.

2024-05-07 | GSE229594 | GEO

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