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Regulation of heterochromatin formation and tumor suppression in leukemia by IKAROS, HDAC1 and EZH2 [ChIP-seq]

GSE261181 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 28 samples Submitted 2024/10/01 Platform GPL34290Platform GPL17021Platform GPL9250Platform GPL21273
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 28 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Mus musculus (mouse)
Samples
28 samples
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
The IKZF1 gene encodes IKAROS – a DNA binding protein that acts as a tumor suppressor in T-cell acute lymphoblastic leukemia (T-ALL). IKAROS can act as a transcriptional repressor via chromatin remodeling, however the mechanisms through which Ikaros exerts its tumor suppressor function via heterochromatin in T-ALL are largely unknown.
Read the full summary ↓
We studied human and mouse T-ALL using loss-of-function and Ikzf1 re-expression approach, along with Ikzf1-wildtype primary human and mouse T-ALL and thymocytes to establish the role of Ikaros and Ikaros-associated protein histone deacetylase 1 (HDAC1) in global regulation of facultative heterochromatin and transcriptional repression in T-ALL. Results identified novel Ikaros and HDAC1 functions in T-ALL: Ikaros and HDAC1 are essential for EZH2 histone methyltransferase activity, and formation of facultative heterochromatin; Recruitment of HDAC1 by Ikaros is critical for establishment of H3K27me3 and repression of active enhancers; and Ikaros-HDAC1 complexes promote formation and expansion of H3K27me3 large organized chromatin lysine domains (LOCKs) and broad genic repression domains (BGRDs) in T-ALL. Our results establish that Ikaros’ tumor suppressor function in T-ALL occurs via activation of EZH2 and HDAC1 function, global regulation of the facultative heterochromatin landscape and silencing of active enhancers that regulate oncogene expression.
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE261181_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1085713 and SRA study SRP494146. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 28 more — browse all 28 samples with per-sample file links →

Datasets on a similar topic

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