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ARID1A regulates DSB repair through chromatin organization and its deficiency triggers DNA damage-mediated immune response [ACT-seq]

GSE249442 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 48 samples Submitted 2024/06/12 Platform GPL21697
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 48 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
Homo sapiens (human)
Samples
48 samples: 18 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
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.
Paper
ARID1A regulates DNA repair through chromatin organization and its deficiency triggers DNA damage-mediated anti-tumor immune responseNucleic acids research · 2024
Summary (written by the submitters)
AT-rich interaction domain protein 1A (ARID1A), a SWI/SNF chromatin remodeling complex subunit, is frequently mutated across various cancer entities. Loss of ARID1A leads to DNA repair defects. Here we show that ARID1A plays epigenetic roles to promote both DNA double-strand breaks (DSBs) repair pathways, non-homologous end-joining (NHEJ) and homologous recombination (HR).
Read the full summary ↓
ARID1A is accumulated at DSBs after DNA damage and regulates chromatin loops formation by recruiting RAD21 and CTCF to DSBs. Simultaneously, ARID1A binds to and promotes the recruitment of HDAC1 and RSF1 to DSBs to control the distribution of activating histone marks and chromatin accessibility leading to eviction of RNAPII and silencing of transcription in transcriptionally active chromatin. ARID1A depletion resulted in enhanced accumulation of micronuclei, activation of cGAS-STING pathway, and an increased expression of immunomodulatory cytokines upon ionizing radiation. Furthermore, low ARID1A expression in cancer patients receiving radiotherapy was associated with higher infiltration of several immune cells. The high mutation rate of ARID1A in various cancer types highlights its clinical relevance as a promising biomarker that correlates with the level of immune regulatory cytokines and estimates the levels of tumor-infiltrating immune cells, which can predict the response to the combination of radio- and immunotherapy.
Published in
ARID1A regulates DNA repair through chromatin organization and its deficiency triggers DNA damage-mediated anti-tumor immune response
Bakr A, Della Corte G, Veselinov O et al. · Nucleic acids research 2024 · PMID 38587186 · doi:10.1093/nar/gkae233
This dataset
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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.

Series matrix ↓
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 GSE249442_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

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 PRJNA1049042 and SRA study SRP476013. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38587186) ↗
Study design
18 conditions, mostly in triplicate
KO_T0_H2AK118ac ×3 KO_T0_IgG ×3 KO_T4_H2AK118ac ×3 KO_T4_IgG ×3 KO_UT_H2AK118ac ×3 KO_UT_IgG ×3 WT_T0_H2AK118ac ×3 WT_T0_IgG ×3 +10 more

Supports a between-group comparison across 48 samples.

How we read this: 18 replicated groups read from 48 sample titles; they account for 48 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

+ 8 more — browse all 48 samples with per-sample file links →

Datasets on a similar topic

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