GEO series

Regulation of transcription patterns, poly(ADP-ribose), and RNA-DNA hybrids by the ATM protein kinase

GSE233479 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 52 samples Submitted 2024/03/01 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 52 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: 52 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.
Paper: Regulation of transcription patterns, poly(ADP-ribose), and RNA-DNA hybrids by the ATM protein kinaseCell reports · 2024

Summary (written by the submitters)

The ATM protein kinase is a master regulator of the DNA damage response and also an important sensor of oxidative stress in mammals. Loss of ATM or its ability to be activated by reactive oxygen species (ROS) generates high levels of ROS and an excess of single-strand DNA breaks in non-dividing human cells. Here we map locations of poly-ADP-ribose and RNA-DNA hybrid accumulation genome-wide in post-mitotic human neurons with ATM inhibition and find that these locations are coincident with promoter regions, active transcription histone marks, and sequences with high GC content.

Read the full summary ↓

Antioxidant treatment reverses the accumulation of R-loops in transcribed regions, consistent with the central role of ROS in promoting these lesions. In A-T patient cerebellum tissue, RNAseq analyses show large-scale transcriptional changes that correlate with both expression level and GC content of transcribed genes. Based on these results we postulate that transcription-associated lesions accumulate in ATM-deficient neurons and that the single-strand breaks and PARylation at these sites ultimately generate changes in transcription that compromise cerebellum function and lead to neurodegeneration of this tissue over time in A-T patients.

Published in

Regulation of transcription patterns, poly(ADP-ribose), and RNA-DNA hybrids by the ATM protein kinase

Woolley PR, Wen X, Conway OM et al. · Cell reports 2024 · PMID 38442018 · doi:10.1016/j.celrep.2024.113896

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 GSE233479_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 PRJNA976332 and SRA study SRP439599. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38442018) ↗

Samples in this study

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+ 52 more — browse all 52 samples with per-sample file links →

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