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Binding of MYC to nascent RNA suppresses innate immune signaling by R-loop-derived RNA-DNA hybrids [ChIP_Rx]

GSE281611 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 44 samples Submitted 2026/02/09 Platform GPL30173Platform GPL30172
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 44 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
44 samples: 19 conditions, mostly in duplicateGroups 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
MYC binding to nascent RNA suppresses innate immune signaling by R-loop-derived RNA-DNA hybridsCell · 2026
Summary (written by the submitters)
In response to perturbed transcription elongation, the MYC oncoprotein multimerizes and undergoes a phase transition. The underlying mechanisms and their function are unknown. Here, we demonstrate that MYC globally relocalizes from its canonical positions on DNA to nascent RNA in response to the accumulation of intronic RNA. Binding of MYC to RNA induces MYC to form multimers that concentrate the nuclear exosome - a 3'-5' RNA exonuclease - and its targeting complexes around double-stranded RNA and R-loops.
Read the full summary ↓
MYC harbors four RNA-binding regions (RBRI–IV), which overlap with evolutionarily conserved regions. Of these, RBRIII promotes MYC multimerization and is necessary for recruiting the exosome to R-loops. While RBRIII is dispensable for MYC-dependent transcriptional activation and pancreatic tumor cell proliferation in culture, it is indispensable for sustaining tumor growth in vivo. Via RBRIII, MYC suppresses the accumulation of R-loop-derived RNA-DNA hybrids and prevents them from binding to the pattern recognition receptor TLR3 and activating the innate immune kinase TBK1. Our data demonstrate that MYC has mechanistically distinct functions in transcription and RNA metabolism, and that its phase transition is an RNA-driven stress response that suppresses the accumulation of immunogenic RNA-DNA hybrids.
Published in
MYC binding to nascent RNA suppresses innate immune signaling by R-loop-derived RNA-DNA hybrids
Uhl L, Aziba A, Löbbert S et al. · Cell 2026 · PMID 41576951 · doi:10.1016/j.cell.2025.12.019
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 GSE281611_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 PRJNA1184797 and SRA study SRP544524. Searching any of these in the dataset finder brings you back here.

Study design
19 conditions, mostly in duplicate
ChIP_Rx_U2OSMYCtetOn_Input_DMSO ×2 ChIP_Rx_U2OSMYCtetOn_Input_CBL0137 ×2 ChIP_Rx_U2OSMYCtetOn_Input_PlaB ×2 ChIP_Rx_U2OSMYCtetOn_MYC_IP_DMSO ×2 ChIP_Rx_U2OSMYCtetOn_MYC_IP_CBL0137 ×2 ChIP_Rx_U2OSMYCtetOn_MYC_IP_PlaB ×2 ChIP_Rx_U2OSMYCtetOn_RNAPII_CBL ×2 ChIP_Rx_U2OSMYCtetOn_RNAPII_DMSO ×2 +17 more

Supports a between-group comparison across 38 samples.

How we read this: 19 replicated groups read from 44 sample titles; they account for 38 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

+ 4 more — browse all 44 samples with per-sample file links →

Datasets on a similar topic

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