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Cytoplasmic ATM restricts oncolytic VSVΔ51 replication by sustaining TBK1-IRF3 signaling in glioblastoma cells

GSE342072 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/08/05 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 12 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Topic
GlioblastomaThis series is part of our curated briefing on it.
Samples
12 samples: 3 × LN-18 wild-type mock vs 3 × LN-18 sgATM mock vs 3 × LN-18 wild-type VSVΔ51 vs 3 × LN-18 sgATM VSVΔ51Groups 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.
Summary (written by the submitters)
ATM is a nuclear DNA damage response kinase with tumor-suppressive functions, but its cytoplasmic function during virus infection remains poorly understood. Here, we identify cytoplasmic ATM as an antiviral factor that restricts oncolytic virus (OVs) replication. Infection with oncolytic VSVΔ51 triggered CRM1-dependent nuclear export of ATM, generating cytoplasmic ATM that associated with viral dsRNA-containing complexes.
Read the full summary ↓
Blocking ATM nuclear export or inhibiting ATM attenuated type I interferon induction, thereby licensing viral replication. Mechanistically, cytoplasmic ATM interacted with the ubiquitin-like domain of TBK1 and sustained TBK1-IRF3 signaling. ATM inhibition potentiated oncolytic cytotoxicity and promoted immunogenic cell death in cancer cells. In multiple tumor models, pharmacological inhibition or genetic loss of ATM cooperated with VSVΔ51 to suppress tumor growth, prolong survival of mice, and promote durable antitumor immunity. These findings reveal the cytoplasmic function of ATM in antiviral innate immunity and identify it as a therapeutic vulnerability for improving oncolytic virotherapy.
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 GSE342072_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1505557 and SRA study SRP723061. Searching any of these in the dataset finder brings you back here.

Study design
3 × LN-18 wild-type mock vs 3 × LN-18 sgATM mock vs 3 × LN-18 wild-type VSVΔ51 vs 3 × LN-18 sgATM VSVΔ51

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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
More Glioblastoma datasets

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.