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Transcriptomic investigation of differential cellular reprogramming of infected cells by human adenovirus 5 E1A mutants

GSE288390 Homo sapiens (human) RNA-seq (gene expression) 10 samples Submitted 2025/04/24 Platform GPL16791
At a glance

RNA-seq (gene expression) · human · 10 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)
Samples
10 samples: 5 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
Cellular transcriptomics of arrested normal lung fibroblasts IMR-90 infected with Human Adenovirus 5 E1A mutantsPloS one · 2025
Summary (written by the submitters)
Induction of S-phase is paramount to the replication of most human DNA viruses. Human adenoviruses have evolved sophisticated mechanisms that drive the infected cells into S-phase to ensure that viral genomes are efficiently replicated. We have identified an E1A mutant, E1A289Rdl2-11/YC, that disrupts the canonical means of S-phase induction by E1A.
Read the full summary ↓
Specifically, this mutant abrogates binding of E1A to the E2F/DP complex as well as to the retinoblastoma protein. Yet, we show that this mutant can still effectively drive the infected cell into S-phase. We explore potential mechanisms of how this occurs via cellular transcriptomic analysis 16 hours after infection. We show that this mutant induces many cell-cycle specific genes to drive S-phase. Interestingly, MYC mRNA is significantly upregulated by this mutant as compared to other viruses investigated. This MYC upregulation, together with normal expression of E4orf6/7 in this mutant, may contribute to efficient S-phase induction. We also demonstrate that this mutant is unable to effectively suppress innate immune response to infection, likely due to loss of p300/CBP binding caused by deletion of E1A residues 2 to 11.
Published in
Cellular transcriptomics of arrested normal lung fibroblasts IMR-90 infected with Human Adenovirus 5 E1A mutants
Helwer R, Pelka P · PloS one 2025 · PMID 40424376 · doi:10.1371/journal.pone.0323494
This dataset
Open GSE288390 in finder → Find more human RNA-seq datasets →
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 GSE288390_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: 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 PRJNA1217341 and SRA study SRP560706. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40424376) ↗
Study design
5 conditions, mostly in duplicate
Mock.biol ×2 E1A.WT.dl309.biol ×2 E1A.289R.pm975.biol ×2 E1A.243R.dl520.biol ×2 E1A.289R.YCD.biol ×2

Supports a between-group comparison across 10 samples.

How we read this: 5 replicated groups read from 10 sample titles; they account for 10 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
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