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Ribosome biogenesis mediates the translational increase of codon non-optimal transcripts during IFN stimulation

GSE281848 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2026/05/01 Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 24 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
24 samples: 8 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.
Summary (written by the submitters)
The interferon response is a signaling pathway unique to vertebrates that links the innate and adaptive immune responses. Interferons signal through a cascade of factors including the JAK-STAT pathway to induce the transcription of hundreds of interferon stimulated genes (ISGs). Although the main interferon signal transduction pathways and ISGs have been elucidated, translational regulation of ISG transcripts has not been fully investigated.
Read the full summary ↓
Prior work demonstrated that ribosomal protein RPL28 negatively regulates a subset of ISGs; however, we find that this effect may be due to a reduction in overall ribosome availability. Multi-omics analysis of RNA-seq and LC-MS/MS data reveal proteins that are translationally up-regulated during BOP1 knockdown and IFN-β stimulation, including an enrichment of ISGs. Analysis of codon optimality demonstrates a significant reduction in codon optimality for proteins that are translationally up-regulated during BOP1 knockdown and IFN-β stimulation. Extremely codon-optimized and -non-optimized reporter constructs were tested under these conditions and demonstrate that BOP1 knockdown increases translation of the non-optimal reporter during IFN stimulation. We propose that this is a form of translational fine-tuning of the IFN in order to ensure the production of integral proteins during times of cellular stress when translation machinery may be inhibited.
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 GSE281848_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 PRJNA1185811 and SRA study SRP545111. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in triplicate
A549 cells, BOP1 siRNA, mock, 8h, ×3 A549 cells, BOP1 siRNA, mock, 12h, ×3 A549 cells, BOP1 siRNA, IFN, 8h, ×3 A549 cells, BOP1 siRNA, IFN, 12h, ×3 A549 cells, control FLuc siRNA, mock, 8h, ×3 A549 cells, control FLuc siRNA, mock, 12h, ×3 A549 cells, control FLuc siRNA, IFN, 8h, ×3 A549 cells, control FLuc siRNA, IFN, 12h, ×3

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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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