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Targeting Fused in Sarcoma (FUS): A Novel Antisense Strategy for Treating Idiopathic Pulmonary Fibrosis [RNA-Seq IPF]

GSE310473 Homo sapiens (human) RNA-seq (gene expression) 16 samples Submitted 2026/01/26 Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 16 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
16 samples: 4 × scr-ION-363 vs 4 × ION-363 vs 4 × scr-siFUS vs 4 × siFUSGroups 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
Targeting fused in sarcoma (FUS): a novel antisense strategy for treating idiopathic pulmonary fibrosisSignal transduction and targeted therapy · 2026
Summary (written by the submitters)
Fused in Sarcoma (FUS) is a highly conserved RNA-binding protein with essential roles in RNA processing and genomic stability. While extensively studied in the context of neurodegeneration, its involvement in fibrotic diseases—particularly idiopathic pulmonary fibrosis (IPF)—remains largely unexplored. This study investigates the pathological role of FUS in IPF and assesses its viability as a therapeutic target.
Read the full summary ↓
Specifically, we examine how FUS dysregulation contributes to fibrotic signaling and evaluate whether therapeutic silencing of FUS offers a rational strategy to modulate disease progression. Functional assays were performed on primary lung fibroblasts derived from healthy donors and IPF patients to assess the effects of FUS overexpression and knockdown. Precision-cut lung slices (PCLS) and 3D-alveolosphere cultures from IPF patients were treated with a FUS-targeted antisense oligonucleotide (ASO;ION363). FUS-RNA interactions were mapped using CLIP-Seq, and global transcriptional changes following FUS inhibition were analyzed via RNA sequencing. FUS overexpression in healthy fibroblasts promoted proliferation, while its knockdown attenuated the hyperproliferative phenotype in IPF fibroblasts. IPF cells demonstrated aberrant cytoplasmic mislocalization of FUS. Standard-of-care treatments (pirfenidone, nintedanib) reduced FUS expression in PCLS. CLIP-Seq revealed FUS binding to a distinct set of pro-fibrotic RNAs in IPF. ION363 treatment downregulated fibrotic gene programs, including those linked to ECM remodeling, TGF-β signaling, and epithelial dysfunction. On the contrary, ION363 promoted functional markers and improved morphology in patient derived 3D-alveolospheres. We conclude that FUS is a pivotal regulator of fibrotic signaling in IPF and targeting FUS via ASO represents a promising therapeutic avenue for IPF.
Published in
Targeting fused in sarcoma (FUS): a novel antisense strategy for treating idiopathic pulmonary fibrosis
Katariya BB, Chillappagari S, Arnold L et al. · Signal transduction and targeted therapy 2026 · PMID 41741410 · doi:10.1038/s41392-026-02585-9
This dataset
Open GSE310473 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 GSE310473_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 PRJNA1366400 and SRA study SRP646858. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41741410) ↗
Study design
4 × scr-ION-363 vs 4 × ION-363 vs 4 × scr-siFUS vs 4 × siFUS

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 16 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
Datasets on a similar topic

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