← BioTransfer GEO Dataset Finder
GEO series

Proteolethargy is a pathogenic mechanism in chronic disease

GSE273733 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/01/15 Platform GPL24676
Summary
The pathogenic mechanisms of many diseases are well understood at the molecular level, but there are prevalent syndromes associated with pathogenic signaling, such as diabetes and chronic inflammation, where our understanding is more limited. Here we report that pathogenic signaling suppresses the mobility of a spectrum of proteins that play essential roles in cellular functions known to be dysregulated in these chronic diseases. The reduced protein mobility, which we call proteolethargy, was linked to cysteine residues in the affected proteins and signaling-related increases in excess reactive oxygen species. Diverse pathogenic stimuli, including hyperglycemia, dyslipidemia and inflammation, produce similar reduced protein mobility phenotypes. We propose that proteolethargy is an overlooked cellular mechanism that may account for various pathogenic features of diverse chronic diseases.
Published in
Proteolethargy is a pathogenic mechanism in chronic disease
Dall'Agnese A, Zheng MM, Moreno S et al. · Cell 2025 · PMID 39610243 · doi:10.1016/j.cell.2024.10.051
This dataset
Download

Direct links to NCBI, no account and no request form: the whole study as GSE273733_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1142944 and SRA study SRP523663. Searching any of these in the dataset finder brings you back here.

Samples in this study

The sample list for this study is not cached yet. Press Sort into groups and it will be fetched from NCBI.

+ 6 more — browse all 6 samples with per-sample file links →

Similar datasets

Search all human RNA-seq datasets in GEO →

Share this dataset

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.