ArticleG3 (Bethesda, Md.)2026
Analysis of proteasome stress in different cell types defines a conserved transcriptional response signature and its modulation with aging.
Article in G3 (Bethesda, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
The proteasome is essential for proteostasis. Transcriptional induction of proteasomal components occurs when the proteasome is inhibited, but an overview of the transcriptional responses caused by proteasome perturbation is missing. Here, we profiled transcriptional changes caused by chemical and genetic proteasome inhibition and defined time-dose responses in cells and organoids. Induction of proteasome components varied by cell type and inhibition mode, whereas other responses were consistent, including upregulation of chaperones and secreted factors, and repression of cell cycle regulators. A proteasome stress response signature was defined based on the genes consistently modulated across systems, and applying this signature to aging datasets revealed activation of this stress response in some tissues, including skeletal muscle. Moreover, secreted factors within the signature showed similar age-related changes in human plasma, suggesting systemic activation of this stress response with aging. Together, these findings define a transcriptional signature for monitoring proteasome stress during aging and age-related diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.