ArticleAging cell2025
STN1 Shields CTC1 From TRIM32-Mediated Ubiquitination to Prevent Cellular Aging.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- STN1 upregulation promotes PARPi resistance in BRCA2-deficient cancer cells via replication fork protection and suppression of ssDNA gap formation.NAR cancer · 2026Article
- STN1 upregulation promotes PARPi resistance in BRCA2-deficient cancer cells via replication fork protection and suppression of ssDNA gap formation.bioRxiv : the preprint server for biology · 2026Article
- Conditional deletion of human STN1 leads to telomere dysfunction, genome instability and proliferation defects.Journal of cell science · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
The CST (CTC1-STN1-TEN1) complex, a single-stranded DNA (ssDNA) binding complex, is essential for telomere maintenance and genome stability. Depletion of either CTC1 or STN1 results in cellular senescence, while mutations in these components are associated with severe hereditary disorders. In this study, we demonstrate that the direct STN1-CTC1 interaction stabilizes CTC1 by preventing its degradation via TRIM32 mediated ubiquitination. Functional assays indicate that TRIM32 and the CTC1/STN1 complex exert opposing effects on cellular proliferation. Additionally, transcriptomic analysis of large-scale RNA sequencing data from the Genotype-Tissue Expression (GTEx) reveals inverse expression patterns of TRIM32 and CTC1/STN1 during somatic cell aging. Structural modeling using AlphaFold3 predicts that the TRIM32-CTC1 interaction occurs at the OB-G domain of CTC1, with the binding interface positioned near the STN1-interacting region, termed the "cleft" motif. Mechanistically, STN1 likely associates with the OB-G domain of CTC1, competing with TRIM32 for binding sites and thereby interfering with TRIM32-mediated ubiquitination of CTC1. Collectively, our findings identify STN1 as a critical regulator of CST complex integrity and cellular aging by safeguarding CTC1 from TRIM32-driven ubiquitin-proteasome degradation.
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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 Socratic graph.