ArticleBiochemical and biophysical research communications2025
Loss of DNA replication fork protection by TIMELESS degradation supports oncogene-induced senescence.
Article in Biochemical and biophysical research communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Tilting the balance of life and death: navigating DNA replication stress in cancer therapy.Experimental & molecular medicine · 2026Review
- Disrupted renal clock and blood pressure rhythms in type 2 diabetic nephropathy.Clinical science (London, England : 1979) · 2026Article
- ZMYM3 S464: a potential phospho-regulatory hub in epigenetic remodeling and oncogenesis.Molecular genetics and genomics : MGG · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Oncogene-induced senescence (OIS) is a potent barrier that limits tumorigenesis. While persistent DNA replication stress accompanied by cellular hyperproliferation is considered an underlying basis of OIS, the molecular mechanisms through which oncogenes elicit genome instability remain unclear. Here, we identify a distinct cellular process in which DNA replication fork stalling is linked to senescence in response to oncogenic signaling. We demonstrate that TIMELESS (TIM), an essential regulatory component of the fork protection complex that supports the integrity of the replisome, is downregulated in non-transformed human cell lines that undergo OIS by HRAS
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