ArticleNature chemical biology2026
Stabilization of AFF1 by PARylation ensures transcriptional restart after DNA damage.
Article in Nature chemical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Targeting cuproptosis opens a new chapter of nanomedicine: a scientometric and graphical analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- PANoptosis: potential new targets and therapeutic prospects in digestive diseases.Apoptosis : an international journal on programmed cell death · 2025Review
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Precise control of transcription is essential for cell survival under stress conditions, including DNA damage. While mechanisms of DNA damage-induced transcriptional silencing are well characterized, how transcription resumes remains less understood. Here we identify a new role for poly(ADP-ribose) polymerase 1 (PARP1) in transcriptional restart during the DNA damage response (DDR) through a mechanism termed poly(ADP-ribose)-mediated stabilization (PARSTA) of AFF1. Upon DNA damage, PARP1 binds to and PARylates AFF1 in a region targeted by the E3 ligase Siah1, preventing AFF1 ubiquitination and promoting its stability. This stabilization supports efficient transcriptional recovery after DNA damage. Notably, cells resistant to genotoxic stress exhibit elevated PARP1 activity and AFF1 levels, while AFF1 depletion impairs DNA repair and survival. Together, these findings expand PARP1's role to the transcriptional recovery phase in DDR and suggest that targeting the PARSTA pathway may offer therapeutic potential in diseases characterized by hyperactive PARP1 and elevated levels of AFF1.
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Registered trials
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