ArticleClinical and translational medicine2025
H1N76/77 deamidation facilitates chromatin remodelling and genome stability during DNA damage repair.
Article in Clinical and translational medicine, 2025. 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
Chromatin relaxation is a permissiven progress for DNA repair through enabling repair factors to access the damaged DNA. Linker histone H1 is important in maintaining chromatin compaction under physiological state. The recent evidence highlights the importance of H1 modifications in response to cellular stress. Following DNA double-strand breaks, the metabolic enzyme phosphorylated CTP synthase 1 (CTPS1) functions as a deamidase, catalyzing the rapid conversion of H1 residues Asn76 and Asn77 into aspartate. This modification enables subsequent acetylation at Lys75 by the histone acetyltransferase p300, thereby reducing H1-DNA affinity and promoting chromatin decompaction. This sequential modification-H1 deamidation followed by acetylation-facilitates the recruitment of repair factors involving both homologous recombination and non-homologous end joining repair pathways, and consequently promoting DNA repair. Importantly, high expression of CTPS1 is associated with resistance to radiotherapy in mouse models and clinical cancer patients, suggesting that the CTPS1 may serve as a potential therapeutic target. While targeting CTPS1 may offer opportunities to enhance radiosensitivity of cancer patients, challenges related to specificity and off-target effects require further studies. This article highlights an emerging role of H1 modification in the DNA damage repair and discusses the therapeutic potential of manipulating H1 deamidation in cancer treatment.
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.