Evidence map›Paper›PMID 42575441›Full record

ArticleThe Journal of biological chemistry2026

ATR-dependent phosphorylation of the histone acetyltransferase HBO1 suppresses chromatin binding and promotes replication stress responses.

Chunyan Zong, Jiamin Zhang, Zhe Zhang, Yujuan Cai, Yiran Wang, Yan Fang, Guopei Zheng, Qian Li, Lulu Wang, Jianfeng Shen

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Chunyan ZongDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China; Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: zong_chunyan@163.com.
Jiamin ZhangDepartment of Chemical Biology, School of Pharmacy, Tianjin Medical University, Tianjin, China.
Zhe ZhangDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yujuan CaiDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yiran WangDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yan FangDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China.
Guopei ZhengDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China.
Qian LiDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China.
Lulu WangDepartment of Chemical Biology, School of Pharmacy, Tianjin Medical University, Tianjin, China. Electronic address: wanglulu@tmu.edu.cn.
Jianfeng ShenDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, China; Institute of Translational Medicine, National Facility for Translational Medicine, Shanghai Jiao Tong University, Shanghai, China. Electronic address: jfshen@shsmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence has shown that histone acetyltransferase binding to ORC1 (HBO1) serves as an oncoprotein, warranting the use of the small molecule inhibitor WM-3835 for cancer therapy. However, HBO1 is ubiquitously expressed in both tumor and normal tissues, with potential to increase the risk of systemic toxicity. This unmet need highlights the importance of identifying suitable biomarkers to predict the sensitivity to HBO1 inhibitor. Here, we show that ATR, a key regulator of DNA replication stress, is a novel interacting partner of HBO1. In addition, we reveal a regulatory function of HBO1 in DNA replication stress responses, in an ATR-dependent manner. Mechanistically, ATR mediated HBO1 Ser50/53 phosphorylation interferes with the genomic binding of HBO1 and regulates gene expression. Notably, overexpression of HBO1 mutated at the ATR phosphorylation site (S50/53A) dampens the expression of DNA repair related genes and suppresses tumor colony formation, consistent with the observations of WM-3835 treatment. Inhibition of ATR significantly antagonized the sensitivity to WM-3835 treatment. Collectively, our findings uncovered a previously unidentified role of HBO1 in the regulation of replication stress and discovered ATR as a potential biomarker for WM-3835 treatment.

Indexed as

ATRHBO1histone acetyltransferasephosphorylationreplication stress

Identifiers

PMID42575441
PMCPMC13570308

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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.