Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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
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.
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
12 authors.
Zheng Li *Guangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.ORCID http://orcid.org/0000-0002-5071-8470
Xingxuan Wu *Guangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.
Liu LiuCollege of Life Sciences, Capital Normal University, Beijing, China.
Shaohong RaoGuangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.
Yanting LiaoGuangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.
Mengting LiuGuangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.
Bin PengGuangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.
Qiongdan ZhangSchool of Biological Sciences, The University of Hong Kong, Hong Kong, China.
Yisui XiaSouth China Hospital, Guangdong Key Laboratory for Genome Stability & Disease Prevention, Shenzhen University Medical School, Shenzhen, China.ORCID http://orcid.org/0000-0002-5576-2147
Shunichi TakedaGuangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China. stakeda@szu.edu.cn.ORCID http://orcid.org/0000-0002-7924-7991
Xingzhi XuGuangdong Key Laboratory for Genome Stability & Disease Prevention and Carson International Cancer Center, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China. Xingzhi.Xu@szu.edu.cn.ORCID http://orcid.org/0000-0002-4459-2082
Funding
MOST | National Key Research and Development Program of China (NKPs) 2022YFA1302804MOST | National Natural Science Foundation of China (NSFC) 32090031MOST | National Natural Science Foundation of China (NSFC) 32250710138MOST | National Natural Science Foundation of China (NSFC) 82072947MOST | National Natural Science Foundation of China (NSFC) U24A20740Pearl River Talent Recruitment Program 2021JC02Y089Shenzhen Medical Research Fund D2403014Shenzhen Municipal Science and Technology Innovation Council | Shenzhen Science and Technology Innovation Program () JCYJ20220818095605011Shenzhen Municipal Science and Technology Innovation Council | Shenzhen Science and Technology Innovation Program () JCYJ20220818095616035
6 · The paper itself
Abstract
Modification with UFM1 (UFMylation) is essential for cell proliferation, but its precise mechanism of action is unclear. Furthermore, the UFMylation pathway has been associated with microcephalic primordial dwarfism (MPD) disorders, and mutations causative for MPD are also identified in genes encoding components of the replicative DNA helicase complex, including the MCM hexamer. Here, we reveal that UFMylation regulates DNA replication, and that all MPD-associated mutations in UFMylation enzymes impair replication. Mechanistically, the UFM1 E3 ligase UFL1 catalyzes Lys583 UFMylation of MCM5, a critical component of the CMG replicative DNA helicase complex. Mutation of Lys583 blocking this UFMylation event destabilizes the helicase complex, delaying origin firing and slowing replication fork progression. We conclude that MCM5 UFMylation is essential for efficient origin firing and replication fork progression, both of which ensure accurate DNA replication, cell proliferation, and prevention of MPD disorders.
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.
MCM5 UFMylation regulates replication origin firing and fork progression. · full record | OpenQuestion