Evidence map›Paper›PMID 36094642›Full record

ArticleInvestigative ophthalmology & visual science2022

UBE3D Is Involved in Blue Light-Induced Retinal Damage by Regulating Double-Strand Break Repair.

Ningda Xu, Yue Liu, Shanshan Nai, Yong Tao, Yuehe Ding, Lemei Jia, Qizhi Geng, Jie Li, Yujing Bai, Gong-Hong Wei and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Investigative ophthalmology & visual science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 7 citations in OpenAlex.

  1. BlingLifeJournal of microbiology and biotechnology · 2025
    Article
4 · The record

Corrections and comments

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

17 authors at 7 institutions in 2 countries.

Ningda XuDepartment of Ophthalmology, Eye Diseases and Optometry Institute, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, College of Optometry, Peking University Health Science Center, Peking University People's Hospital Beijing, China.
Yue LiuBeijing Key Laboratory of DNA Damage Response and College of Life Science, Capital Normal University, Beijing, China.
Shanshan NaiBeijing Key Laboratory of DNA Damage Response and College of Life Science, Capital Normal University, Beijing, China.
Yong TaoDepartment of Ophthalmology, Beijing Chaoyang Hospital, Capital Medical University, Chaoyang District, Beijing, China.
Yuehe DingNational Institute of Biological Sciences, Beijing, China.
Lemei JiaNational Institute of Biological Sciences, Beijing, China.
Qizhi GengBeijing Key Laboratory of DNA Damage Response and College of Life Science, Capital Normal University, Beijing, China.
Jie LiBeijing Key Laboratory of DNA Damage Response and College of Life Science, Capital Normal University, Beijing, China.
Yujing BaiDepartment of Ophthalmology, Eye Diseases and Optometry Institute, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, College of Optometry, Peking University Health Science Center, Peking University People's Hospital Beijing, China.
Gong-Hong WeiBiocenter Oulu, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
Meng-Qiu DongNational Institute of Biological Sciences, Beijing, China.
Linyi LuoDepartment of Ophthalmology and Visual Sciences, Affiliated Dongguan Hospital, Southern Medical University, Guangdong, China.
Mingwei ZhaoDepartment of Ophthalmology, Eye Diseases and Optometry Institute, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, College of Optometry, Peking University Health Science Center, Peking University People's Hospital Beijing, China.
Xingzhi XuBeijing Key Laboratory of DNA Damage Response and College of Life Science, Capital Normal University, Beijing, China.
Xiao-Xin LiDepartment of Ophthalmology, Eye Diseases and Optometry Institute, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, College of Optometry, Peking University Health Science Center, Peking University People's Hospital Beijing, China.
Jing LiBeijing Key Laboratory of DNA Damage Response and College of Life Science, Capital Normal University, Beijing, China.
Lvzhen HuangDepartment of Ophthalmology, Eye Diseases and Optometry Institute, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, College of Optometry, Peking University Health Science Center, Peking University People's Hospital Beijing, China.
Capital Normal University · CNNational Institute of Biological Sciences, Beijing · CNPeking University · CNPeking University People's Hospital · CNBeijing Chaoyang Emergency Medical Center · CNShanghai Medical College of Fudan University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Age-related macular degeneration (AMD) is currently the leading cause of blindness worldwide. Previously, we identified ubiquitin-protein ligase E3D (UBE3D) as an AMD-associated protein for East Asian populations, and here we further demonstrate that UBE3D could be associated with DNA damage response. Methods: The established I-SceI-inducible GFP reporter system was used to explore the effect of UBE3D on homologous recombination. Immunoprecipitation-mass spectrometry (MS) was used to explore potential UBE3D-interacting proteins and validated with coimmunoprecipitation assays and the pulldown assays. Micrococcal nuclease (MNase) assays were used to investigate the function of UBE3D on heterochromatin de-condensation upon DNA damage. An aged mouse model of blue light-induced eye damage was constructed, and electroretinography (ERG) and optical coherence tomography (OCT) were performed to compare the differences between wild-type and UBE3D+/- mice. Results: First, we show that GFP-UBE3D is recruited to damage sites by PCNA, through a PCNA-interacting protein (PIP) box. Furthermore, UBE3D interacts with KAP1 via R377R378 and oxidation of the AMD-associated V379M mutation abolishes KAP1-UBE3D binding. By MNase assays, UBE3D depletion reduces the chromatin relaxation levels upon DNA damage. In addition, UBE3D depletion renders less KAP1 recruitment. Compared with wild type, blue light induces less damage in UBE3D+/- mice as measured by ERG and OCT, consistent with our biochemical results. Conclusions: Hence, we propose that one potential mechanism that UBE3D-V379M contributes to AMD pathogenesis might be via defective DNA damage repair linked with oxidative stress and our results offered a potential direction for the treatment of AMD.

Indexed as

Macular DegenerationAnimalsDNA DamageElectroretinographyLightMiceProliferating Cell Nuclear AntigenUbiquitin-Protein LigasesProliferating Cell Nuclear AntigenUbe2cbp protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID36094642
PMCPMC9482326
OpenAlexW4295501199

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.