Evidence map›Paper›PMID 27203177›Full record

ArticleMolecular cell2016

Autophagic UVRAG Promotes UV-Induced Photolesion Repair by Activation of the CRL4(DDB2) E3 Ligase.

Yongfei Yang, Shanshan He, Qiaoxiu Wang, Fan Li, Mi-Jeong Kwak, Sally Chen, Douglas O'Connell, Tian Zhang, Sara Dolatshahi Pirooz, Yong Heui Jeon and 7 more

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

Article in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Autophagy Paradox: Strategizing Treatment Modality in Melanoma.Current treatment options in oncology · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. CRL4AOncogene · 2021
    Article
  14. Article
  15. Review
  16. Article
  17. How autophagy is tied to inflammation and cancer.Molecular & cellular oncology · 2020
    Article
  18. Article
  19. Article
  20. Review
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 4 institutions in 3 countries.

Yongfei YangDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Shanshan HeDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Qiaoxiu WangDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Fan LiDivision of Infectious Diseases, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA 90027, USA.
Mi-Jeong KwakDepartment of Biological Sciences, KAIST Institute for Biocentury, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Republic of Korea.
Sally ChenDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Douglas O'ConnellDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Tian ZhangDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Sara Dolatshahi PiroozDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Yong Heui JeonDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Nyam-Osor ChimgeDepartment of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Baruch FrenkelDepartment of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Younho ChoiDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Grace M AldrovandiDivision of Infectious Diseases, Department of Pediatrics, Children's Hospital Los Angeles, Los Angeles, CA 90027, USA.
Byung-Ha OhDepartment of Biological Sciences, KAIST Institute for Biocentury, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Republic of Korea.
Zengqiang YuanState Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Chengyu LiangDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. Electronic address: chengyu.liang@med.usc.edu.
University of Southern California · USChildren's Hospital of Los Angeles · USKorea Advanced Institute of Science and Technology · KRInstitute of Biophysics · CN

Funding

Role of UVRAG-mediated Autophagy in Tumor SuppressionR01CA140964 · NCI · WISTAR INSTITUTE · PI LIANG, CHENGYU · 2009 to 2025
$5.4M
Role of viral BCI-2 mediated anti-apoptosis and-autophagyR01AI073099 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JUNG, JAE U · 2007 to 2017
$4.3M
NCI NIH HHS R01 CA140964NIAID NIH HHS R01 AI073099
6 · The paper itself

Abstract

UV-induced DNA damage, a major risk factor for skin cancers, is primarily repaired by nucleotide excision repair (NER). UV radiation resistance-associated gene (UVRAG) is a tumor suppressor involved in autophagy. It was initially isolated as a cDNA partially complementing UV sensitivity in xeroderma pigmentosum (XP), but this was not explored further. Here we show that UVRAG plays an integral role in UV-induced DNA damage repair. It localizes to photolesions and associates with DDB1 to promote the assembly and activity of the DDB2-DDB1-Cul4A-Roc1 (CRL4(DDB2)) ubiquitin ligase complex, leading to efficient XPC recruitment and global genomic NER. UVRAG depletion decreased substrate handover to XPC and conferred UV-damage hypersensitivity. We confirmed the importance of UVRAG for UV-damage tolerance using a Drosophila model. Furthermore, increased UV-signature mutations in melanoma correlate with reduced expression of UVRAG. Our results identify UVRAG as a regulator of CRL4(DDB2)-mediated NER and suggest that its expression levels may influence melanoma predisposition.

Indexed as

DNA DamageUltraviolet RaysAnimalsAutophagyCarrier ProteinsCullin ProteinsDNA-Binding ProteinsDNA RepairDrosophila melanogasterDrosophila ProteinsEnzyme ActivationHEK293 CellsHeLa CellsHumansMelanoma, ExperimentalProteolysisCarrier ProteinsCUL4A protein, humanCul4a protein, mouseCullin ProteinsDDB1 protein, humanDdb1 protein, mouseDDB2 protein, humanDdb2 protein, mouseDNA-Binding ProteinsDrosophila ProteinsGAL4 protein, DrosophilaIL17RB protein, humanRBX1 protein, humanRBX1 protein, mouseReceptors, Interleukin-17Transcription FactorsTumor Suppressor ProteinsUbiquitin-Protein LigasesUVRAG protein, DrosophilaUVRAG protein, humanUVRAG protein, mouse

Identifiers

PMID27203177
PMCPMC4875571
OpenAlexW2394915104

What OpenQuestion holds

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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.