Evidence map›Paper›PMID 28380355›Full record

ArticleCell reports2017

DGCR8 Mediates Repair of UV-Induced DNA Damage Independently of RNA Processing.

Philamer C Calses, Kiranjit K Dhillon, Nyka Tucker, Yong Chi, Jen-Wei Huang, Masaoki Kawasumi, Paul Nghiem, Yemin Wang, Bruce E Clurman, Celine Jacquemont and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Regulation of the microprocessor by post-translational modifications.Frontiers in cell and developmental biology · 2025
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  9. HER2-driven breast cancer suppression by the JNK signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Embryonic microRNAs are essential for bovine preimplantation embryo development.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Review
  12. DISE/6mer seed toxicity-a powerful anti-cancer mechanism with implications for other diseases.Journal of experimental & clinical cancer research : CR · 2021
    Review
  13. Article
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  18. ETMR: a tumor entity in its infancy.Acta neuropathologica · 2020
    Review
  19. Review
  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

14 authors at 6 institutions in 2 countries.

Philamer C CalsesDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Molecular and Cellular Biology Graduate Program, University of Washington, 1959 NE Pacific, HSB T-466, Seattle, WA 98195-7275, USA.
Kiranjit K DhillonDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA.
Nyka TuckerDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA.
Yong ChiDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Clinical Research, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA.
Jen-Wei HuangDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Molecular and Cellular Biology Graduate Program, University of Washington, 1959 NE Pacific, HSB T-466, Seattle, WA 98195-7275, USA.
Masaoki KawasumiDivision of Dermatology, Department of Medicine, University of Washington, 850 Republican St., Seattle, WA 98109-4714, USA.
Paul NghiemDivision of Dermatology, Department of Medicine, University of Washington, 850 Republican St., Seattle, WA 98109-4714, USA.
Yemin WangDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA.
Bruce E ClurmanDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Clinical Research, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA.
Celine JacquemontDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA.
Philip R GafkenProteomics Core Facility, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., DE-352, Seattle, WA 98109-1024, USA.
Kaoru SugasawaBiosignal Research Center, Organization of Advanced Science and Technology, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo 657-8501, Japan.
Masafumi SaijoGraduate School of Frontier Biosciences, Osaka University, Yamadaoka 1-3, Suita, Osaka 565-0871, Japan.
Toshiyasu TaniguchiDivision of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., C1-015, Seattle, WA 98109-1024, USA; Department of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan. Electronic address: ttaniguc@fhcrc.org.
Fred Hutch Cancer Center · USUniversity of Washington · USKobe University · JPOsaka University · JPSeattle Pacific University · USTokai University · JP

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Thomas James Lynch · 1985 to 2026
$296.4M
TRAINING IN MOLECULAR AND CELLULAR BIOLOGYT32GM007270 · NIGMS · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2020
$21.0M
The replication checkpoint and genomic fidelity in skinR01AR049832 · NIAMS · UNIVERSITY OF WASHINGTON · PI NGHIEM, PAUL · 2003 to 2014
$3.6M
Mechanisms of UV-Induced DNA Damage Responses and Carcinogenesis in SkinR01AR067722 · NIAMS · UNIVERSITY OF WASHINGTON · PI NGHIEM, PAUL · 2015 to 2020
$2.0M
The Fanconi Anemia-BRCA Pathway And Chemosensitivity of Human CancerR01CA125636 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TANIGUCHI, TOSHIYASU · 2007 to 2011
$1.6M
MicroRNAs Regulating The Fanconi Anemia-BRCA PathwayR21HL092978 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TANIGUCHI, TOSHIYASU · 2008 to 2009
$468k
The DGCR8-mediated UV response pathwayR21ES026326 · NIEHS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TANIGUCHI, TOSHIYASU · 2016 to 2016
$264k
Howard Hughes Medical InstituteNCI NIH HHS P30 CA015704NCI NIH HHS R01 CA125636NHLBI NIH HHS R21 HL092978NIAMS NIH HHS R01 AR049832NIAMS NIH HHS R01 AR067722NIEHS NIH HHS R21 ES026326NIGMS NIH HHS T32 GM007270
6 · The paper itself

Abstract

Ultraviolet (UV) radiation is a carcinogen that generates DNA lesions. Here, we demonstrate an unexpected role for DGCR8, an RNA binding protein that canonically functions with Drosha to mediate microRNA processing, in the repair of UV-induced DNA lesions. Treatment with UV induced phosphorylation on serine 153 (S153) of DGCR8 in both human and murine cells. S153 phosphorylation was critical for cellular resistance to UV, the removal of UV-induced DNA lesions, and the recovery of RNA synthesis after UV exposure but not for microRNA expression. The RNA-binding and Drosha-binding activities of DGCR8 were not critical for UV resistance. DGCR8 depletion was epistatic to defects in XPA, CSA, and CSB for UV sensitivity. DGCR8 physically interacted with CSB and RNA polymerase II. JNKs were involved in the UV-induced S153 phosphorylation. These findings suggest that UV-induced S153 phosphorylation mediates transcription-coupled nucleotide excision repair of UV-induced DNA lesions in a manner independent of microRNA processing.

Indexed as

DNA DamageAnimalsAnisomycinAnthracenesDNADNA RepairHCT116 CellsHeLa CellsHumansMAP Kinase Kinase 4MiceMicroRNAsPhosphorylationRibonuclease IIIRNA-Binding ProteinsRNA Polymerase IIAnisomycinAnthracenesDGCR8 protein, humanDNADROSHA protein, humanMAP Kinase Kinase 4MicroRNAspyrazolanthroneRibonuclease IIIRNA-Binding ProteinsRNA Polymerase IIDGCR8DNA repairDroshaJNKmicroRNAtranscription-coupled nucleotide excision repairUV radiation

Identifiers

PMID28380355
PMCPMC5423785
OpenAlexW2604283208

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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.