Evidence map›Paper›PMID 30445466›Full record

ArticleNucleic acids research2019

RNF8 mediates NONO degradation following UV-induced DNA damage to properly terminate ATR-CHK1 checkpoint signaling.

Rakesh Deshar, Wonjin Yoo, Eun-Bee Cho, Sungjoo Kim, Jong-Bok Yoon

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Frontiers in molecular biosciences · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

5 authors at 2 institutions in 1 country.

Rakesh DesharDepartment of Medical Lifesciences, The Catholic University of Korea, Seoul 137-701, Korea.
Wonjin YooDepartment of Biochemistry, College of Life Science & Biotechnology, Yonsei University, Seoul 120-749, Korea.
Eun-Bee ChoDepartment of Biochemistry, College of Life Science & Biotechnology, Yonsei University, Seoul 120-749, Korea.
Sungjoo KimDepartment of Medical Lifesciences, The Catholic University of Korea, Seoul 137-701, Korea.
Jong-Bok YoonDepartment of Biochemistry, College of Life Science & Biotechnology, Yonsei University, Seoul 120-749, Korea.
Yonsei University · KRCatholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNF8 plays a critical role in DNA damage response (DDR) to initiate ubiquitination-dependent signaling. To better characterize the role of RNF8 in UV-induced DDR, we searched for novel substrates of RNF8 and identified NONO as one intriguing substrate. We found that: (i) RNF8 ubiquitinates NONO and (ii) UV radiation triggers NONO ubiquitination and its subsequent degradation. Depletion of RNF8 inhibited UV-induced degradation of NONO, suggesting that RNF8 targets NONO for degradation in response to UV damage. In addition, we found that 3 NONO lysine residues (positions 279, 290 and 295) are important for conferring its instability in UV-DDR. Depletion of RNF8 or expression of NONO with lysine to arginine substitutions at positions 279, 290 and 295 prolonged CHK1 phosphorylation over an extended period of time. Furthermore, expression of the stable mutant, but not wild-type NONO, induced a prolonged S phase following UV exposure. Stable cell lines expressing the stable NONO mutant showed increased UV sensitivity in a clonogenic survival assay. Since RNF8 recruitment to the UV-damaged sites is dependent on ATR, we propose that RNF8-mediated NONO degradation and subsequent inhibition of NONO-dependent chromatin loading of TOPBP1, a key activator of ATR, function as a negative feedback loop critical for turning off ATR-CHK1 checkpoint signaling in UV-DDR.

Indexed as

DNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsCell LineCheckpoint Kinase 1DNA-Binding ProteinsHumansLysineNuclear Matrix-Associated ProteinsOctamer Transcription FactorsRNA-Binding ProteinsSignal TransductionS PhaseUbiquitinationUbiquitin-Protein LigasesUltraviolet RaysAtaxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 1CHEK1 protein, humanDNA-Binding ProteinsLysineNONO protein, humanNuclear Matrix-Associated ProteinsOctamer Transcription FactorsRNA-Binding ProteinsRNF8 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID30445466
PMCPMC6344893
OpenAlexW2900642666

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.