Evidence map›Paper›PMID 22039351›Full record

ArticlePLoS biology2011

Regulation of nucleotide excision repair by UV-DDB: prioritization of damage recognition to internucleosomal DNA.

Jia Fei, Nina Kaczmarek, Andreas Luch, Andreas Glas, Thomas Carell, Hanspeter Naegeli

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Article
  3. UV-B-induced modulation of constitutive heterochromatin content in Arabidopsis thaliana.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023
    Article
  4. Article
  5. DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Formation and Recognition of UV-Induced DNA Damage within Genome Complexity.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

Jia FeiInstitute of Pharmacology and Toxicology, University of Zürich-Vetsuisse, Zürich, Switzerland.
Nina Kaczmarek
Andreas Luch
Andreas Glas
Thomas Carell
Hanspeter Naegeli
University of Zurich · CHLudwig-Maximilians-Universität München · DEFederal Institute for Risk Assessment · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

How tightly packed chromatin is thoroughly inspected for DNA damage is one of the fundamental unanswered questions in biology. In particular, the effective excision of carcinogenic lesions caused by the ultraviolet (UV) radiation of sunlight depends on UV-damaged DNA-binding protein (UV-DDB), but the mechanism by which this DDB1-DDB2 heterodimer stimulates DNA repair remained enigmatic. We hypothesized that a distinctive function of this unique sensor is to coordinate damage recognition in the nucleosome repeat landscape of chromatin. Therefore, the nucleosomes of human cells have been dissected by micrococcal nuclease, thus revealing, to our knowledge for the first time, that UV-DDB associates preferentially with lesions in hypersensitive, hence, highly accessible internucleosomal sites joining the core particles. Surprisingly, the accompanying CUL4A ubiquitin ligase activity is necessary to retain the xeroderma pigmentosum group C (XPC) partner at such internucleosomal repair hotspots that undergo very fast excision kinetics. This CUL4A complex thereby counteracts an unexpected affinity of XPC for core particles that are less permissive than hypersensitive sites to downstream repair subunits. That UV-DDB also adopts a ubiquitin-independent function is evidenced by domain mapping and in situ protein dynamics studies, revealing direct but transient interactions that promote a thermodynamically unfavorable β-hairpin insertion of XPC into substrate DNA. We conclude that the evolutionary advent of UV-DDB correlates with the need for a spatiotemporal organizer of XPC positioning in higher eukaryotic chromatin.

Indexed as

DNA DamageDNA RepairAnimalsBenzoatesCHO CellsCricetinaeCullin ProteinsDNADNA-Binding ProteinsFuransGene Knockdown TechniquesHEK293 CellsHeLa CellsHumansNucleosomesProtein Binding4(4-(5-nitro-furan-2-ylmethylene)-3,5-dioxo-pyrazolidin-1-yl)-benzoic acid ethyl esterBenzoatesCUL4A protein, humanCullin ProteinsDDB2 protein, humanDNADNA-Binding ProteinsFuransNucleosomesPyrazolesPyrimidine DimersUbiquitin-Activating EnzymesXPC protein, human

Identifiers

PMID22039351
PMCPMC3201922
OpenAlexW2133251151

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.