Evidence map›Paper›PMID 8710877›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

Ultraviolet-induced movement of the human DNA repair protein, Xeroderma pigmentosum type G, in the nucleus.

M S Park, J A Knauf, S H Pendergrass, C H Coulon, G F Strniste, B L Marrone, M A MacInnes

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. XPG: its products and biological roles.Advances in experimental medicine and biology · 2008
    Review
  7. Article
  8. Article
  9. Article
  10. Translocation of Cockayne syndrome group A protein to the nuclear matrix: possible relevance to transcription-coupled DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Molecular cloning and structural analysis of the functional mouse genomic XPG gene.Mammalian genome : official journal of the International Mammalian Genome Society · 1996
    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

7 authors at 1 institution in 1 country.

M S ParkLife Sciences Division, Los Alamos National Laboratory, NM 87545, USA. park@telomere.lanl.gov
J A Knauf
S H Pendergrass
C H Coulon
G F Strniste
B L Marrone
M A MacInnes
Los Alamos National Laboratory · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Xeroderma pigmentosum type G (XPG) is a human genetic disease exhibiting extreme sensitivity to sunlight. XPG patients are defective XPG endonuclease, which is an enzyme essential for DNA repair of the major kinds of solar ultraviolet (UV)-induced DNA damages. Here we describe a novel dynamics of this protein within the cell nucleus after UV irradiation of human cells. Using confocal microscopy, we have localized the immunofluorescent, antigenic signal of XPG protein to foci throughout the cell nucleus. Our biochemical studies also established that XPG protein forms a tight association with nuclear structure(s). In human skin fibroblast cells, the number of XPG foci decreased within 2 h after UV irradiation, whereas total nuclear XPG fluorescence intensity remained constant, suggesting redistribution of XPG from a limited number of nuclear foci to the nucleus overall. Within 8 h after UV, most XPG antigenic signal was found as foci. Using beta-galactosidase-XPG fusion constructs (beta-gal-XPG) transfected into HeLa cells, we have identified a single region of XPG that is evidently responsible both for foci formation and for the UV dynamic response. The fusion protein carrying the C terminus of XPG (amino acids 1146-1185) localized beta-gal specific antigenic signal to foci and to the nucleolus regions. After UV irradiation, antigenic beta-gal translocated reversibly from the subnuclear structures to the whole nucleus with kinetics very similar to the movements of XPG protein. These findings lead us to propose a model in which distribution of XPG protein may regulate the rate of DNA repair within transcriptionally active and inactive compartments of the cell nucleus.

Indexed as

DNA RepairUltraviolet RaysAmino Acid SequenceCell CompartmentationCell NucleusDNA-Binding ProteinsDNA Excision Repair Protein ERCC-5EndonucleasesFluorescent Antibody Technique, IndirectHeLa CellsHumansMicroscopy, ConfocalMolecular Sequence DataNuclear ProteinsPeptidesRecombinant Fusion ProteinsDNA-Binding ProteinsDNA Excision Repair Protein ERCC-5EndonucleasesNuclear ProteinsPeptidesRecombinant Fusion ProteinsTranscription Factors

Identifiers

PMID8710877
PMCPMC38677
OpenAlexW2033613599

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.