Evidence map›Paper›PMID 18068156›Full record

ArticleExperimental cell research2008

DNA polymerase eta reduces the gamma-H2AX response to psoralen interstrand crosslinks in human cells.

Seiki Mogi, Christina E Butcher, Dennis H Oh

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. The Fanconi anaemia pathway: new players and new functions.Nature reviews. Molecular cell biology · 2016
    Review
  8. Article
  9. Review
  10. Review
  11. The Fanconi anemia pathway in replication stress and DNA crosslink repair.Cellular and molecular life sciences : CMLS · 2012
    Review
  12. Article
  13. Article
  14. DNA interstrand crosslink repair in mammalian cells: step by step.Critical reviews in biochemistry and molecular biology · 2010
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Seiki MogiDepartment of Dermatology, University of California, San Francisco, and Dermatology Research Unit, San Francisco VA Medical Center 94121, USA.
Christina E Butcher
Dennis H Oh
University of California, San Francisco · US

Funding

Mechanism of Triplex DNA Damage and Repair in Skin CellsR01CA105958 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI OH, DENNIS H · 2003 to 2007
$1.1M
NCI NIH HHS CA105958NCI NIH HHS R01 CA105958
6 · The paper itself

Abstract

DNA interstrand crosslinks are processed by multiple mechanisms whose relationships to each other are unclear. Xeroderma pigmentosum-variant (XP-V) cells lacking DNA polymerase eta are sensitive to psoralen photoadducts created under conditions favoring crosslink formation, suggesting a role for translesion synthesis in crosslink repair. Because crosslinks can lead to double-strand breaks, we monitored phosphorylated H2AX (gamma-H2AX), which is typically generated near double-strand breaks but also in response to single-stranded DNA, following psoralen photoadduct formation in XP-V fibroblasts to assess whether polymerase eta is involved in processing crosslinks. In contrast to conditions favoring monoadducts, conditions favoring psoralen crosslinks induced gamma-H2AX levels in both XP-V and nucleotide excision repair-deficient XP-A cells relative to control repair-proficient cells; ectopic expression of polymerase eta in XP-V cells normalized the gamma-H2AX response. In response to psoralen crosslinking, gamma-H2AX as well as 53BP1 formed coincident foci that were more numerous and intense in XP-V and XP-A cells than in controls. Psoralen photoadducts induced gamma-H2AX throughout the cell cycle in XP-V cells. These results indicate that polymerase eta is important in responding to psoralen crosslinks, and are consistent with a model in which nucleotide excision repair and polymerase eta are involved in processing crosslinks and avoiding gamma-H2AX associated with double-strand breaks and single-stranded DNA in human cells.

Indexed as

DNA Breaks, Double-StrandedDNA RepairCell CycleCell Line, TransformedDNA AdductsDNA-Directed DNA PolymeraseFurocoumarinsHistonesHumansUltraviolet RaysXeroderma PigmentosumY-Family DNA PolymerasesDNA AdductsDNA-Directed DNA PolymeraseFurocoumarinsH2AX protein, humanHistonespsoralen-DNA adductRad30 proteinY-Family DNA Polymerases

Identifiers

PMID18068156
PMCPMC2267924
OpenAlexW2032316865

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.