Evidence map›Paper›PMID 24351291›Full record

ArticleCancer research2014

FANCJ localization by mismatch repair is vital to maintain genomic integrity after UV irradiation.

Shawna Guillemette, Amy Branagan, Min Peng, Aashana Dhruva, Orlando D Schärer, Sharon B Cantor

Abstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Type-I Interferon Signaling in Fanconi Anemia.Frontiers in cellular and infection microbiology · 2022
    Review
  6. Article
  7. Review
  8. The repair geneOncology reviews · 2021
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. The Fanconi anaemia pathway: new players and new functions.Nature reviews. Molecular cell biology · 2016
    Review
  15. FANCJ at the FORK.Mutation research · 2016
    Review
  16. Article
  17. Article
  18. Article
  19. What is wrong with Fanconi anemia cells?Cell cycle (Georgetown, Tex.) · 2014
    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

6 authors at 3 institutions in 1 country.

Shawna GuillemetteAuthors' Affiliations: Department of Cancer Biology, University of Massachusetts Medical School, Women's Cancers Program, UMASS Memorial Cancer Center, Worcester, Massachusetts; and Department of Pharmacological Sciences & Department of Chemistry, Stony Brook University, Stony Brook, New York.
Amy Branagan
Min Peng
Aashana Dhruva
Orlando D Schärer
Sharon B Cantor
UMass Memorial Health Care · USUniversity of Massachusetts Chan Medical School · USStony Brook University · US

Funding

BACH1/FANCJ Checkpoint, Recombination, and ChemoresistanceR01CA129514 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CANTOR, SHARON B · 2007 to 2011
$1.6M
NCI NIH HHS R01 CA129514NCI NIH HHS R01 CA129514-01A1
6 · The paper itself

Abstract

Nucleotide excision repair (NER) is critical for the repair of DNA lesions induced by UV radiation, but its contribution in replicating cells is less clear. Here, we show that dual incision by NER endonucleases, including XPF and XPG, promotes the S-phase accumulation of the BRCA1 and Fanconi anemia-associated DNA helicase FANCJ to sites of UV-induced damage. FANCJ promotes replication protein A phosphorylation and the arrest of DNA synthesis following UV irradiation. Interaction defective mutants of FANCJ reveal that BRCA1 binding is not required for FANCJ localization, whereas interaction with the mismatch repair (MMR) protein MLH1 is essential. Correspondingly, we find that FANCJ, its direct interaction with MLH1, and the MMR protein MSH2 function in a common pathway in response to UV irradiation. FANCJ-deficient cells are not sensitive to killing by UV irradiation, yet we find that DNA mutations are significantly enhanced. Thus, we considered that FANCJ deficiency could be associated with skin cancer. Along these lines, in melanoma we found several somatic mutations in FANCJ, some of which were previously identified in hereditary breast cancer and Fanconi anemia. Given that, mutations in XPF can also lead to Fanconi anemia, we propose collaborations between Fanconi anemia, NER, and MMR are necessary to initiate checkpoint activation in replicating human cells to limit genomic instability.

Indexed as

DNA Mismatch RepairBasic-Leucine Zipper Transcription FactorsCell Line, TumorDNA DamageDNA RepairDNA ReplicationFanconi Anemia Complementation Group ProteinsGenomic InstabilityHumansModels, BiologicalMutationPhosphorylationProtein TransportReplication Protein AS PhaseUltraviolet RaysBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsFanconi Anemia Complementation Group ProteinsReplication Protein A

Identifiers

PMID24351291
PMCPMC5402619
OpenAlexW2149484928

What OpenQuestion holds

Textmetadata
LicenceTDM
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.