Evidence map›Paper›PMID 22744751›Full record

ReviewCellular and molecular life sciences : CMLS2012

The Fanconi anemia pathway in replication stress and DNA crosslink repair.

Mathew J K Jones, Tony T Huang

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Mitomycin C-induced DNA double-strand breaks are enhanced by catalytical inactivation of DNA polymerase κ in mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Helicase HELQ: Molecular Characters Fit for DSB Repair Function.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

2 authors.

Mathew J K JonesDepartment of Biochemistry, New York University School of Medicine, 550 First Ave., MSB 399, New York, NY, 10016, USA.
Tony T Huang

Funding

Role of Deubiquitination in Fanconi Anemia Cancer Susceptibility PathwayR01GM084244 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, TONY TUNG · 2009 to 2013
$2.3M
NIGMS NIH HHS R01 GM084244
6 · The paper itself

Abstract

Interstand crosslinks (ICLs) are DNA lesions where the bases of opposing DNA strands are covalently linked, inhibiting critical cellular processes such as transcription and replication. Chemical agents that generate ICLs cause chromosomal abnormalities including breaks, deletions and rearrangements, making them highly genotoxic compounds. This toxicity has proven useful for chemotherapeutic treatment against a wide variety of cancer types. The majority of our understanding of ICL repair in humans has been uncovered through analysis of the rare genetic disorder Fanconi anemia, in which patients are extremely sensitive to crosslinking agents. Here, we discuss recent insights into ICL repair gained using new repair assays and highlight the role of the Fanconi anemia repair pathway during replication stress.

Indexed as

DNA DamageCross-Linking ReagentsDNADNA RepairDNA ReplicationFanconi AnemiaFanconi Anemia Complementation Group ProteinsHumansModels, GeneticSignal TransductionCross-Linking ReagentsDNAFanconi Anemia Complementation Group Proteins

Identifiers

PMID22744751
PMCPMC3890373

What OpenQuestion holds

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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.