Evidence map›Paper›PMID 19965384›Full record

ArticleScience (New York, N.Y.)2009

The Fanconi anemia pathway promotes replication-dependent DNA interstrand cross-link repair.

Puck Knipscheer, Markus Räschle, Agata Smogorzewska, Milica Enoiu, The Vinh Ho, Orlando D Schärer, Stephen J Elledge, Johannes C Walter

Abstract read
In one paragraph

Article in Science (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 359 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
359citing papers in PubMed, 1 pooled it
–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

359 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Treatment of Fanconi Anemia-Associated Head and Neck Cancer: Opportunities to Improve Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Pooled it
  2. Article
  3. Article
  4. Chromosome-Level Genome Assembly ofJournal of fungi (Basel, Switzerland) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Proteome-widebioRxiv : the preprint server for biology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

299 more citing papers are in PubMed but not listed here.

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

8 authors.

Puck KnipscheerDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Markus Räschle
Agata Smogorzewska
Milica Enoiu
The Vinh Ho
Orlando D Schärer
Stephen J Elledge
Johannes C Walter

Funding

MOLECULAR IMMUNOLOGY AND TUMOR BIOLOGYT32CA009216 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI David Michael Langenau · 1985 to 2026
$10.6M
Properties of the eukaryotic replicative DNA helicaseR01GM062267 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALTER, JOHANNES · 2001 to 2014
$4.1M
Genetics of Cell Cycle &DNA Damage Regulation in YeastR37GM044664 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI ELLEDGE, STEPHEN J · 2003 to 2012
$3.5M
Howard Hughes Medical InstituteNCI NIH HHS T32 CA009216NCI NIH HHS T32CA09216NIGMS NIH HHS GM62267NIGMS NIH HHS R01 GM062267NIGMS NIH HHS R37 GM044664
6 · The paper itself

Abstract

Fanconi anemia is a human cancer predisposition syndrome caused by mutations in 13 Fanc genes. The disorder is characterized by genomic instability and cellular hypersensitivity to chemicals that generate DNA interstrand cross-links (ICLs). A central event in the activation of the Fanconi anemia pathway is the mono-ubiquitylation of the FANCI-FANCD2 complex, but how this complex confers ICL resistance remains enigmatic. Using a cell-free system, we showed that FANCI-FANCD2 is required for replication-coupled ICL repair in S phase. Removal of FANCD2 from extracts inhibits both nucleolytic incisions near the ICL and translesion DNA synthesis past the lesion. Reversal of these defects requires ubiquitylated FANCI-FANCD2. Our results show that multiple steps of the essential S-phase ICL repair mechanism fail when the Fanconi anemia pathway is compromised.

Indexed as

DNA RepairDNA ReplicationAnimalsCell-Free SystemChromatinDNADNA DamageFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsMolecular Sequence DataRecombinant ProteinsSignal TransductionS PhaseUbiquitinated ProteinsUbiquitinationChromatinDNAFANCI Protein, XenopusFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsRecombinant ProteinsUbiquitinated ProteinsXenopus Proteins

Identifiers

PMID19965384
PMCPMC2909596

What OpenQuestion holds

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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.