Evidence map›Paper›PMID 17396147›Full record

ArticleThe EMBO journal2007

FAAP100 is essential for activation of the Fanconi anemia-associated DNA damage response pathway.

Chen Ling, Masamichi Ishiai, Abdullah Mahmood Ali, Annette L Medhurst, Kornelia Neveling, Reinhard Kalb, Zhijiang Yan, Yutong Xue, Anneke B Oostra, Arleen D Auerbach and 7 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The EMBO journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

94 citing papers in PubMed, 174 citations in OpenAlex.

  1. Review
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  4. Article
  5. Another Fanconi anemia gene joins the club.The Journal of clinical investigation · 2025
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  6. Review
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  15. Review
  16. DNA polymerase ι compensates for Fanconi anemia pathway deficiency by countering DNA replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Article

34 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

17 authors at 9 institutions in 4 countries.

Chen LingLaboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Masamichi Ishiai
Abdullah Mahmood Ali
Annette L Medhurst
Kornelia Neveling
Reinhard Kalb
Zhijiang Yan
Yutong Xue
Anneke B Oostra
Arleen D Auerbach
Maureen E Hoatlin
Detlev Schindler
Hans Joenje
Johan P de Winter
Minoru Takata
Amom Ruhikanta Meetei
Weidong Wang
Amsterdam UMC Location VUmc · NLNational Institute on Aging · USUniversity of Würzburg · DEKawasaki Medical School · JPCincinnati Children's Hospital Medical Center · USNational Institutes of Health · USOregon Health & Science University · USRockefeller University · USUniversity of Cincinnati Medical Center · US

Funding

FANCONI ANEMIA--HETEROGENEITY AND CARRIER DETECTIONR37HL032987 · NHLBI · ROCKEFELLER UNIVERSITY · PI AUERBACH, ARLEEN D · 1997 to 2007
$3.2M
Protein Complexes Involved In Fanconi AnemiaZ01AG000688 · NIA · NATIONAL INSTITUTE ON AGING · PI WANG, WEIDONG · 2002 to 2008
$1.5M
Functional Analysis of the Fanconi PathwayR01CA112775 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI HOATLIN, MAUREEN E · 2005 to 2009
$1.4M
The Risk of Cancer in Fanconi Anemia HeterozygotesR01CA082678 · NCI · UNIVERSITY OF NEW MEXICO · PI BERWICK, MARIANNE · 2001 to 2005
$1.2M
NCI NIH HHS CA112775NCI NIH HHS R01 CA082678NCI NIH HHS R01 CA112775NCI NIH HHS R01CA82678NHLBI NIH HHS R37 HL032987NHLBI NIH HHS R37HL32987
6 · The paper itself

Abstract

The Fanconi anemia (FA) core complex plays a central role in the DNA damage response network involving breast cancer susceptibility gene products, BRCA1 and BRCA2. The complex consists of eight FA proteins, including a ubiquitin ligase (FANCL) and a DNA translocase (FANCM), and is essential for monoubiquitination of FANCD2 in response to DNA damage. Here, we report a novel component of this complex, termed FAAP100, which is essential for the stability of the core complex and directly interacts with FANCB and FANCL to form a stable subcomplex. Formation of this subcomplex protects each component from proteolytic degradation and also allows their coregulation by FANCA and FANCM during nuclear localization. Using siRNA depletion and gene knockout techniques, we show that FAAP100-deficient cells display hallmark features of FA cells, including defective FANCD2 monoubiquitination, hypersensitivity to DNA crosslinking agents, and genomic instability. Our study identifies FAAP100 as a new critical component of the FA-BRCA DNA damage response network.

Indexed as

DNA DamageBRCA1 ProteinBRCA2 ProteinDNA-Binding ProteinsDNA HelicasesFanconi Anemia Complementation Group L ProteinHeLa CellsHumansModels, MolecularMultiprotein ComplexesOligonucleotidesRNA InterferenceBRCA1 ProteinBRCA2 ProteinDNA-Binding ProteinsDNA HelicasesFAAP100 protein, humanFANCL protein, humanFANCM protein, humanFanconi Anemia Complementation Group L ProteinMultiprotein ComplexesOligonucleotides

Identifiers

PMID17396147
PMCPMC1852792
OpenAlexW2085909080

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.