Evidence map›Paper›PMID 19519404›Full record

ReviewCurrent molecular medicine2009

FANCJ helicase operates in the Fanconi Anemia DNA repair pathway and the response to replicational stress.

Yuliang Wu, Robert M Brosh

Open access · greenAbstract readReview
In one paragraph

Review in Current molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. The repair geneOncology reviews · 2021
    Article
  9. Biogenesis of Iron-Sulfur Clusters and Their Role in DNA Metabolism.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Decreased FANCJ caused by 5FU contributes to the increased sensitivity to oxaliplatin in gastric cancer cells.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2013
    Article
  18. Article
  19. Article
  20. 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 at 1 institution in 1 country.

Yuliang WuLaboratory of Molecular Gerontology, National Institute on Aging, NIH, NIH Biomedical Research Center, Baltimore, MD 21224, USA.
Robert M Brosh
National Institute on Aging · US

Funding

Roles Of DNA Helicases In Pathways Required For Maintenance Of Genomic StabilityZIAAG000741 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$7.6M
Fanconi Anemia PathwayZIAAG000753 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$4.3M
Roles Of Dna Helicases:Pathways Required For MaintenanceZ01AG000741 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT M · 2001 to 2008
$1.1M
Intramural NIH HHS Z01 AG000741
6 · The paper itself

Abstract

Fanconi anemia (FA) is an autosomal recessive disorder characterized by multiple congenital anomalies, progressive bone marrow failure, and high cancer risk. Cells from FA patients exhibit spontaneous chromosomal instability and hypersensitivity to DNA interstrand cross-linking (ICL) agents. Although the precise mechanistic details of the FA/BRCA pathway of ICL-repair are not well understood, progress has been made in the identification of the FA proteins that are required for the pathway. Among the 13 FA complementation groups from which all the FA genes have been cloned, only a few of the FA proteins are predicted to have direct roles in DNA metabolism. One of the more recently identified FA proteins, shown to be responsible for complementation of the FA complementation group J, is the BRCA1 Associated C-terminal Helicase (BACH1, designated FANCJ), originally identified as a protein associated with breast cancer. FANCJ has been proposed to function downstream of FANCD2 monoubiquitination, a critical event in the FA pathway. Evidence supports a role for FANCJ in a homologous recombination (HR) pathway of double strand break (DSB) repair. In this review, we will summarize the current knowledge in terms of FANCJ functions through its enzymatic activities and protein interactions. The molecular roles of FANCJ in DNA repair and the response to replicational stress will be discussed.

Indexed as

Amino Acid SequenceAnimalsBasic-Leucine Zipper Transcription FactorsDNADNA Breaks, Double-StrandedDNA RepairDNA ReplicationFanconi AnemiaFanconi Anemia Complementation Group ProteinsHumansModels, BiologicalMolecular Sequence DataSubstrate SpecificityBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsDNAFanconi Anemia Complementation Group Proteins

Identifiers

PMID19519404
PMCPMC2763586
OpenAlexW2090377588

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.