Evidence map›Paper›PMID 25070891›Full record

ArticleThe Journal of biological chemistry2014

The Fanconi anemia proteins FANCD2 and FANCJ interact and regulate each other's chromatin localization.

Xiaoyong Chen, James B Wilson, Patricia McChesney, Stacy A Williams, Youngho Kwon, Simonne Longerich, Andrew S Marriott, Patrick Sung, Nigel J Jones, Gary M Kupfer

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  11. The Fanconi anaemia pathway: new players and new functions.Nature reviews. Molecular cell biology · 2016
    Review
  12. FANCJ at the FORK.Mutation research · 2016
    Review
  13. Review
  14. Article
  15. Article
  16. 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

10 authors at 3 institutions in 2 countries.

Xiaoyong ChenFrom the Departments of Pediatrics.
James B Wilsonthe Department of Molecular and Clinical Cancer Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool L3 9TA, United Kingdom.
Patricia McChesneyFrom the Departments of Pediatrics.
Stacy A WilliamsFrom the Departments of Pediatrics.
Youngho KwonMolecular Biophysics and Biochemistry, Yale University School of Medicine, Section of Hematology/Oncology, New Haven, Connecticut 06520.
Simonne LongerichMolecular Biophysics and Biochemistry, Yale University School of Medicine, Section of Hematology/Oncology, New Haven, Connecticut 06520.
Andrew S Marriottthe Department of Biochemistry, Institute of Integrative Biology, University of Liverpool, Liverpool L69 7ZB, United Kingdom, and.
Patrick SungMolecular Biophysics and Biochemistry, Yale University School of Medicine, Section of Hematology/Oncology, New Haven, Connecticut 06520.
Nigel J Jonesthe Department of Biochemistry, Institute of Integrative Biology, University of Liverpool, Liverpool L69 7ZB, United Kingdom, and.
Gary M KupferFrom the Departments of Pediatrics, Pathology, and gary.kupfer@yale.edu.
Yale University · USUniversity of Liverpool · GBPediatrics and Genetics · US

Funding

Yale University Clinical and Translational Science Award ProgramUL1TR000142 · NCATS · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2012 to 2015
$31.8M
The Fanconi Anemia Core and D2 ComplexesR01HL063776 · NHLBI · YALE UNIVERSITY · PI KUPFER, GARY M. · 2000 to 2014
$5.3M
Molecular Basis of BRCA2-mediated DNA Repair and Cancer AvoidanceR01ES015252 · NIEHS · YALE UNIVERSITY · PI SUNG, PATRICK · 2007 to 2016
$3.8M
NCATS NIH HHS UL1 TR000142NHLBI NIH HHS R01 HL063776NHLBI NIH HHS R01-HL063776NIEHS NIH HHS R01 ES015252NIEHS NIH HHS R01-ES015252
6 · The paper itself

Abstract

Fanconi anemia is a genetic disease resulting in bone marrow failure, birth defects, and cancer that is thought to encompass a defect in maintenance of genomic stability. Mutations in 16 genes (FANCA, B, C, D1, D2, E, F, G, I, J, L, M, N, O, P, and Q) have been identified in patients, with the Fanconi anemia subtype J (FA-J) resulting from homozygous mutations in the FANCJ gene. Here, we describe the direct interaction of FANCD2 with FANCJ. We demonstrate the interaction of FANCD2 and FANCJ in vivo and in vitro by immunoprecipitation in crude cell lysates and from fractions after gel filtration and with baculovirally expressed proteins. Mutation of the monoubiquitination site of FANCD2 (K561R) preserves interaction with FANCJ constitutively in a manner that impedes proper chromatin localization of FANCJ. FANCJ is necessary for FANCD2 chromatin loading and focus formation in response to mitomycin C treatment. Our results suggest not only that FANCD2 regulates FANCJ chromatin localization but also that FANCJ is necessary for efficient loading of FANCD2 onto chromatin following DNA damage caused by mitomycin C treatment.

Indexed as

Protein BindingBasic-Leucine Zipper Transcription FactorsChromatinDNA-Binding ProteinsDNA DamageDNA RepairFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsGenomic InstabilityHumansMutationBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsChromatinDNA-Binding ProteinsFANCD2 protein, humanFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsCancer BiologyDNA Damage ResponseDNA RepairFANCD2FANCJFanconi AnemiaGenetic DiseaseGenomic Instability

Identifiers

PMID25070891
PMCPMC4162179
OpenAlexW1990098145

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.