Evidence map›Paper›PMID 26336824›Full record

ArticleOncotarget2015

FANCJ protein is important for the stability of FANCD2/FANCI proteins and protects them from proteasome and caspase-3 dependent degradation.

David W Clark, Kaushlendra Tripathi, Josephine C Dorsman, Komaraiah Palle

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Journal of breast cancer · 2017
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. FANCI is a negative regulator of Akt activation.Cell cycle (Georgetown, Tex.) · 2016
    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

4 authors at 3 institutions in 2 countries.

David W ClarkDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA.
Kaushlendra TripathiDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA.
Josephine C DorsmanDepartment of Clinical Genetics, Section Oncogenetics, VU University Medical Center, Amsterdam, The Netherlands.
Komaraiah PalleDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA.
USA Mitchell Cancer Institute · USAmsterdam UMC Location VUmc · NLUniversity of South Alabama · US

Funding

Ras18-mediated Fanconi Anemia pathway activation in response to camptothecinR01GM098956 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PALLE, KOMARAIAH · 2012 to 2016
$1.1M
NIGMS NIH HHS R01 GM098956NIGMS NIH HHS R01GM098956
6 · The paper itself

Abstract

Fanconi anemia (FA) is a rare genome instability syndrome with progressive bone marrow failure and cancer susceptibility. FANCJ is one of 17 genes mutated in FA-patients, comprises a DNA helicase that is vital for properly maintaining genomic stability and is known to function in the FA-BRCA DNA repair pathway. While exact role(s) of FANCJ in this repair process is yet to be determined, it is known to interact with primary effector FANCD2. However, FANCJ is not required for FANCD2 activation but is important for its ability to fully respond to DNA damage. In this report, we determined that transient depletion of FANCJ adversely affects stability of FANCD2 and its co-regulator FANCI in multiple cell lines. Loss of FANCJ does not significantly alter cell cycle progression or FANCD2 transcription. However, in the absence of FANCJ, the majority of FANCD2 is degraded by both the proteasome and Caspase-3 dependent mechanism. FANCJ is capable of complexing with and stabilizing FANCD2 even in the absence of a functional helicase domain. Furthermore, our data demonstrate that FANCJ is important for FANCD2 stability and proper activation of DNA damage responses to replication blocks induced by hydroxyurea.

Indexed as

Basic-Leucine Zipper Transcription FactorsCaspase 3Cell Line, TumorDNA DamageDNA RepairEnzyme StabilityFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsGene Expression Regulation, NeoplasticHumansHydroxyureaProteasome Endopeptidase ComplexProteasome InhibitorsProtein BindingProteolysisBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsCASP3 protein, humanCaspase 3FANCD2 protein, humanFANCI protein, humanFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group ProteinsHydroxyureaProteasome Endopeptidase ComplexProteasome Inhibitorscaspase-3FANCD2FANCJFanconi anemiaproteasome

Identifiers

PMID26336824
PMCPMC4745694
OpenAlexW1860817424

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.