Evidence map›Paper›PMID 42062396›Full record

ArticleScientific reports2026

Differential regulation of retinoic acid metabolism in Fanconi anemia.

Justin L Blaize, Bahaa M Noori, Kelsey P Hunter, Kathryn A Henrikson, Janet A Atoyan, Alan A Ardito, Abygail G Chapdelaine, Gongqin Sun, Frank X Donovan, Settara C Chandrasekharappa and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Justin L BlaizeDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.
Bahaa M NooriDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.
Kelsey P HunterDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.
Kathryn A HenriksonDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.
Janet A AtoyanDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.
Alan A ArditoTherapeutic Sciences Graduate Program, Brown University, Providence, RI, USA.
Abygail G ChapdelaineDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.
Gongqin SunDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.
Frank X DonovanCancer Genetics and Comparative Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Settara C ChandrasekharappaCancer Genetics and Comparative Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Detlev SchindlerDepartment of Human Genetics, University of Wurzburg, Wurzburg, Germany.
Niall G HowlettDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA. nhowlett@uri.edu.

Funding

Training CoreP20GM103430 · NIGMS · UNIVERSITY OF RHODE ISLAND · PI Christopher Lee Hemme · 2012 to 2026
$63.6M
NHLBI NIH HHS HL149907NIGMS NIH HHS P20GM103430
6 · The paper itself

Abstract

Fanconi anemia (FA) is a genetic disease characterized by congenital abnormalities and increased risk for bone marrow failure and cancer. FA is caused by mutation of 23 genes, the protein products of which function in the maintenance of genome stability. An important role for the FA proteins in the repair of DNA interstrand crosslinks (ICLs) has been established. While the endogenous sources of ICLs relevant to the pathophysiology of FA have yet to be determined, a role for the FA proteins in the detoxification of reactive metabolic aldehydes has been established. To discover new metabolic pathways linked to FA, we performed RNA-seq analysis on a previously established isogenic FA-D2 patient cell model. Multiple retinoic acid metabolism and signaling genes were differentially expressed in the FA-D2 patient cells, including ALDH1A1 and RDH10, two key enzymes in the retinoic acid pathway. Increased levels of ALDH1A1 and RDH10 were confirmed by immunoblotting. FA-D2 (FANCD2

Indexed as

Fanconi AnemiaTretinoinAldehyde Dehydrogenase 1 FamilyCell LineDNA DamageDNA RepairFanconi Anemia Complementation Group D2 ProteinHumansRetinal DehydrogenaseSignal TransductionAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanFANCD2 protein, humanFanconi Anemia Complementation Group D2 ProteinRetinal DehydrogenaseTretinoinChromosome stabilityDNA repairFanconi anemiaRetinoic acid

Identifiers

PMID42062396
PMCPMC13324539

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Registered trials

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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.