Evidence map›Paper›PMID 30995231›Full record

ArticlePloS one2019

QDPR homologues in Danio rerio regulate melanin synthesis, early gliogenesis, and glutamine homeostasis.

Maximilian Breuer, Luca Guglielmi, Matthias Zielonka, Verena Hemberger, Stefan Kölker, Jürgen G Okun, Georg F Hoffmann, Matthias Carl, Sven W Sauer, Thomas Opladen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Experimental Animal Models of Phenylketonuria: Pros and Cons.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Article
  5. Article
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  8. 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 2 institutions in 2 countries.

Maximilian BreuerUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.
Luca GuglielmiHeidelberg University, Medical Faculty Mannheim, Department of Cell and Molecular Biology, Mannheim, Germany.
Matthias ZielonkaUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.ORCID 0000-0001-9653-2914
Verena HembergerUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.
Stefan KölkerUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.
Jürgen G OkunUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.
Georg F HoffmannUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.
Matthias CarlHeidelberg University, Medical Faculty Mannheim, Department of Cell and Molecular Biology, Mannheim, Germany.
Sven W SauerUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.
Thomas OpladenUniversity Children's Hospital, Division of Child Neurology and Metabolic Diseases, Heidelberg, Germany.ORCID 0000-0003-4349-7662
Heidelberg University · DEUniversity of Trento · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dihydropteridine reductase (QDPR) catalyzes the recycling of tetrahydrobiopterin (BH4), a cofactor in dopamine, serotonin, and phenylalanine metabolism. QDPR-deficient patients develop neurological symptoms including hypokinesia, truncal hypotonia, intellectual disability and seizures. The underlying pathomechanisms are poorly understood. We established a zebrafish model for QDPR deficiency and analyzed the expression as well as function of all zebrafish QDPR homologues during embryonic development. The homologues qdpra is essential for pigmentation and phenylalanine metabolism. Qdprb1 is expressed in the proliferative zones of the optic tectum and eye. Knockdown of qdprb1 leads to up-regulation of pro-proliferative genes and increased number of phospho-histone3 positive mitotic cells. Expression of neuronal and astroglial marker genes is concomitantly decreased. Qdprb1 hypomorphic embryos develop microcephaly and reduced eye size indicating a role for qdprb1 in the transition from cell proliferation to differentiation. Glutamine accumulation biochemically accompanies the developmental changes. Our findings provide novel insights into the neuropathogenesis of QDPR deficiency.

Indexed as

GlutamineMelaninsPhenylketonuriasZebrafishAnimalsCell ProliferationDihydropteridine ReductaseDisease Models, AnimalGene Knockdown TechniquesHumansNeurogliaZebrafish ProteinsDihydropteridine ReductaseGlutamineMelaninsZebrafish Proteins

Identifiers

PMID30995231
PMCPMC6469847
OpenAlexW2936128237

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.