Evidence map›Paper›PMID 22147205›Full record

ReviewMammalian genome : official journal of the International Mammalian Genome Society2012

Canine models of copper toxicosis for understanding mammalian copper metabolism.

Hille Fieten, Peter A J Leegwater, Adrian L Watson, Jan Rothuizen

Open access · hybridAbstract readReview
In one paragraph

Review in Mammalian genome : official journal of the International Mammalian Genome Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Pedigree study of the heredity of copper-associated hepatitis in Dalmatians in Japan.The Canadian veterinary journal = La revue veterinaire canadienne · 2022
    Article
  5. The Rat Genome Database (RGD) facilitates genomic and phenotypic data integration across multiple species for biomedical research.Mammalian genome : official journal of the International Mammalian Genome Society · 2022
    Article
  6. Copper-associated hepatitis in a young Dalmatian dog in Japan.The Journal of veterinary medical science · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Animal models of Wilson disease.Journal of neurochemistry · 2018
    Review
  14. Article
  15. Canine Models for Copper Homeostasis Disorders.International journal of molecular sciences · 2016
    Review
  16. Article
  17. Article
  18. Distinct phenotype of a Wilson disease mutation reveals a novel trafficking determinant in the copper transporter ATP7B.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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 2 institutions in 1 country.

Hille FietenDepartment of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 108, 3584 CM Utrecht, The Netherlands. H.Fieten@uu.nl
Peter A J Leegwater
Adrian L Watson
Jan Rothuizen
Utrecht University · NLWaltham Centre for Pet Nutrition

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary forms of copper toxicosis exist in man and dogs. In man, Wilson's disease is the best studied disorder of copper overload, resulting from mutations in the gene coding for the copper transporter ATP7B. Forms of copper toxicosis for which no causal gene is known yet are recognized as well, often in young children. Although advances have been made in unraveling the genetic background of disorders of copper metabolism in man, many questions regarding disease mechanisms and copper homeostasis remain unanswered. Genetic studies in the Bedlington terrier, a dog breed affected with copper toxicosis, identified COMMD1, a gene that was previously unknown to be involved in copper metabolism. Besides the Bedlington terrier, a number of other dog breeds suffer from hereditary copper toxicosis and show similar phenotypes to humans with copper storage disorders. Unlike the heterogeneity of most human populations, the genetic structure within a purebred dog population is homogeneous, which is advantageous for unraveling the molecular genetics of complex diseases. This article reviews the work that has been done on the Bedlington terrier, summarizes what was learned from studies into COMMD1 function, describes hereditary copper toxicosis phenotypes in other dog breeds, and discusses the opportunities for genome-wide association studies on copper toxicosis in the dog to contribute to the understanding of mammalian copper metabolism and copper metabolism disorders in man.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCopperDisease Models, AnimalDog DiseasesDogsHepatolenticular DegenerationHumansMetal Metabolism, Inborn ErrorsMutationAdaptor Proteins, Signal TransducingCarrier ProteinsCopper

Identifiers

PMID22147205
PMCPMC3275736
OpenAlexW2112206095

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.