Evidence map›Paper›PMID 31484196›Full record

ArticlePloS one2019

A large deletion in the GP9 gene in Cocker Spaniel dogs with Bernard-Soulier syndrome.

Fabio Gentilini, Maria Elena Turba, Fiorella Giancola, Roberto Chiocchetti, Chiara Bernardini, Markéta Dajbychova, Vidhya Jagannathan, Michaela Drögemüller, Cord Drögemüller

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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. One Health: Animal Models of Heritable Human Bleeding Diseases.Animals : an open access journal from MDPI · 2022
    Review
  3. 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

9 authors at 2 institutions in 2 countries.

Fabio GentiliniDepartment of Veterinary Medical Sciences, University of Bologna, Bologna, Italy.ORCID 0000-0002-0970-4827
Maria Elena TurbaGenefast, Forlì, Italy.
Fiorella GiancolaDepartment of Veterinary Medical Sciences, University of Bologna, Bologna, Italy.
Roberto ChiocchettiDepartment of Veterinary Medical Sciences, University of Bologna, Bologna, Italy.
Chiara BernardiniDepartment of Veterinary Medical Sciences, University of Bologna, Bologna, Italy.
Markéta DajbychovaGenomia, Plzen, Czech Republic.ORCID 0000-0001-5344-5263
Vidhya JagannathanInstitute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Michaela DrögemüllerInstitute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Cord DrögemüllerInstitute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
University of Bologna · ITUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inherited bleeding disorders including abnormalities of platelet number and function rarely occur in a variety of dog breeds, but are probably underdiagnosed. Genetically characterized canine forms of platelet disorders provide valuable large animal models for understanding similar platelet disorders in people. Breed-specific disease associated genetic variants in only eight different genes are known to cause intrinsic platelet disorders in dogs. However, the causative genetic variant in many dog breeds has until now remained unknown. Four cases of a mild to severe bleeding disorder in Cocker Spaniel dogs are herein presented. The affected dogs showed a platelet adhesion defect characterized by macrothrombocytopenia with variable platelet counts resembling human Bernard-Soulier syndrome (BSS). Furthermore, the lack of functional GPIb-IX-V was demonstrated by immunocytochemistry. Whole genome sequencing of one affected dog and visual inspection of the candidate genes identified a deletion in the glycoprotein IX platelet (GP9) gene. The GP9 gene encodes a subunit of a platelet surface membrane glycoprotein complex; this functions as a receptor for von Willebrand factor, which initiates the maintenance of hemostasis after injury. Variants in human GP9 are associated with Bernard-Soulier syndrome, type C. The deletion spanned 2460 bp, and included a significant part of the single coding exon of the canine GP9 gene on dog chromosome 20. The variant results in a frameshift and premature stop codon which is predicted to truncate almost two-thirds of the encoded protein. PCR-based genotyping confirmed recessive inheritance. The homozygous variant genotype seen in affected dogs did not occur in 98 control Cocker Spaniels. Thus, it was concluded that the structural variant identified in the GP9 gene was most likely causative for the BSS-phenotype in the dogs examined. These findings provide the first large animal GP9 model for this group of inherited platelet disorders and greatly facilitate the diagnosis and identification of affected and/or normal carriers in Cocker Spaniels.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseSequence DeletionAnimalsBernard-Soulier SyndromeDog DiseasesDogsMalePedigreePlatelet Glycoprotein GPIb-IX ComplexPlatelet Glycoprotein GPIb-IX Complex

Identifiers

PMID31484196
PMCPMC6726462
OpenAlexW2972094456

What OpenQuestion holds

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LicenceCC BY
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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.