Evidence map›Paper›PMID 39593234›Full record

ArticleAnimal genetics2025

Identification of a de novo missense variant in the BRI3BP gene in a Holstein calf with congenital cardiac malformation and carpus valgus.

Chang He, Llorenç Grau-Roma, Robin Schmid, Irene M Häfliger, Mireille Meylan, Cord Drögemüller, Joana G P Jacinto

Abstract readCase Reports
In one paragraph

Article in Animal genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Chang HeInstitute of Animal Pathology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.
Llorenç Grau-RomaInstitute of Animal Pathology, Vetsuisse Faculty, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0000-0002-9406-8844
Robin SchmidClinic for Ruminants, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0009-0003-6678-4661
Irene M HäfligerInstitute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0000-0002-5648-963X
Mireille MeylanClinic for Ruminants, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0000-0003-0191-5686
Cord DrögemüllerInstitute of Genetics, Vetsuisse Faculty, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0000-0001-9773-522X
Joana G P JacintoClinic for Ruminants, Department of Clinical Veterinary Medicine, Vetsuisse Faculty, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0000-0002-6438-7975

Funding

Arbeitsgemeinschaft Schweizerischer Rinderzüchter (ASR), Zollikofen, SwitzerlandFederal Office for Agriculture (FOAG), Bern, Switzerland
6 · The paper itself

Abstract

Congenital malformations in cattle pose a diagnostic challenge with limited treatment options and are often associated with a guarded prognosis. The aim of this study was to characterize the clinicopathological phenotype of a viable calf with complex congenital heart defects and carpus valgus, and to identify a possible genetic cause using a whole genome sequencing trio approach. A 3-month-old female Holstein calf was referred for respiratory distress and congenital carpal deviation. Clinicopathologic findings included ventricular septal defect, ventricular dilatation, atrioventricular valve dysplasia, an overriding aorta, and unilateral carpus valgus. Genetic analysis revealed a private heterozygous missense variant in BRI3BP affecting an evolutionarily conserved residue (c.478G>A; p.Val160Ile). The variant was predicted to be deleterious and was present only in the affected calf and was absent in more than 5100 sequenced bovine genomes, including both parents, indicating a de novo origin. This study implicates an important role for the uncharacterized BRI3 binding protein in cardiac and possibly also bone development. By presenting the first BRI3BP-related disease model, this study demonstrates the potential to gain new insights into the function of individual genes by using phenotypically well-studied spontaneous mutants in large animals, and it provides a novel candidate gene for similar conditions in humans.

Indexed as

Cattle DiseasesHeart Defects, CongenitalMutation, MissenseNeoplasm ProteinsAnimalsCattleFemalePhenotypeNeoplasm ProteinsBRI3 binding proteincattlecongenital heart defectlarge animal modelprecision medicineventricular septal defect

Identifiers

PMID39593234
PMCPMC11666921

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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.