Evidence map›Paper›PMID 30845214›Full record

ArticlePloS one2019

A novel nonsense variant in SUPT20H gene associated with Rheumatoid Arthritis identified by Whole Exome Sequencing of multiplex families.

Maëva Veyssiere, Javier Perea, Laetitia Michou, Anne Boland, Christophe Caloustian, Robert Olaso, Jean-François Deleuze, François Cornelis, Elisabeth Petit-Teixeira, Valérie Chaudru

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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Genome-wide association study of aromatase inhibitor discontinuation due to musculoskeletal symptoms.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022
    Trial
  2. Review
  3. Frontiers in genetics · 2024
    Article
  4. Article
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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 4 institutions in 2 countries.

Maëva VeyssiereGenHotel-Univ Evry, University of Paris Saclay, Evry, France.ORCID 0000-0001-8985-9257
Javier PereaGenHotel-Univ Evry, University of Paris Saclay, Evry, France.
Laetitia MichouDivision of Rheumatology, Department of Medicine, CHU de Québec-Université Laval, QC, Québec, Canada.ORCID 0000-0002-8364-4164
Anne BolandCentre National de Recherche en Génomique Humaine-François Jacob Institute, CEA, Evry, France.
Christophe CaloustianCentre National de Recherche en Génomique Humaine-François Jacob Institute, CEA, Evry, France.
Robert OlasoCentre National de Recherche en Génomique Humaine-François Jacob Institute, CEA, Evry, France.
Jean-François DeleuzeCentre National de Recherche en Génomique Humaine-François Jacob Institute, CEA, Evry, France.
François CornelisGenHotel-Auvergne-Auvergne University, Genetic Department, CHU Clermont-Ferrand, Clermont-Ferrand, France.
Elisabeth Petit-TeixeiraGenHotel-Univ Evry, University of Paris Saclay, Evry, France.
Valérie ChaudruGenHotel-Univ Evry, University of Paris Saclay, Evry, France.
Commissariat à l'Énergie Atomique et aux Énergies Alternatives · FRUniversité Paris-Saclay · FRUniversité Clermont Auvergne · FRUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The triggering and development of Rheumatoid Arthritis (RA) is conditioned by environmental and genetic factors. Despite the identification of more than one hundred genetic variants associated with the disease, not all the cases can be explained. Here, we performed Whole Exome Sequencing in 9 multiplex families (N = 30) to identify rare variants susceptible to play a role in the disease pathogenesis. We pre-selected 77 genes which carried rare variants with a complete segregation with RA in the studied families. Follow-up linkage and association analyses with pVAAST highlighted significant RA association of 43 genes (p-value < 0.05 after 106 permutations) and pinpointed their most likely causal variant. We re-sequenced the 10 most significant likely causal variants (p-value ≤ 3.78*10-3 after 106 permutations) in the extended pedigrees and 9 additional multiplex families (N = 110). Only one SNV in SUPT20H: c.73A>T (p.Lys25*), presented a complete segregation with RA in an extended pedigree with early-onset cases. In summary, we identified in this study a new variant associated with RA in SUPT20H gene. This gene belongs to several biological pathways like macro-autophagy and monocyte/macrophage differentiation, which contribute to RA pathogenesis. In addition, these results showed that analyzing rare variants using a family-based approach is a strategy that allows to identify RA risk loci, even with a small dataset.

Indexed as

AdultArthritis, RheumatoidAutophagyCell DifferentiationCodon, NonsenseExomeExome SequencingFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMacrophagesMaleMonocytesPedigreeTranscription FactorsCodon, NonsenseTranscription Factors

Identifiers

PMID30845214
PMCPMC6405192
OpenAlexW2950191394

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.