Evidence map›Paper›PMID 34195596›Full record

ArticleMatrix biology plus2021

A new mouse mutant with cleavage-resistant versican and isoform-specific versican mutants demonstrate that proteolysis at the Glu

Sumeda Nandadasa, Cyril Burin des Roziers, Christopher Koch, Karin Tran-Lundmark, María T Dours-Zimmermann, Dieter R Zimmermann, Sophie Valleix, Suneel S Apte

Open access · goldAbstract read
In one paragraph

Article in Matrix biology plus, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. An Overview of ADAMTS Proteases.Methods in molecular biology (Clifton, N.J.) · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Proteolysis: a key post-translational modification regulating proteoglycans.American journal of physiology. Cell physiology · 2022
    Review
  9. Article
  10. Defining the versican interactome in lung health and disease.American journal of physiology. Cell physiology · 2022
    Review
  11. Article
  12. Article
  13. 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

8 authors at 4 institutions in 4 countries.

Sumeda NandadasaDepartment of Biomedical Engineering-ND20, Cleveland Clinic Lerner Research Institute, 9500 Euclid Avenue, Cleveland, OH 44195, United States.
Cyril Burin des RoziersInstitut Cochin, Inserm U1016 - CNRS UMR8104 - Paris Descartes University Medical School, 24, Rue du faubourg Saint Jacques, 75014 Paris, France.
Christopher KochDepartment of Biomedical Engineering-ND20, Cleveland Clinic Lerner Research Institute, 9500 Euclid Avenue, Cleveland, OH 44195, United States.
Karin Tran-LundmarkDepartment of Experimental Medical Science and Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden.
María T Dours-ZimmermannDepartment of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.
Dieter R ZimmermannDepartment of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.
Sophie ValleixInstitut Cochin, Inserm U1016 - CNRS UMR8104 - Paris Descartes University Medical School, 24, Rue du faubourg Saint Jacques, 75014 Paris, France.
Suneel S ApteDepartment of Biomedical Engineering-ND20, Cleveland Clinic Lerner Research Institute, 9500 Euclid Avenue, Cleveland, OH 44195, United States.
Cleveland Clinic Lerner College of Medicine · USCentre National de la Recherche Scientifique · FRUniversity Hospital of Zurich · CHLund University · SE

Funding

VERSICAN PROTEOLYSIS AND REGULATION OF VASCULAR SMOOTH MUSCLEP01HL107147 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI LAUER, MARK E · 2011 to 2017
$16.1M
NHLBI NIH HHS P01 HL107147
6 · The paper itself

Abstract

Two inherent challenges in the mechanistic interpretation of protease-deficient phenotypes are defining the specific substrate cleavages whose reduction generates the phenotypes and determining whether the phenotypes result from loss of substrate function, substrate accumulation, or loss of a function(s) embodied in the substrate fragments. Hence, recapitulation of a protease-deficient phenotype by a cleavage-resistant substrate would stringently validate the importance of a proteolytic event and clarify the underlying mechanisms. Versican is a large proteoglycan required for development of the circulatory system and proper limb development, and is cleaved by ADAMTS proteases at the Glu

Indexed as

ADAMTSExtracellular matrixLimb developmentMetalloproteaseProteoglycanSyndactyly

Identifiers

PMID34195596
PMCPMC8233476
OpenAlexW3160885242

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.