Evidence map›Paper›PMID 25339693›Full record

ArticleOpen biology2014

Understanding the functional difference between growth arrest-specific protein 6 and protein S: an evolutionary approach.

Romain A Studer, Fred R Opperdoes, Gerry A F Nicolaes, André B Mulder, René Mulder

Open access · goldAbstract read
In one paragraph

Article in Open biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Protein S Protects against Podocyte Injury in Diabetic Nephropathy.Journal of the American Society of Nephrology : JASN · 2018
    Article
  10. Mouse macrophages show different requirements for phosphatidylserine receptor Tim4 in efferocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  11. 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

5 authors at 4 institutions in 3 countries.

Romain A StuderEuropean Molecular Biology Laboratory-European Bioinformatics Institute (EMBL-EBI), Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK.
Fred R OpperdoesLaboratory of Biochemistry, de Duve Institute and Université catholique de Louvain, Brussels 1200, Belgium.
Gerry A F NicolaesDepartment of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
André B MulderDepartment of Laboratory Medicine, University Medical Centre Groningen, Groningen, The Netherlands.
René MulderDepartment of Laboratory Medicine, University Medical Centre Groningen, Groningen, The Netherlands r.mulder01@umcg.nl.
University Medical Center Groningen · NLde Duve Institute · BEEuropean Bioinformatics Institute · GBMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although protein S (PROS1) and growth arrest-specific protein 6 (GAS6) proteins are homologous with a high degree of structural similarity, they are functionally different. The objectives of this study were to identify the evolutionary origins from which these functional differences arose. Bioinformatics methods were used to estimate the evolutionary divergence time and to detect the amino acid residues under functional divergence between GAS6 and PROS1. The properties of these residues were analysed in the light of their three-dimensional structures, such as their stability effects, the identification of electrostatic patches and the identification potential protein-protein interaction. The divergence between GAS6 and PROS1 probably occurred during the whole-genome duplications in vertebrates. A total of 78 amino acid sites were identified to be under functional divergence. One of these sites, Asn463, is involved in N-glycosylation in GAS6, but is mutated in PROS1, preventing this post-translational modification. Sites experiencing functional divergence tend to express a greater diversity of stabilizing/destabilizing effects than sites that do not experience such functional divergence. Three electrostatic patches in the LG1/LG2 domains were found to differ between GAS6 and PROS1. Finally, a surface responsible for protein-protein interactions was identified. These results may help researchers to analyse disease-causing mutations in the light of evolutionary and structural constraints, and link genetic pathology to clinical phenotypes.

Indexed as

AlgorithmsAmino AcidsAnimalsBinding SitesBlood ProteinsCiona intestinalisComputational BiologyDatabases, ProteinEvolution, MolecularGlycosylationGrowth Arrest-Specific Protein 6HumansIntercellular Signaling Peptides and ProteinsMutationPhenotypePhylogenyAmino AcidsBlood ProteinsGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsPROS1 protein, humanProtein Sevolutiongrowth arrest-specific protein 6protein S

Identifiers

PMID25339693
PMCPMC4221892
OpenAlexW2120702845

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.