Evidence map›Paper›PMID 30083158›Full record

ArticleFrontiers in immunology2018

Functional Characterization of Alternative and Classical Pathway C3/C5 Convertase Activity and Inhibition Using Purified Models.

Seline A Zwarthoff, Evelien T M Berends, Sanne Mol, Maartje Ruyken, Piet C Aerts, Mihály Józsi, Carla J C de Haas, Suzan H M Rooijakkers, Ronald D Gorham

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025
    Review
  8. Functional Characterization of Anti-C3bBb Autoantibodies and C3 Glomerulopathy Phenotype.Journal of the American Society of Nephrology : JASN · 2025
    Article
  9. Article
  10. Article
  11. The Complement System.Advances in experimental medicine and biology · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024
    Review
  16. Novel Role of theInternational journal of molecular sciences · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. The human factor H protein family - an update.Frontiers in immunology · 2024
    Review
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 3 institutions in 2 countries.

Seline A ZwarthoffDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Evelien T M BerendsDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Sanne MolDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Maartje RuykenDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Piet C AertsDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Mihály JózsiDepartment of Immunology, ELTE Eötvös Loránd University, Budapest, Hungary.
Carla J C de HaasDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Suzan H M RooijakkersDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Ronald D GorhamDepartment of Medical Microbiology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
University Medical Center Utrecht · NLUtrecht University · NLEötvös Loránd University · HU

Funding

European Research Council 639209
6 · The paper itself

Abstract

Complement is essential for the protection against infections; however, dysregulation of complement activation can cause onset and progression of numerous inflammatory diseases. Convertase enzymes play a central role in complement activation and produce the key mediators of complement: C3 convertases cleave C3 to generate chemoattractant C3a and label target cells with C3b, which promotes phagocytosis; C5 convertases cleave C5 into chemoattractant C5a, and C5b, which drives formation of the membrane attack complex. Since convertases mediate nearly all complement effector functions, they are ideal targets for therapeutic complement inhibition. A unique feature of convertases is their covalent attachment to target cells, which effectively confines complement activation to the cell surface. However, surface localization precludes detailed analysis of convertase activation and inhibition. In our previous work, we developed a model system to form purified alternative pathway (AP) C5 convertases on C3b-coated beads and quantify C5 conversion

Indexed as

complementcomplement therapeuticsconvertase enzymesinflammatory diseaseinnate immunitymulti-molecular proteases

Identifiers

PMID30083158
PMCPMC6064732
OpenAlexW2883602848

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.