Evidence map›Paper›PMID 22610094›Full record

ArticleThe Journal of biological chemistry2012

Annexin A1 interaction with the FPR2/ALX receptor: identification of distinct domains and downstream associated signaling.

Stefania Bena, Vincenzo Brancaleone, Ji Ming Wang, Mauro Perretti, Roderick J Flower

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

80 citing papers in PubMed, 140 citations in OpenAlex.

  1. Review
  2. Article
  3. More Than a Cleanup Crew: The Expanding Biology of Efferocytosis.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  4. Article
  5. Article
  6. M2 Macrophage-Derived Extracellular Vesicles Reprogram Immature Neutrophils into Anxa1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Review
  8. Article
  9. Bacterial and host interactions inFrontiers in microbiology · 2025
    Review
  10. Article
  11. Annexin A1 in the nervous and ocular systems.Neural regeneration research · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

20 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Stefania BenaWilliam Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Vincenzo Brancaleone
Ji Ming Wang
Mauro Perretti
Roderick J Flower
William Harvey Research Institute · GBCenter for Cancer Research · USQueen Mary University of London · GB

Funding

The Role of Cellular Receptors Involved in Inflammation and Tumor ProgressionZIABC010015 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 2009 to 2023
$6.3M
Wellcome Trust 086867/Z/08
6 · The paper itself

Abstract

Understanding how proresolving agonists selectively activate FPR2/ALX is a crucial step in the clarification of proresolution molecular networks that can be harnessed for the design of novel therapeutics for inflammatory disease. FPR2/ALX, a G protein-coupled receptor belonging to the formyl peptide receptor (FPR) family, conveys the biological functions of a variety of ligands, including the proresolution mediators annexin A1 (AnxA1) and lipoxin A(4), as well as the activating and proinflammatory protein serum amyloid A. FPR2/ALX is the focus of intense screening for novel anti-inflammatory therapeutics, and the small molecule compound 43 was identified as a receptor ligand. Here, we used chimeric FPR1 and FPR2/ALX clones (stably transfected in HEK293 cells) to identify the N-terminal region and extracellular loop II as the FPR2/ALX domain required for AnxA1-mediated signaling. Genomic responses were also assessed with domain-specific effects emerging, so the N-terminal region is required for AnxA1 induction of JAG1 and JAM3, whereas it is dispensable for modulation of SGPP2. By comparison, serum amyloid A non-genomic responses were reliant on extracellular loops I and II, whereas the small molecule compound 43 activated extracellular loop I with downstream signaling dependent on transmembrane region II. In desensitization experiments, the N-terminal region was dispensable for AnxA1-induced FPR2/ALX down-regulation in both the homologous and heterologous desensitization modes.

Indexed as

Annexin A1Blotting, WesternCalciumFlow CytometryHEK293 CellsHumansNeutrophilsProtein BindingProtein Structure, TertiaryReceptors, Formyl PeptideReceptors, LipoxinSerum Amyloid A ProteinSignal TransductionAnnexin A1CalciumFPR2 protein, humanReceptors, Formyl PeptideReceptors, LipoxinSerum Amyloid A Protein

Identifiers

PMID22610094
PMCPMC3397896
OpenAlexW2014462125

What OpenQuestion holds

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LicenceCC BY-NC
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.