Evidence map›Paper›PMID 21741965›Full record

ArticleEuropean journal of pharmacology2011

G protein coupled receptor specificity for C3a and compound 48/80-induced degranulation in human mast cells: roles of Mas-related genes MrgX1 and MrgX2.

Sakeen W Kashem, Hariharan Subramanian, Sarah J Collington, Paola Magotti, John D Lambris, Hydar Ali

Open access · greenAbstract read
In one paragraph

Article in European journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed, 108 citations in OpenAlex.

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  8. Metabolic Consequences of IgE- and Non-IgE-Mediated Mast Cell Degranulation.Journal of immunology (Baltimore, Md. : 1950) · 2021
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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

6 authors at 1 institution in 1 country.

Sakeen W KashemDepartment of Pathology, School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States.
Hariharan Subramanian
Sarah J Collington
Paola Magotti
John D Lambris
Hydar Ali
University of Pennsylvania · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
G Protein Coupled Receptor Signaling in Mast CellsR01HL085774 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ALI, HYDAR · 2008 to 2011
$1.6M
Adapter molecules on C3a receptor signaling in mast cellsR56AI080852 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI ALI, HYDAR · 2009 to 2009
$358k
NHLBI NIH HHS HL085774NHLBI NIH HHS R01 HL085774NIAID NIH HHS AI068730NIAID NIH HHS AI080852NIAID NIH HHS P01 AI068730NIAID NIH HHS R56 AI080852
6 · The paper itself

Abstract

Although human mast cells express G protein coupled receptors for the anaphylatoxin C3a, previous studies indicated that C3a causes mast cell degranulation, at least in part, via a C3a receptor-independent mechanism similar to that proposed for polycationic molecules such as compound 48/80. The purpose of the present study was to delineate the receptor specificity of C3a-induced degranulation in human mast cells. We found that C3a, a C3a receptor "superagonist" (E7) and compound 48/80 induced Ca(2+) mobilization and degranulation in a differentiated human mast cell line, LAD2. However, C3a and E7 caused Ca(2+) mobilization in an immature mast cell line, HMC-1 but compound 48/80 did not. We have previously shown that LAD2 cells express MrgX1 and MrgX2 but HMC-1 cells do not. To delineate the receptor specificity for C3a and compound 48/80 further, we generated stable transfectants expressing MrgX1 and MrgX2 in a rodent mast cell line, RBL-2H3 cells. We found that compound 48/80 caused degranulation in RBL-2H3 cells expressing MrgX1 and MrgX2 but C3a did not. By contrast, E7 activated RBL-2H3 cells expressing MrgX2 but not MrgX1. These findings demonstrate that in contrast to previous reports, C3a and compound 48/80 do not use a shared mechanism for mast cell degranulation. It shows that while compound 48/80 utilizes MrgX1 and MrgX2 for mast cell degranulation C3a does not. It further reveals the novel finding that the previously characterized synthetic peptide, C3a receptor "superagonist" E7 activates human mast cells via two mechanisms; one involving the C3a receptor and the other MrgX2.

Indexed as

Amino Acid SequenceCell DegranulationCell LineComplement C3aHumansMast CellsMolecular Sequence DataNerve Tissue ProteinsPeptide Fragmentsp-Methoxy-N-methylphenethylamineProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledReceptors, NeuropeptideSubstrate SpecificityComplement C3amas-related gene-X1 receptor, humanMRGPRX2 protein, humanNerve Tissue ProteinsPeptide Fragmentsp-Methoxy-N-methylphenethylamineProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledReceptors, Neuropeptide

Identifiers

PMID21741965
PMCPMC3169012
OpenAlexW2162787809

What OpenQuestion holds

Textmetadata
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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.