Evidence map›Paper›PMID 18207701›Full record

ArticleCellular signalling2008

Synergistic activation of phospholipases Cgamma and Cbeta: a novel mechanism for PI3K-independent enhancement of FcepsilonRI-induced mast cell mediator release.

Hye Sun Kuehn, Michael A Beaven, Hong-Tao Ma, Mi-Sun Kim, Dean D Metcalfe, Alasdair M Gilfillan

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Inside-Out Control of Fc-Receptors.Frontiers in immunology · 2019
    Review
  5. Article
  6. Article
  7. Article
  8. Natural killer cell deficiency.The Journal of allergy and clinical immunology · 2013
    Review
  9. Phospholipase C-β in immune cells.Advances in biological regulation · 2013
    Review
  10. Review
  11. Article
  12. Article
  13. IL-33 induces a hyporesponsive phenotype in human and mouse mast cells.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Article
  14. Article
  15. Stem cell factor programs the mast cell activation phenotype.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Hye Sun KuehnLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892-1881, USA.
Michael A Beaven
Hong-Tao Ma
Mi-Sun Kim
Dean D Metcalfe
Alasdair M Gilfillan
National Heart Lung and Blood Institute · USNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

SECRETION OF MEDIATORS FROM MAST CELLSZ01HL000990 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI BEAVEN, MICHAEL A · 1987 to 2008
$1.6M
Integrated Signaling Pathways for the Enhancement of Mast Cell ActivationZ01AI000965 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI METCALFE, DEAN D · 2006 to 2008
$772k
Intramural NIH HHS Z01 AI000965
6 · The paper itself

Abstract

Antigen/IgE-mediated mast cell activation via FcvarepsilonRI can be markedly enhanced by the activation of other receptors expressed on mast cells and these receptors may thus contribute to the allergic response in vivo. One such receptor family is the G protein-coupled receptors (GPCRs). Although the signaling cascade linking FcvarepsilonRI aggregation to mast cell activation has been extensively investigated, the mechanisms by which GPCRs amplify this response are relatively unknown. To investigate this, we utilized prostaglandin (PG)E2 based on initial studies demonstrating its greater ability to augment antigen-mediated degranulation in mouse mast cells than other GPCR agonists examined. This enhancement, and the ability of PGE2 to amplify antigen-induced calcium mobilization, was independent of phosphoinositide 3-kinase but was linked to a pertussis toxin-sensitive synergistic translocation to the membrane of phospholipase (PL)Cgamma and PLCbeta and to an enhancement of PLCgamma phosphorylation. This "trans-synergistic" activation of PLCbeta and gamma, in turn, enhanced production of inositol 1,4,5-trisphosphate, store-operated calcium entry, and activation of protein kinase C (PKC) (alpha and beta). These responses were critical for the promotion of degranulation. This is the first report of synergistic activation between PLCgamma and PLCbeta that permits reinforcement of signals for degranulation in mast cells.

Indexed as

Cell DegranulationSignal TransductionAnimalsAntigensCalcium SignalingCell MembraneCells, CulturedCytokinesDinoprostoneEnzyme ActivationHypersensitivityInositol 1,4,5-TrisphosphateMacrophagesMiceMice, Inbred C57BLPertussis ToxinAntigensCytokinesDinoprostoneInositol 1,4,5-TrisphosphatePertussis ToxinPhosphatidylinositol 3-KinasesPhospholipase C betaPhospholipase C gammaProtein Kinase CProtein Kinase C-alphaProtein Kinase C betaReceptors, IgEReceptors, Prostaglandin E

Identifiers

PMID18207701
PMCPMC2692074
OpenAlexW1978243682

What OpenQuestion holds

Textmetadata
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.