Evidence map›Paper›PMID 10662774›Full record

ArticleThe Journal of cell biology2000

Cdc42 and Rac stimulate exocytosis of secretory granules by activating the IP(3)/calcium pathway in RBL-2H3 mast cells.

E Hong-Geller, R A Cerione

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 145 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. MYO1F Regulates IgE and MRGPRX2-Dependent Mast Cell Exocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Rho GTPases in platelet function.Journal of thrombosis and haemostasis : JTH · 2013
    Review
  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

2 authors at 1 institution in 1 country.

E Hong-GellerDepartment of Molecular Medicine, Cornell University, Ithaca, New York 14853, USA.
R A Cerione
Cornell University · US

Funding

Roles of Cdc42 and its signaling partners in cell growth and differentiationR01GM047458 · NIGMS · CORNELL UNIVERSITY ITHACA · PI CERIONE, RICHARD A. · 1992 to 2016
$5.6M
NIGMS NIH HHS GM47458NIGMS NIH HHS R01 GM047458
6 · The paper itself

Abstract

We have expressed dominant-active and dominant-negative forms of the Rho GTPases, Cdc42 and Rac, using vaccinia virus to evaluate the effects of these mutants on the signaling pathway leading to the degranulation of secretory granules in RBL-2H3 cells. Dominant-active Cdc42 and Rac enhance antigen-stimulated secretion by about twofold, whereas the dominant-negative mutants significantly inhibit secretion. Interestingly, treatment with the calcium ionophore, A23187, and the PKC activator, PMA, rescues the inhibited levels of secretion in cells expressing the dominant-negative mutants, implying that Cdc42 and Rac act upstream of the calcium influx pathway. Furthermore, cells expressing the dominant-active mutants exhibit elevated levels of antigen-stimulated IP(3) production, an amplified antigen-stimulated calcium response consisting of both calcium release from internal stores and influx from the extracellular medium, and an increase in aggregate formation of the IP(3) receptor. In contrast, cells expressing the dominant-negative mutants display the opposite phenotypes. Finally, we are able to detect an in vitro interaction between Cdc42 and PLCgamma1, the enzyme immediately upstream of IP(3) formation. Taken together, these findings implicate Cdc42 and Rac in regulating the exocytosis of secretory granules by stimulation of IP(3) formation and calcium mobilization upon antigen stimulation.

Indexed as

Calcium SignalingAnimalsCalcium Channelscdc42 GTP-Binding ProteinCell DegranulationCell LineChlorocebus aethiopsCytoplasmic GranulesDinitrophenolsEgtazic AcidEnzyme ActivationExocytosisGene ExpressionGenetic VectorsGuanosine TriphosphateInositol 1,4,5-TrisphosphateCalcium Channelscdc42 GTP-Binding ProteinDinitrophenolsdinitrophenyl-bovine serum albuminEgtazic AcidGuanosine TriphosphateInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsIsoenzymesPhospholipase C gammaProtein Kinase Crac GTP-Binding ProteinsReceptors, Cytoplasmic and NuclearRecombinant Fusion ProteinsSerum Albumin, BovineType C Phospholipases

Identifiers

PMID10662774
PMCPMC2174803
OpenAlexW2132212780

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.