ArticleProceedings of the National Academy of Sciences of the United States of America2001
Activated Cdc42/Rac reconstitutes Fcepsilon RI-mediated Ca2+ mobilization and degranulation in mutant RBL mast cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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.
Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
- RhoGDI in RBL-2H3 cells acts as a negative regulator of Rho GTPase signaling to inhibit granule exocytosis.Journal of leukocyte biology · 2024Article
- Inhibiting Isoprenylation Suppresses FcεRI-Mediated Mast Cell Function and Allergic Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Novel mediator in anaphylaxis: decreased levels of miR-375-3p in serum and within extracellular vesicles of patients.Frontiers in immunology · 2023Article
- Cell division cycle 42 reflects disease risk, symptoms, Th1/Th2 disproportion, and its short-term variation indicates symptom amelioration after treatment in allergic rhinitis patients.Journal of clinical laboratory analysis · 2022Article
- Review
- Mast cell granule motility and exocytosis is driven by dynamic microtubule formation and kinesin-1 motor function.PloS one · 2022Article
- Myo1f, an Unconventional Long-Tailed Myosin, Is a New Partner for the Adaptor 3BP2 Involved in Mast Cell Migration.Frontiers in immunology · 2019Article
- Roles for lipid heterogeneity in immunoreceptor signaling.Biochimica et biophysica acta · 2016Review
- Roles for Ca2+ mobilization and its regulation in mast cell functions: recent progress.Biochemical Society transactions · 2016Review
- Activation of Cdc42 is necessary for sustained oscillations of Ca2+ and PIP2 stimulated by antigen in RBL mast cells.Biology open · 2014Article
- Mast cell mediators: their differential release and the secretory pathways involved.Frontiers in immunology · 2014Review
- Gene targeting implicates Cdc42 GTPase in GPVI and non-GPVI mediated platelet filopodia formation, secretion and aggregation.PloS one · 2011Article
- Effects of 7,8-dihydro-8-oxo-deoxyguanosine on antigen challenge in ovalbumin-sensitized mice may be mediated by suppression of Rac.British journal of pharmacology · 2009Article
- Rac1 modulates stimulus-evoked Ca(2+) release in neuronal growth cones via parallel effects on microtubule/endoplasmic reticulum dynamics and reactive oxygen species production.Molecular biology of the cell · 2009Article
- Article
- Primary granule exocytosis in human neutrophils is regulated by Rac-dependent actin remodeling.American journal of physiology. Cell physiology · 2008Article
- Clostridium difficile toxins A and B directly stimulate human mast cells.Infection and immunity · 2007Article
- Roles of Rac and p38 kinase in the activation of cytosolic phospholipase A2 in response to PMA.The Biochemical journal · 2005Article
- Mast cells. Receptors, secretagogues, and signaling.Clinical reviews in allergy & immunology · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Antigen stimulation of mast cells via FcepsilonRI, the high-affinity receptor for IgE, triggers a signaling cascade that requires Ca(2+) mobilization for exocytosis of secretory granules during an allergic response. This study investigates critical signaling components by using mutant RBL mast cells that are defective in antigen-stimulated phospholipase Cgamma (PLCgamma) activation, as well as other signaling activities downstream of stimulated tyrosine phosphorylation. We show that the expression of activated versions of the Cdc42 or Rac1 GTPase restores antigen-stimulated Ca(2+) mobilization necessary for degranulation in these mutant cells. Wild-type Cdc42 and Rac1, as well as activated Cdc42 containing effector domain mutations, all fail to restore antigen-stimulated signaling leading to exocytosis. Expression of oncogenic Dbl, a guanine nucleotide exchange factor for Cdc42 and Rac1, partially restores sustained Ca(2+) mobilization and degranulation, suggesting that activation of endogenous Cdc42 and/or Rac1 is impaired in the mutant cells. Overexpression of PLCgamma1 with either activated Cdc42 or Rac1 synergistically stimulates degranulation, consistent with a critical defect in PLCgamma activation in these cells. Thus, our results point to activation of Cdc42 and/or Rac1 playing an essential role in antigen stimulation of early events that culminate in mast cell degranulation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.