ArticlePloS one2014
Involvement of class II phosphoinositide 3-kinase α-isoform in antigen-induced degranulation in RBL-2H3 cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Distinct phosphoinositide signatures orchestrate FcεRI versus MRGPRX2 mast cell secretion.iScience · 2026Article
- An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022Article
- Antiallergic Activity of 6-Deoxy-2-Molecules (Basel, Switzerland) · 2021Article
- PI3KC2β inactivation stabilizes VE-cadherin junctions and preserves vascular integrity.EMBO reports · 2021Article
- A postsynaptic PI3K-cII dependent signaling controller for presynaptic homeostatic plasticity.eLife · 2018Article
- Anti-Allergic Activity of Monoacylated Ascorbic Acid 2-Glucosides.Molecules (Basel, Switzerland) · 2017Article
- Phosphatidlyinositol-3-kinase C2 beta (PI3KC2β) is a potential new target to treat IgE mediated disease.PloS one · 2017Article
- The Central Polybasic Region of the Soluble SNARE (Soluble N-Ethylmaleimide-sensitive Factor Attachment Protein Receptor) Vam7 Affects Binding to Phosphatidylinositol 3-Phosphate by the PX (Phox Homology) Domain.The Journal of biological chemistry · 2016Article
- Inactivation of class II PI3K-C2α induces leptin resistance, age-dependent insulin resistance and obesity in male mice.Diabetologia · 2016Article
- Inactivation of the Class II PI3K-C2β Potentiates Insulin Signaling and Sensitivity.Cell reports · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we present findings that suggest that PI3K-C2α, a member of the class II phosphoinositide 3-kinase (PI3K) subfamily, regulates the process of FcεRI-triggered degranulation. RBL-2H3 cells were transfected with shRNA targeting PI3K-C2α. The knockdown impaired the FcεRI-induced release of a lysosome enzyme, β-hexosaminidase, without affecting the intracellular Ca2+ mobilization. The release of mRFP-tagged neuropeptide-Y, a reporter for the regulated exocytosis, was also decreased in the PI3K-C2α-deficient cells. The release was increased significantly by the expression of the siRNA-resistant version of PI3K-C2α. In wild-type cells, FcεRI stimulation induced the formation of large vesicles, which were associated with CD63, a marker protein of secretory granules. On the vesicles, the existence of PI3K-C2α and PtdIns(3,4)P2 was observed. These results indicated that PI3K-C2α and its product PtdIns(3,4)P2 may play roles in the secretory process.
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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.