ArticleBlood2011
The PI3K pathway drives the maturation of mast cells via microphthalmia transcription factor.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Berberine Inhibits Eczematous SkinInternational journal of molecular sciences · 2026Article
- Longitudinal analysis of influenza vaccination implicates regulation of RIG-I signaling by DNA methylation.Scientific reports · 2024Article
- ATP/IL-33-Co-Sensing by Mast Cells (MCs) Requires Activated c-Kit to Ensure Effective Cytokine Responses.Cells · 2023Article
- Fetal Tissue-Derived Mast Cells (MC) as Experimental Surrogate for In Vivo Connective Tissue MC.Cells · 2022Article
- Anaphylaxis: Focus on Transcription Factor Activity.International journal of molecular sciences · 2021Review
- Challenges and Opportunities for Drug Repositioning in Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Review
- The underestimated role of the microphthalmia-associated transcription factor (MiTF) in normal and pathological haematopoiesis.Cell & bioscience · 2021Review
- Second messenger ApNature communications · 2019Article
- Loss of epigenetic regulator TET2 and oncogenic KIT regulate myeloid cell transformation via PI3K pathway.JCI insight · 2018Article
- Peroxisome proliferator-activated receptor γ agonist suppresses mast cell maturation and induces apoptosis.Molecular medicine reports · 2017Article
- The endocytic pathway in microglia during health, aging and Alzheimer's disease.Ageing research reviews · 2016Review
- TAK1 and IKK2, novel mediators of SCF-induced signaling and potential targets for c-Kit-driven diseases.Oncotarget · 2015Article
- The role of Lin28b in myeloid and mast cell differentiation and mast cell malignancy.Leukemia · 2015Article
- A point mutation in the extracellular domain of KIT promotes tumorigenesis of mast cells via ligand-independent auto-dimerization.Scientific reports · 2015Article
- The CD20 homologue MS4A4 directs trafficking of KIT toward clathrin-independent endocytosis pathways and thus regulates receptor signaling and recycling.Molecular biology of the cell · 2015Article
- Identification of microRNAs regulating the developmental pathways of bone marrow derived mast cells.PloS one · 2014Article
- Unique and redundant roles of class IA PI3Kinase regulatory subunits in mast cell development.Cell cycle (Georgetown, Tex.) · 2013Article
- The role of SHIP in the development and activation of mouse mucosal and connective tissue mast cells.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Mast cell maturation is poorly understood. We show that enhanced PI3K activation results in accelerated maturation of mast cells by inducing the expression of microphthalmia transcription factor (Mitf). Conversely, loss of PI3K activation reduces the maturation of mast cells by inhibiting the activation of AKT, leading to reduced Mitf but enhanced Gata-2 expression and accumulation of Gr1(+)Mac1(+) myeloid cells as opposed to mast cells. Consistently, overexpression of Mitf accelerates the maturation of mast cells, whereas Gata-2 overexpression mimics the loss of the PI3K phenotype. Expressing the full-length or the src homology 3- or BCR homology domain-deleted or shorter splice variant of the p85α regulatory subunit of PI3K or activated AKT or Mitf in p85α-deficient cells restores the maturation but not growth. Although deficiency of both SHIP and p85α rescues the maturation of SHIP(-/-) and p85α(-/-) mast cells and expression of Mitf; in vivo, mast cells are rescued in some, but not all tissues, due in part to defective KIT signaling, which is dependent on an intact src homology 3 and BCR homology domain of p85α. Thus, p85α-induced maturation, and growth and survival signals, in mast cells can be uncoupled.
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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.