ArticleJournal of immunology (Baltimore, Md. : 1950)2012
The transcription factor Zeb2 regulates signaling in mast cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Transcriptional Regulation of Mouse Mast Cell Differentiation and the Role of Human Lung Mast Cells in Airway Inflammation.Immunological reviews · 2025Review
- Decoding the pathogenesis of spermatogenic failure in cryptorchidism through single-cell transcriptomic profiling.Cell reports. Medicine · 2024Article
- Mast Cell Activation Syndrome in COVID-19 and Female Reproductive Function: Theoretical Background vs. Accumulating Clinical Evidence.Journal of immunology research · 2022Review
- Puerarin Prevents Acute Liver InjuryFrontiers in pharmacology · 2021Article
- The Role of Mast Cells in Stroke.Cells · 2019Review
- Genetic Architectures of Childhood- and Adult-Onset Asthma Are Partly Distinct.American journal of human genetics · 2019Article
- ZEB Proteins in Leukemia: Friends, Foes, or Friendly Foes?HemaSphere · 2018Review
- ZEB2 Attenuates LPS-Induced Inflammation by the NF-κB Pathway in HK-2 Cells.Inflammation · 2018Article
- The transcriptional program, functional heterogeneity, and clinical targeting of mast cells.The Journal of experimental medicine · 2017Review
- MicroRNA-145 Increases the Apoptosis of Activated Hepatic Stellate Cells Induced by TRAIL through NF-κB Signaling Pathway.Frontiers in pharmacology · 2017Article
- Epigenetic and transcriptional control of mast cell responses.F1000Research · 2017Review
- The transcription factors ZEB2 and T-bet cooperate to program cytotoxic T cell terminal differentiation in response to LCMV viral infection.The Journal of experimental medicine · 2015Article
- Mast Cell: A Multi-Functional Master Cell.Frontiers in immunology · 2015Review
- Unique transcriptional profile of liver-resident memory CD8+ T cells induced by immunization with malaria sporozoites.Genes and immunityArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mast cell activation results in the release of stored and newly synthesized inflammatory mediators. We found that Zeb2 (also named Sip1, Zfhx1b), a zinc finger transcription factor, regulates both early and late mast cell responses. Transfection with small interfering RNA (siRNA) reduced Zeb2 expression and resulted in decreased FcεRI-mediated degranulation, with a parallel reduction in receptor-induced activation of NFAT and NF-κB transcription factors, but an enhanced response to the LPS-mediated activation of NF-κB. There was variable and less of a decrease in the Ag-mediated release of the cytokines TNF-α, IL-13, and CCL-4. This suggests that low Zeb2 expression differentially regulates signaling pathways in mast cells. Multiple phosphorylation events were impaired that affected molecules both at early and late events in the signaling pathway. The Zeb2 siRNA-treated mast cells had altered cell cycle progression, as well as decreased expression of several molecules including cell surface FcεRI and its β subunit, Gab2, phospholipase-Cγ1, and phospholipase-Cγ2, all of which are required for receptor-induced signal transduction. The results indicate that the transcription factor Zeb2 controls the expression of molecules thereby regulating signaling in mast cells.
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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.