ArticleThe Journal of experimental medicine2001
Essential role of the prosurvival bcl-2 homologue A1 in mast cell survival after allergic activation.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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Who cites it
40 citing papers in PubMed, 106 citations in OpenAlex.
- Unlocking the therapeutic potential of the NFAT pathway in kidney diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Absence of pro-survival A1 has no impact on inflammatory cell survival in vivo during acute lung inflammation and peritonitis.Cell death and differentiation · 2022Article
- Granule Leakage Induces Cell-Intrinsic, Granzyme B-Mediated Apoptosis in Mast Cells.Frontiers in cell and developmental biology · 2021Article
- Clemastine Fumarate Attenuates Myocardial Ischemia Reperfusion Injury Through Inhibition of Mast Cell Degranulation.Frontiers in pharmacology · 2021Article
- Anti-apoptotic A1 is not essential for lymphoma development in Eµ-Myc mice but helps sustain transplanted Eµ-Myc tumour cells.Cell death and differentiation · 2018Article
- Controlling Mast Cell Activation and Homeostasis: Work Influenced by Bill Paul That Continues Today.Frontiers in immunology · 2018Review
- Characterisation of mice lacking all functional isoforms of the pro-survival BCL-2 family member A1 reveals minor defects in the haematopoietic compartment.Cell death and differentiation · 2017Article
- Apoptotic resistance of human skin mast cells is mediated by Mcl-1.Cell death discovery · 2017Article
- Cell cycle and apoptosis regulation by NFAT transcription factors: new roles for an old player.Cell death & disease · 2016Review
- Conditional knockdown of BCL2A1 reveals rate-limiting roles in BCR-dependent B-cell survival.Cell death and differentiation · 2016Article
- Lessons from gain- and loss-of-function models of pro-survival Bcl2 family proteins: implications for targeted therapy.The FEBS journal · 2015Review
- Knockdown of the antiapoptotic Bcl-2 family member A1/Bfl-1 protects mice from anaphylaxis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Targeting the mitochondrial apoptotic pathway: a preferred approach in hematologic malignancies?Cell death & disease · 2014Review
- IgE induces proliferation in human airway smooth muscle cells: role of MAPK and STAT3 pathways.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2013Article
- Regulation of A1 by OX40 contributes to CD8(+) T cell survival and anti-tumor activity.PloS one · 2013Article
- MiR-146a and NF-κB1 regulate mast cell survival and T lymphocyte differentiation.Molecular and cellular biology · 2012Article
- A1/Bfl-1 in leukocyte development and cell death.Experimental cell research · 2012Review
- Targeting antiapoptotic A1/Bfl-1 by in vivo RNAi reveals multiple roles in leukocyte development in mice.Blood · 2012Article
- BCL2A1: the underdog in the BCL2 family.Cell death and differentiation · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mast cells reside in tissues, where upon activation through the high-affinity-IgE-receptor (FcepsilonRI) they degranulate and orchestrate the allergic reaction. Mast cells survive this activation and can thus be reactivated. In this study we demonstrate that this process depends on the pro-survival gene A1. Activation of mast cells through FcepsilonRI resulted in degranulation, strong induction of A1 mRNA and protein, and cell survival. In contrast, A1-deficient mast cells released granule mediators similar to the wild-type control, but the cells did not survive an allergic activation. Furthermore, A1(-/-) mice that had been sensitized and provoked with allergen exhibited a lower number of mast cell compared with littermate controls. The induction of A1 was dependent on calcium, as EDTA prevented A1 expression. The calcium ionophore, ionomycin, induced A1 expression and mast cell survival, whereas compound 48/80, a well-known mast cell secretagogue, did not. This study uncovers the importance of A1 for mast cell survival in allergic reactions, and it proposes A1 as a potential target for the treatment of allergic diseases.
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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.