ArticleThe Journal of experimental medicine1994
IL-5 receptor-mediated tyrosine phosphorylation of SH2/SH3-containing proteins and activation of Bruton's tyrosine and Janus 2 kinases.
Article in The Journal of experimental medicine, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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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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
49 citing papers in PubMed, 176 citations in OpenAlex.
- IL-5 antagonism reverses priming and activation of eosinophils in severe eosinophilic asthma.Mucosal immunology · 2024Article
- Eosinophils: old cells, new directions.Frontiers in medicine · 2024Review
- Enhanced CD19 activity in B cells contributes to immunodeficiency in mice deficient in the ICF syndrome gene Zbtb24.Cellular & molecular immunology · 2023Article
- Taking a Breather: Advances in Interleukin 5 Inhibition for Asthma Relief.International journal of molecular sciences · 2022Review
- Recent advances of eosinophils and its correlated diseases.Frontiers in public health · 2022Review
- Current Perspectives: Evidence to Date on BTK Inhibitors in the Management of Multiple Sclerosis.Drug design, development and therapy · 2022Review
- Targeting Bruton's Tyrosine Kinase in Inflammatory and Autoimmune Pathologies.Frontiers in cell and developmental biology · 2021Review
- The Trinity of Matrix Metalloproteinases, Inflammation, and Cancer: A Literature Review of Recent Updates.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2020Review
- Synergy of Interleukin (IL)-5 and IL-18 in eosinophil mediated pathogenesis of allergic diseases.Cytokine & growth factor reviews · 2019Review
- Integrated Cellular and Plasma Proteomics of Contrasting B-cell Cancers Reveals Common, Unique and Systemic Signatures.Molecular & cellular proteomics : MCP · 2017Article
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- Review
- Structural basis of interleukin-5 dimer recognition by its α receptor.Protein science : a publication of the Protein Society · 2012Article
- Identification of pro-inflammatory cytokines associated with muscle invasive bladder cancer; the roles of IL-5, IL-20, and IL-28A.PloS one · 2012Article
- Differential biological activity of disease-associated JAK2 mutants.FEBS letters · 2011Article
- Interleukin-5 and IL-5 receptor in health and diseases.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2011Review
- Naturally occurring Bruton's tyrosine kinase mutations have no dominant negative effect in an X-linked agammaglobulinaemia cellular model.Clinical and experimental immunology · 2008Article
- Article
- Bruton's tyrosine kinase regulates immunoglobulin promoter activation in association with the transcription factor Bright.Molecular and cellular biology · 2005Article
- Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness.The Journal of experimental medicine · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin 5 (IL-5) induces proliferation and differentiation of B cells and eosinophils by interacting with its receptor (IL-5R) which consists of two distinct polypeptide chains, alpha and beta (beta c). Although both IL-5R alpha and beta c lack a kinase catalytic domain, IL-5 is capable of inducing tyrosine phosphorylation of cellular proteins. We investigated the role of IL-5R alpha in tyrosine phosphorylation of molecules involved in IL-5 signal transduction, using an IL-5-dependent early B cell line, Y16 and transfectants expressing intact or mutant IL-5R alpha together with intact beta c. The results revealed that the transfectants expressing truncated IL-5R alpha, which entirely lacks a cytoplasmic domain, together with beta c, showed neither protein-tyrosine phosphorylation nor proliferation in response to IL-5. This confirms that IL-5R alpha plays a critical role in protein-tyrosine phosphorylation which triggers cell growth. IL-5 stimulation results in rapid tyrosine phosphorylation of beta c and proteins containing Src homology 2 (SH2) and/or SH3 domains such as phosphatidyl-inositol-3 kinase, Shc, Vav, and HS1, suggesting their involvement in IL-5-mediated signal transduction. IL-5 stimulation significantly enhanced activities of Janus 2 and B cell-specific Bruton's tyrosine kinases (JAK2 and Btk) and increased the tyrosine phosphorylation of JAK2 kinase. These results and recent data on signaling of growth factors taken together, multiple biochemical pathways driven by tyrosine kinases such as JAK2 and Btk are involved in IL-5 signal transduction.
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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.