ArticleFrontiers in immunology2019
Cytoskeletal Protein 4.1R Is a Positive Regulator of the FcεRI Signaling and Chemotaxis in Mast Cells.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Cytoskeletal Protein 4.1R Inhibits BCR-Mediated B-Cell Activation by Restraining AKT1 Phosphorylation.Cells · 2026Article
- Article
- Tropomodulin1 exacerbates inflammatory response in macrophages by negatively regulating LPS-induced TLR4 endocytosis.Cellular and molecular life sciences : CMLS · 2024Article
- [Effect of deletion of protein 4.1R on proliferation, apoptosis and glycolysis of hepatocyte HL-7702 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Cytoskeletal Protein 4.1R in Health and Diseases.Biomolecules · 2024Review
- Regulation of microtubule nucleation in mouse bone marrow-derived mast cells by ARF GTPase-activating protein GIT2.Frontiers in immunology · 2024Article
- The Role of Cytoskeleton Protein 4.1 in Immunotherapy.International journal of molecular sciences · 2023Review
- Genome-wide analysis of dysregulated RNA-binding proteins and alternative splicing genes in keloid.Frontiers in genetics · 2023Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein 4.1R, a member of the 4.1 family, functions as a bridge between cytoskeletal and plasma membrane proteins. It is expressed in T cells, where it binds to a linker for activation of T cell (LAT) family member 1 and inhibits its phosphorylation and downstream signaling events after T cell receptor triggering. The role of the 4.1R protein in cell activation through other immunoreceptors is not known. In this study, we used 4.1R-deficient (4.1R-KO) and 4.1R wild-type (WT) mice and explored the role of the 4.1R protein in the high-affinity IgE receptor (FcεRI) signaling in mast cells. We found that bone marrow mast cells (BMMCs) derived from 4.1R-KO mice showed normal growth
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Registered trials
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