ArticleProceedings of the National Academy of Sciences of the United States of America2004
Inositol (1,4,5) trisphosphate 3 kinase B controls positive selection of T cells and modulates Erk activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- Suppression of ITPKB degradation by Trim25 confers TMZ resistance in glioblastoma through ROS homeostasis.Signal transduction and targeted therapy · 2024Article
- Increased Levels of the Parkinson's Disease-Associated Gene ITPKB Correlate with Higher Expression Levels of α-Synuclein, Independent of Mutation Status.International journal of molecular sciences · 2023Article
- Activation of the MAPK pathway mediates resistance to PI3K inhibitors in chronic lymphocytic leukemia.Blood · 2021Article
- Inositol 1,4,5-trisphosphate 3-kinase B promotes CaScience signaling · 2021Article
- Kinase Inhibition as Treatment for Acute and Chronic Graft-Frontiers in immunology · 2021Review
- Severe combined immunodeficiency caused by inositol-trisphosphate 3-kinase B (ITPKB) deficiency.The Journal of allergy and clinical immunology · 2020Article
- Article
- Beyond the CRAC: Diversification of ion signaling in B cells.Immunological reviews · 2019Review
- Role of miRNAs in Alzheimer's Disease and Possible Fields of Application.International journal of molecular sciences · 2019Review
- Inositol-triphosphate 3-kinase B confers cisplatin resistance by regulating NOX4-dependent redox balance.The Journal of clinical investigation · 2019Article
- Regulation of Hematopoietic Cell Development and Function Through Phosphoinositides.Frontiers in immunology · 2018Review
- miR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain.EMBO molecular medicine · 2016Article
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- Article
- Molecular control of PtdIns(3,4,5)P3 signaling in neutrophils.EMBO reports · 2015Review
- Article
- Lipid and Protein Co-Regulation of PI3K Effectors Akt and Itk in Lymphocytes.Frontiers in immunology · 2015Review
- Regulation of the transcriptional program by DNA methylation during human αβ T-cell development.Nucleic acids research · 2015Article
- Calmodulin and PI(3,4,5)P₃ cooperatively bind to the Itk pleckstrin homology domain to promote efficient calcium signaling and IL-17A production.Science signaling · 2014Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms governing positive selection of T cells in the thymus are still incompletely understood. Here, we describe a N-ethyl-N-nitrosourea induced recessive mouse mutant, Ms. T-less, which lacks T cells in the peripheral blood because of a complete block of thymocyte development at the CD4(+)CD8(+) stage. Single nucleotide polymorphism mapping and candidate gene sequencing revealed a nonsense mutation in the inositol (1,4,5) trisphosphate 3 kinase B (Itpkb) gene in Ms. T-less mice. Accordingly, Ms. T-less thymocytes do not show detectable expression of Itpkb protein and have drastically reduced basal inositol (1,4,5) trisphosphate kinase activity. Itpkb converts inositol (1,4,5) trisphosphate to inositol (1,3,4,5) tetrakisphosphate, soluble second messengers that have been implicated in Ca(2+) signaling. Surprisingly, Ca(2+) responses show no significant differences between wild type (WT) and mutant thymocytes. However, extracellular signal-regulated kinase (Erk) activation in response to suboptimal antigen receptor stimulation is attenuated in Ms. T-less thymocytes, suggesting a role for Itpkb in linking T cell receptor signaling to efficient and sustained Erk activation.
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