Bruton's tyrosine kinase controls a sustained calcium signal essential for B lineage development and function
Genetic data support a role for Btk during the B lineage development transitions regulated by signaling through both the pre-B and the B cell antigen receptors. Dysregulated signaling at each of these transitions can result in failure of these cell populations to proliferate and subsequent cell deat...
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 91(1999), 3 vom: 01. Juni, Seite 243-53 |
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| 1. Verfasser: | |
| Format: | Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
1999
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| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Review Receptors, Antigen, B-Cell Protein-Tyrosine Kinases EC 2.7.10.1 Agammaglobulinaemia Tyrosine Kinase EC 2.7.10.2 BTK protein, human |
| Zusammenfassung: | Genetic data support a role for Btk during the B lineage development transitions regulated by signaling through both the pre-B and the B cell antigen receptors. Dysregulated signaling at each of these transitions can result in failure of these cell populations to proliferate and subsequent cell death. Btk-dependent IP3 production is crucial for maintaining the sustained calcium signal in response to BCR engagement and is likely to regulate a subset of transcriptional events essential for B lineage growth or survival. Identification of these Btk-dependent signals will be important in understanding B cell activation, differentiation, and cell death. This information may lead to therapies specifically targeting these events in B cell autoimmunity or malignancy and provide a fuller understanding of the appropriate target populations and potential negative consequences of Btk gene therapy in XLA. Identification of Btk/Tec family kinases in an increasing number of vertebrate and invertebrate cell lineages suggests that the link between Btk and the PLC gamma/IP3/calcium signaling pathways may be broadly conserved |
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| Beschreibung: | Date Completed 25.06.1999 Date Revised 24.02.2022 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |