Search for dissertations about: "Brutons tyrosine kinase"
Showing result 1 - 5 of 10 swedish dissertations containing the words Brutons tyrosine kinase.
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1. Subcellular localization and signalling of Brutons tyrosine kinase (Btk)
Abstract : Brutons tyrosine kinase (Btk) is a non-receptor tyrosine kinase related to the Src family of kinases. Mutations in various parts of the gene have been shown to cause X-linked agammaglobulinemia (XLA), a primary immunodeficiency in humans, characterized by a defect in B-cell development. READ MORE
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2. Structure and function of the SH3 domain from Bruton´s tyrosine kinase
Abstract : .... READ MORE
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3. Molecular dissection of Bruton’s tyrosine kinase signaling in hematopoietic cells using RNAi
Abstract : RNA mediated gene silencing, RNA interference (RNAi), has recently been identified in mammalians. This thesis describes the utilization and development of RNAi based tools for signal transduction research. The effects of Bruton s tyrosine kinase (Btk) down-regulation with RNAi have been studied with gene expression profiling in hematopoietic cells. READ MORE
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4. Characterization of ankyrin repeat domain 54 (ANKRD54) and its role on the regulation and subcellular localization of Bruton’s tyrosine kinase (BTK)
Abstract : Bruton's tyrosine kinase (BTK) is an important cytoplasmic signaling protein, where the kinase activity plays a pivotal role in the development, proliferation and differentiation of B-cell lineages. Ankyrin repeat domain 54 (ANKRD54) is a nuclear-resident adaptor protein, where the ankyrin domain repeats are critical for specific protein-protein interaction, while the NLS and NES motifs control the nucleo-cytoplasmic shuttling ability. READ MORE
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5. Transcription factors regulating the Btk promoter
Abstract : Bruton's agammaglobulinemia tyrosine kinase (Btk) is a cytoplasmic tyrosine kinase-related to the Src family of kinases. Mutations in various parts of the gene have been shown to lead to X-linked agammaglobulinemia, an immunodeficiency disease which is characterized by a defect in B-cell development. READ MORE