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- W2337873670 abstract "Mutation of Bruton's tyrosine kinase (Btk) causes human X-linke( agammaglobulinemia and murine X-linked immunodeficiency syn drome (xid). Quantitative aspects of B lymphocyte developmen and function have been demonstrated to depend on Btk level ii vivo by using a murine transgenic model system. A sensitivi intracellular immunofluorescent assay was developed to measur Btk protein on a per cell basis to test the hypothesis that its dosag< is dynamically regulated during B cell development or functiona responses. Marrow-derived hematopoietic stem cells, commoi lymphoid progenitor cells, and developing B and myeloid lineage expressed Btk protein at comparable levels. Resting peripheral I lineage cells had a significantly lower amount of Btk than marrow derived cells in both wild-type and xid mice. Activation of the B cel antigen receptor up-regulated Btk protein level 10-fold withii several hours by a phosphatidylinositol 3-kinase-dependent, post transcriptional mechanism. In contrast, the protein level of Btl R28C in activated B lymphocytes from xid mice remained lovv Bypass of the antigen receptor signaling pathways by treatment o cells with phorbol myristic acid and ionomycin rescued up-regula tion of Btk protein in xid splenic B cells. These combined result suggest that certain receptor signals mediated by Btk regulate th( level of expression of Btk protein in responding B lymphocytes tl potentiate signal transduction. Dynamic regulation of Btk proteii dosage is an additional mechanism to modulate B lymphocyti immune functions." @default.
- W2337873670 created "2016-06-24" @default.
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- W2337873670 date "2016-01-01" @default.
- W2337873670 modified "2023-09-24" @default.
- W2337873670 title "Posttranscriptional regulal kinase expression in antig splenic B cells" @default.
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