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• W1858702144 startingPage "C1665" @default.
• W1858702144 abstract "β-Adrenergic receptor (βAR) activation and/or increases in cAMP regulate growth and proliferation of a variety of cells and, in some cells, promote cell death. In the current studies we addressed the mechanism of this growth reduction by examining βAR-mediated effects in the murine T-lymphoma cell line S49. Wild-type S49 cells, derived from immature thymocytes (CD4 + /CD8 + ) undergo growth arrest and subsequent death when treated with agents that increase cAMP levels (e.g., βAR agonists, 8-bromo-cAMP, cholera toxin, forskolin). Morphological and biochemical criteria indicate that this cell death is a result of apoptosis. In cyc − and kin − S49 cells, which lack G s α and functional protein kinase A (PKA), respectively, βAR activation of G s α and cAMP action via PKA are critical steps in this apoptotic pathway. S49 cells that overexpress Bcl-2 are resistant to cAMP-induced apoptosis. We conclude that βAR activation induces apoptosis in immature T lymphocytes via G s α and PKA, while overexpression of Bcl-2 prevents cell death. βAR/cAMP/PKA-mediated apoptosis may provide a means to control proliferation of immature T cells in vivo." @default.
• W1858702144 created "2016-06-24" @default.
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• W1858702144 date "2000-11-01" @default.
• W1858702144 modified "2023-10-10" @default.
• W1858702144 title "β-Adrenergic receptor/cAMP-mediated signaling and apoptosis of S49 lymphoma cells" @default.
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• W1858702144 doi "https://doi.org/10.1152/ajpcell.2000.279.5.c1665" @default.
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