Altered subcellular distribution and activity of protein kinase C (PKC) is associated with transmembrane signalling in a variety of systems in which receptor occupancy leads to increased hydrolysis of polyphosphoinositides. Here we report evidence that in B lymphocytes, cyclic-cAMP-generating signal transduction pathways can activate translocation of PKC from the cytosol to the nucleus. Elevated cAMP levels and translocation of PKC to the nucleus are induced by antibodies against Ia antigens in normal B lymphocytes. Further, cAMP analogues mediate the translocation of PKC to the nucleus of these cells. These findings suggest that in physiological situations, ligation of B-lymphocyte Ia molecules by helper T cells leads to increased cAMP production which in turn causes PKC translocation to the nucleus. In view of recent observations that antibodies against Ia antigens induce differentiation of B cells, we conclude that nuclear PKC may function in the regulation of gene expression.
During the development of a system, software modules can be viewed in terms of their commitments: the constraints imposed by their own structure and behavior, and by their relationships with other modules in terms of resource consumption, data requirements, etc.. The Comet system uses explicit representation and reasoning with commitments to aid the software design and development process in particular, to lead software developers to make decisions that result in reuse. Developers can examine the commitments that must be met in order to include an existing module, and can explore how commitments change when modules are modi ed. Comet has been applied to the domain of sensor-based tracker software.
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