Agonist mediated cell responses

Figure 3. Scheme of ceramidases regulation in agonist mediated cell responses. 

Vorderstrasse, B., Cundiff, J., and Lawrence, B.P., Developmental exposure to the potent aryl hydrocarbon receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs the cell-mediated immune response to infection with influenza A virus, but enhances elements of innate immunity, J. Immunotoxicol., 1, 103, 2004. 

For the 3 adrenoceptor, and many other serpentine receptors, 3-arrestin binding also accelerates endocytosis of receptors from the plasma membrane. Endocytosis of receptors promotes their dephosphorylation, by a receptor phosphatase that is present at high concentration on endosome membranes, and receptors then return to the plasma membrane. This helps explain the ability of cells to recover receptor-mediated signaling responsiveness very efficiently after agonist-induced desensitization. 

The dose level of -agonists affects the response obtained, the optimum dose often varies for the different production parameters measured. The mode of action of -agonists is poorly understood, but their interaction with membrane-bound receptors increases lipolysis in adipose cells and stimulates hypertrophy in muscle fibers. Although -agonists are known to stimulate the secretion of growth hormone and insulin, there is no direct evidence that these hormones mediate the tissue responses to the drug. 

All agonist-induced platelet responses, including shape change, aggregation, adhesion and secretion are inhibited by increased intracellular cAMP levels (1). Synthesis of cAMP in the platelet is stimulated by the binding of mediators, such as prostacyclin and adenosine, to cell surfece receptors ( ) coupled to GTP binding proteins (Fig. 1). 

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