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CAMP-induced influx

Fig. 5 Proposed signal transduction mechanisms that stimulate the pheromone biosynthetic pathway in Helicoverpa zea and Bombyx mori. It is proposed that PBAN binds to a G protein-coupled receptor present in the cell membrane that upon PBAN binding will induce a receptor-activated calcium channel to open causing an influx of extracellular calcium. This calcium binds to calmodulin and in the case of B. mori will directly stimulate a phosphatase that will dephosphorylate and activate a reductase in the biosynthetic pathway. In H. zea the calcium-calmodulin will activate adenylate cyclase to produce cAMP that will then act through kinases and/or phosphatases to stimulate acetyl-CoA carboxylase in the biosynthetic pathway... Fig. 5 Proposed signal transduction mechanisms that stimulate the pheromone biosynthetic pathway in Helicoverpa zea and Bombyx mori. It is proposed that PBAN binds to a G protein-coupled receptor present in the cell membrane that upon PBAN binding will induce a receptor-activated calcium channel to open causing an influx of extracellular calcium. This calcium binds to calmodulin and in the case of B. mori will directly stimulate a phosphatase that will dephosphorylate and activate a reductase in the biosynthetic pathway. In H. zea the calcium-calmodulin will activate adenylate cyclase to produce cAMP that will then act through kinases and/or phosphatases to stimulate acetyl-CoA carboxylase in the biosynthetic pathway...
The Di receptor is typically associated with the stimulation of adenylyl cyclase (Table 9-1) for example, Di-receptor-induced smooth muscle relaxation is presumably due to cAMP accumulation in the smooth muscle of those vascular beds in which dopamine is a vasodilator. D2 receptors have been found to inhibit adenylyl cyclase activity, open potassium channels, and decrease calcium influx. [Pg.175]

Soroker and Rafaeli, 1995). This confirmed that calcium is involved in pheromone biosynthesis and that there is a cross-talk between the two messengers, since the increase in calcium, as a result of the ionophores, induced the increase in cAMP. This reinforces the hypothesis that cAMP stimulation occurs downstream of the calcium influx (Jurenka et al., 1991c Soroker and Rafaeli, 1995). [Pg.120]

Liberation of fatty acids induced by phospholipases is connected with a decrease in the pH. We speculate therefore that this change in pH together with the change in cell wall organization induced by lysolecithins may cause the influx of Ca " ions into the cell, where Ca " -ions together with cAMP activate phosphorylation. [Pg.66]

Its primary action is inhibiting the release of GH from the pituitary gland. Somatostatin al.so suppresses the release of both insulin and glucagon. It causes a decrease in both cAMP levels and adenylate cyclase activity. It also inhibits calcium ion influx into the pituitary cells and suppresses glucose-induced pancreatic insulin secretion by activating and deactivating potassium ion and calcium ion permeability, respcc-tively. The chemistry. SARs, and potential clinical applications have been reviewed.--- ... [Pg.845]


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See also in sourсe #XX -- [ Pg.497 ]

See also in sourсe #XX -- [ Pg.25 , Pg.497 ]




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CAMP

Influx

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