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Review
. 2000 Nov 21;97(24):12933-4.
doi: 10.1073/pnas.97.24.12933.

Calcium signaling and acute pancreatitis: specific response to a promiscuous messenger

A B Parekh  1
Affiliations
Review

Calcium signaling and acute pancreatitis: specific response to a promiscuous messenger

A B Parekh. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Figure 1
Figure 1
Model for calcium signaling after activation of cholecystokinin receptors. Low (physiological) levels of cholecystokinin utilize mainly the NAADP/cADPR pathway. Calcium release by cADPR acting on an open ryanodine-sensitive receptor exerts positive feedback on the receptor as well as adjacent ones, resulting in regenerative calcium-induced calcium release and thus oscillations in intracellular free calcium concentration. This pathway is shown in red. Calcium release by cADPR can also interact synergistically with InsP3 to facilitate further calcium release via open InsP3 receptors. However, physiological levels of cholecystokinin do not increase the levels of InsP3. Higher concentrations of cholecystokinin trigger a robust increase in InsP3, and this results in calcium mobilization from InsP3-sensitive calcium stores. The fall in calcium concentration within the stores activates store-operated calcium entry that underlies the sustained phase of the calcium signal under these conditions. This pathway is shown in blue. The calcium entry and not the oscillatory response results in the premature activation of trypsin within the zymogen granules.
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Comment on

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