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Epidermal growth factor: intracellular Ca 2+ inhibits its association with pancreatic acini and A431 cells
Author(s) -
Logsdon Craig D.,
Williams John A.
Publication year - 1983
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(83)80312-3
Subject(s) - epidermal growth factor , cholecystokinin , secretagogue , intracellular , bombesin , carbachol , endocrinology , medicine , cholinergic , chemistry , growth factor , biology , microbiology and biotechnology , biochemistry , neuropeptide , receptor , secretion , stimulation
The uptake of 125 I‐labeled epidermal growth factor ( 125 I‐EGF) by mouse pancreatic acini was inhibited (40–50%) by the secretagogue cholecystokinin octapeptide (CCK 8 ). Analysis of competitive binding data showed that the apparent K d of EEG binding increased 135% while the binding capacity was only slightly altered (30% increase). That the effect of CCK 8 on acini was mediated by intracellular Ca 2+ was indicated by the following: (i) Inhibition of 125 I‐EGF binding to acini was dose‐dependent and paralleled the known abilities of CCK 8 , its analogs, and the cholinergic secretagogue carbachol to induce Ca 2+ efflux from acini; and (ii) addition of the Ca 2+ ionophore A23187 also inhibited 125 I‐EGF binding. In addition, EGF association with A431 cells was also inhibited by A23187 in the presence but not the absence of Ca 2+ .