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1 al, mucous neck, and chief cells, but not to enterochromaffin-like-cell.
2 th parietal cells and histamine release from enterochromaffin-like cells.
3 ndirectly by releasing histamine from fundic enterochromaffin-like cells.
5 e, with a decrease in number of parietal and enterochromaffin-like cells and an increase in number of
6 hormone-like hormone in histamine-secreting enterochromaffin-like cells and hepcidin in acid-secreti
7 irculating gastrin leads to proliferation of enterochromaffin-like cells and to the development of ga
8 tic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin cell popula
9 ance of the gastric mucosa, proliferation of enterochromaffin-like cells, and neoplastic transformati
10 ctivity was localized to the cell surface of enterochromaffin-like cells, and of myenteric and submuc
11 n, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in in
12 y regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and s
13 rboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia.
14 , parietal and zymogenic, but not for pit or enterochromaffin-like cell lineages in the oxyntic gastr
15 INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited
17 MAT2 alone is expressed in histamine-storing enterochromaffin-like cells of the oxyntic mucosa of the
19 s, including the role of hypergastrinemia on enterochromaffin-like cell proliferation and its relatio
21 for VMAT2 in the transport of histamine into enterochromaffin-like cell secretory vesicles, and with
23 the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a
24 ric neuroendocrine tumours (NETs) arise from enterochromaffin-like cells, which are located in oxynti
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