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2 rboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia.
3 , parietal and zymogenic, but not for pit or enterochromaffin-like cell lineages in the oxyntic gastr
4 INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited
6 s, including the role of hypergastrinemia on enterochromaffin-like cell proliferation and its relatio
7 for VMAT2 in the transport of histamine into enterochromaffin-like cell secretory vesicles, and with
8 tic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin cell popula
10 e, with a decrease in number of parietal and enterochromaffin-like cells and an increase in number of
11 hormone-like hormone in histamine-secreting enterochromaffin-like cells and hepcidin in acid-secreti
12 irculating gastrin leads to proliferation of enterochromaffin-like cells and to the development of ga
13 n, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in in
14 MAT2 alone is expressed in histamine-storing enterochromaffin-like cells of the oxyntic mucosa of the
18 the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a
20 ance of the gastric mucosa, proliferation of enterochromaffin-like cells, and neoplastic transformati
21 ctivity was localized to the cell surface of enterochromaffin-like cells, and of myenteric and submuc
22 y regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and s
23 ric neuroendocrine tumours (NETs) arise from enterochromaffin-like cells, which are located in oxynti
26 reotide was infused for 72 hours to suppress enterochromaffin-like (ECL) cell and gastrin cell functi
30 een three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell,
32 PYY inhibits histamine release from isolated enterochromaffin-like (ECL) cells by stimulation of a se
33 to isolate enriched serotonin-secreting and enterochromaffin-like (ECL) cells from the stomach and t
34 ecretion and in vitro histamine release from enterochromaffin-like (ECL) cells in responses to tumor
35 and II) involve the transformation of naive enterochromaffin-like (ECL) cells to the neoplastic stat
36 ucing parietal cells and histamine-secreting enterochromaffin-like (ECL) cells, and the expression of
37 Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormon
41 per was to define physiological responses of enterochromaffin-like, gastrin, and somatostatin cells i
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