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1 ts a tonic inhibitory influence on parietal, enterochromaffin-like, and gastrin cells.
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
5 ine transport into secretory vesicles of the enterochromaffin-like cell of the gastric corpus.
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
9 al, mucous neck, and chief cells, but not to enterochromaffin-like-cell.
10 zymes and an increase in histamine-secreting enterochromaffin-like cells (ECLs).
11 e, with a decrease in number of parietal and enterochromaffin-like cells and an increase in number of
12  hormone-like hormone in histamine-secreting enterochromaffin-like cells and hepcidin in acid-secreti
13 irculating gastrin leads to proliferation of enterochromaffin-like cells and to the development of ga
14 n, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in in
15 t the difference between beta cells and awry enterochromaffin-like cells is a gradient of cell states
16 MAT2 alone is expressed in histamine-storing enterochromaffin-like cells of the oxyntic mucosa of the
17 rstitial cells of Cajal of the intestine and enterochromaffin-like cells of the stomach.
18                                          All enterochromaffin-like cells respond to cholecystokinin-B
19                     Histamine, released from enterochromaffin-like cells stimulates the parietal cell
20  the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a
21                 It is synthesized by gastric enterochromaffin-like cells, a specific set of hypothala
22 ance of the gastric mucosa, proliferation of enterochromaffin-like cells, and neoplastic transformati
23 ctivity was localized to the cell surface of enterochromaffin-like cells, and of myenteric and submuc
24 y regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and s
25 ric neuroendocrine tumours (NETs) arise from enterochromaffin-like cells, which are located in oxynti
26               CDX2 emerged as a regulator of enterochromaffin-like cells, which we show resemble a tr
27 ndirectly by releasing histamine from fundic enterochromaffin-like cells.
28 th parietal cells and histamine release from enterochromaffin-like cells.
29 reotide was infused for 72 hours to suppress enterochromaffin-like (ECL) cell and gastrin cell functi
30 nderlie the pathogenesis of multiple gastric enterochromaffin-like (ECL) cell carcinoids.
31 etion by regulating basal and gastrin-driven enterochromaffin-like (ECL) cell histamine release.
32              Gastric carcinoids evolved from enterochromaffin-like (ECL) cell hyperplasia are usually
33 een three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell,
34 ut and mucosal proliferation may involve the enterochromaffin-like (ECL) cell.
35 d stimulates the secretion of histamine from enterochromaffin-like (ECL) cells and subsequently acid
36 PYY inhibits histamine release from isolated enterochromaffin-like (ECL) cells by stimulation of a se
37  to isolate enriched serotonin-secreting and enterochromaffin-like (ECL) cells from the stomach and t
38 ecretion and in vitro histamine release from enterochromaffin-like (ECL) cells in responses to tumor
39  and II) involve the transformation of naive enterochromaffin-like (ECL) cells to the neoplastic stat
40 rinemia-induced neoplastic transformation of enterochromaffin-like (ECL) cells to tumor status.
41 ucing parietal cells and histamine-secreting enterochromaffin-like (ECL) cells, and the expression of
42   Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormon
43  PACAP receptors (PAC1) are found on gastric enterochromaffin-like (ECL) cells.
44 bits Ca2+ signaling and histamine release in enterochromaffin-like (ECL) cells.
45  which exerts a tonic restraint on parietal, enterochromaffin-like (ECL), and gastrin cells.
46 per was to define physiological responses of enterochromaffin-like, gastrin, and somatostatin cells i
47  of the three major gastric endocrine cells (enterochromaffin-like, gastrin, and somatostatin).