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1 xpressed by most epithelial cells, including enterochromaffin and goblet cells.
2 r persistent changes in mucosal immunocytes, enterochromaffin and mast cells, enteric nerves, and the
3 s in other inflammatory components including enterochromaffin and mast cells.
4 e populations, and identify Lmx1a as a novel enterochromaffin cell marker that is also essential for
5                                          The enterochromaffin cell population was decreased in severe
6 er RNA, encoding the rate-limiting enzyme in enterochromaffin cell serotonin (5-hydroxytryptamine [5H
7                       Paracrine signaling by enterochromaffin cells (EC), which release 5-HT, has not
8 biota promote 5-HT biosynthesis from colonic enterochromaffin cells (ECs), which supply 5-HT to the m
9 onstrated that 5-HT released from intestinal enterochromaffin cells activates 5-HT3 receptors on vaga
10     5-Hydroxytryptamine (5-HT) released from enterochromaffin cells activates secretory and peristalt
11  5-Hydroxytryptamine (5-HT) is released from enterochromaffin cells and activates neural reflex progr
12 e of 5-hydroxytryptamine (5-HT) from mucosal enterochromaffin cells and activation of 5-HT(3) recepto
13 e transcription factor Lmx1a is expressed in enterochromaffin cells and functions downstream of Nkx2.
14              Serotonin is also released from enterochromaffin cells and inflammatory/immune cells to
15 sis, consistent with localization of TGR5 to enterochromaffin cells and intrinsic primary afferent ne
16 med FFA2 and FFA3, are expressed in duodenal enterochromaffin cells and L cells, respectively.
17 vious results showing guanylin expression in enterochromaffin cells appear to be a consequence of ant
18              These findings imply a role for enterochromaffin cells as "glucose sensors" during inges
19           We show that the number of mucosal enterochromaffin cells containing 5-HT changes with the
20 tion to neurons, a subset of 5-HT-containing enterochromaffin cells expressed 5-HT1A immunoreactivity
21                                      Mucosal enterochromaffin cells have been postulated to be pressu
22 onsistent with the hypothesis that 5-HT from enterochromaffin cells in response to mucosal stimuli in
23  neurons were activated by 5-HT release from enterochromaffin cells in the mucosa.
24                           5-HT released from enterochromaffin cells initiates peristaltic, secretory,
25                 Expression of uroguanylin in enterochromaffin cells is consistent with the hypothesis
26                              5HT produced by enterochromaffin cells is critical in motility and secre
27 g kg-1) indicating that endogenous 5-HT from enterochromaffin cells is not essential for transduction
28 imiting biosynthetic enzyme for serotonin in enterochromaffin cells of the duodenum.
29  a decrease in the synthesis of serotonin by enterochromaffin cells of the gut.
30 , it is unclear whether they act directly on enterochromaffin cells or indirectly through an intermed
31 kx2.2 mutant conditions, serotonin-producing enterochromaffin cells were the most severely reduced en
32 icate goblet cells, whereas others implicate enterochromaffin cells).
33 ivity was abundant in both enteric plexuses, enterochromaffin cells, and pancreatic ganglia.
34 release serotonin (5-hydroxytryptamine) from enterochromaffin cells, and stretch reflexes that determ
35 erotonin (5-HT), which abounds in intestinal enterochromaffin cells, is released in response to vario
36 athematical modeling, we show that, in human enterochromaffin cells, Myrip (1) inhibits a class of SG
37                Human BON cells, derived from enterochromaffin cells, were treated with D-glucose, gal
38  release of endogenous 5-HT from the mucosal enterochromaffin cells, which acts on the 5-HT3 receptor
39 e adult stage in a subset of enteroendocrine/enterochromaffin cells.
40  by 5-hydroxytryptamine (5-HT) released from enterochromaffin cells.
41 g cells are identified as a subpopulation of enterochromaffin cells.
42  in neuroendocrine, including chromaffin and enterochromaffin, cells.
43 sults suggest that mechanical stimulation of enterochromaffin-derived BON cells directly or indirectl
44                                ABSTRACT: The enterochromaffin (EC) cell in the gastrointestinal (GI)
45                                          The enterochromaffin (EC) cell in the gastrointestinal (GI)
46                                              Enterochromaffin (EC) cell numbers (cells producing 5-HT
47  KEY POINTS: The gastrointestinal epithelial enterochromaffin (EC) cell synthesizes the vast majority
48              The gastrointestinal epithelial enterochromaffin (EC) cell synthesizes the vast majority
49        The gut contains a large 5-HT pool in enterochromaffin (EC) cells and a smaller 5-HT pool in t
50     In the gastrointestinal (GI) epithelium, enterochromaffin (EC) cells are enteroendocrine cells re
51                                 Serotonergic enterochromaffin (EC) cells are proposed to fulfill this
52                                              Enterochromaffin (EC) cells are sensors that detect chem
53 , whereas the number of serotonin-expressing enterochromaffin (EC) cells is decreased dramatically.
54 esis that the secretion of 5-HT from mucosal enterochromaffin (EC) cells is essential for the manifes
55 used by the secretion of serotonin (5-HT) by enterochromaffin (EC) cells of the mucosal epithelium.
56 hat 5-hydroxytryptamine (5-HT) released from enterochromaffin (EC) cells plays an important role in t
57      It is a paracrine messenger utilized by enterochromaffin (EC) cells, which function as sensory t
58 oendocrine tumors believed to originate from enterochromaffin (EC) cells.
59 ed to quantify the number of 5-HT-expressing enterochromaffin (EC) cells.
60 s localized to subpopulations of G cells and enterochromaffin (EC) cells; neither was found in antral
61 reotide was infused for 72 hours to suppress enterochromaffin-like (ECL) cell and gastrin cell functi
62 nderlie the pathogenesis of multiple gastric enterochromaffin-like (ECL) cell carcinoids.
63 etion by regulating basal and gastrin-driven enterochromaffin-like (ECL) cell histamine release.
64              Gastric carcinoids evolved from enterochromaffin-like (ECL) cell hyperplasia are usually
65 een three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell,
66 ut and mucosal proliferation may involve the enterochromaffin-like (ECL) cell.
67 PYY inhibits histamine release from isolated enterochromaffin-like (ECL) cells by stimulation of a se
68  to isolate enriched serotonin-secreting and enterochromaffin-like (ECL) cells from the stomach and t
69 ecretion and in vitro histamine release from enterochromaffin-like (ECL) cells in responses to tumor
70  and II) involve the transformation of naive enterochromaffin-like (ECL) cells to the neoplastic stat
71 ucing parietal cells and histamine-secreting enterochromaffin-like (ECL) cells, and the expression of
72   Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormon
73  PACAP receptors (PAC1) are found on gastric enterochromaffin-like (ECL) cells.
74 bits Ca2+ signaling and histamine release in enterochromaffin-like (ECL) cells.
75  which exerts a tonic restraint on parietal, enterochromaffin-like (ECL), and gastrin cells.
76 rboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia.
77 , parietal and zymogenic, but not for pit or enterochromaffin-like cell lineages in the oxyntic gastr
78 INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited
79 ine transport into secretory vesicles of the enterochromaffin-like cell of the gastric corpus.
80 s, including the role of hypergastrinemia on enterochromaffin-like cell proliferation and its relatio
81 for VMAT2 in the transport of histamine into enterochromaffin-like cell secretory vesicles, and with
82 tic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin cell popula
83 e, with a decrease in number of parietal and enterochromaffin-like cells and an increase in number of
84  hormone-like hormone in histamine-secreting enterochromaffin-like cells and hepcidin in acid-secreti
85 irculating gastrin leads to proliferation of enterochromaffin-like cells and to the development of ga
86 n, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in in
87 MAT2 alone is expressed in histamine-storing enterochromaffin-like cells of the oxyntic mucosa of the
88 rstitial cells of Cajal of the intestine and enterochromaffin-like cells of the stomach.
89                                          All enterochromaffin-like cells respond to cholecystokinin-B
90                     Histamine, released from enterochromaffin-like cells stimulates the parietal cell
91  the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a
92                 It is synthesized by gastric enterochromaffin-like cells, a specific set of hypothala
93 ance of the gastric mucosa, proliferation of enterochromaffin-like cells, and neoplastic transformati
94 ctivity was localized to the cell surface of enterochromaffin-like cells, and of myenteric and submuc
95 y regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and s
96 ric neuroendocrine tumours (NETs) arise from enterochromaffin-like cells, which are located in oxynti
97 ndirectly by releasing histamine from fundic enterochromaffin-like cells.
98 th parietal cells and histamine release from enterochromaffin-like cells.
99 ts a tonic inhibitory influence on parietal, enterochromaffin-like, and gastrin cells.
100 per was to define physiological responses of enterochromaffin-like, gastrin, and somatostatin cells i
101  of the three major gastric endocrine cells (enterochromaffin-like, gastrin, and somatostatin).
102 al, mucous neck, and chief cells, but not to enterochromaffin-like-cell.
103 l root ganglion neurons from rats and in the enterochromaffin model cell line QGP-1, from which serot

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