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1 We also performed RNA sequencing analysis of ECL cells.
2 sor cells to produce the coupled G-cells and ECL cells.
3 ation may involve the enterochromaffin-like (ECL) cell.
4  are found on gastric enterochromaffin-like (ECL) cells.
5  histamine release in enterochromaffin-like (ECL) cells.
6 nin-B (CCK-B), now termed CCK2, receptors on ECL cells activates histidine decarboxylase, releases hi
7 found to coincide with other markers of both ECL cells and mast cells.
8 rin exerts a mitogenic function primarily on ECL cells and progenitor cells in the gastric isthmus.
9  72 hours to suppress enterochromaffin-like (ECL) cell and gastrin cell function.
10 ion of histamine from enterochromaffin-like (ECL) cells and subsequently acid from parietal cells in
11 nd -38 dose-dependently raise [Ca(2+)](i) in ECL cells, and stimulated histamine release.
12 d histamine-secreting enterochromaffin-like (ECL) cells, and the expression of genes associated with
13      It is proposed that the G-cells and the ECL cells are coupled by the couplet molecules gastrin a
14 , and histamine, from enterochromaffin-like (ECL) cells, are two of the hormones that regulate gastri
15 ated with histamine synthesis and storage in ECL cells, as well as acutely stimulating acid secretion
16 E. coli LPS had a weak stimulatory effect on ECL cell BrdU uptake at 10(-6) mol/L but had no effect o
17 stimulates histamine secretion from isolated ECL cells, but its physiologic role, if any, is not know
18      NGASP stimulates histamine release from ECL cells, but the release is not mediated via CCK-B/gas
19 release from isolated enterochromaffin-like (ECL) cells by stimulation of a selective Y receptor.
20                                      Gastric ECL-cell carcinoid is an independent tumor type of MEN-1
21 5 of 20 (75%) MEN-1-ZES carcinoids, and each ECL-cell carcinoid with LOH showed deletion of the wild-
22 s of multiple gastric enterochromaffin-like (ECL) cell carcinoids.
23 re investigated in a short-term 90%-95% pure ECL cell culture system.
24 ium signaling and histamine release from the ECL cells due to activation of a Gi,o protein-coupled re
25 rotonin-secreting and enterochromaffin-like (ECL) cells from the stomach and to clarify their cellula
26 that substantial neurohormonal modulation of ECL cell function exists.
27 n, the effect of lipopolysaccharide (LPS) on ECL cell function in vitro was investigated.
28 , there were marked reductions in markers of ECL cell function, e.g., histidine decarboxylase and chr
29 stric ECL cell that inhibits gastrin-induced ECL cell histamine release and Ca2+ entry by activation
30                                Inhibition of ECL cell histamine release and calcium signaling is prod
31            To test whether H. pylori affects ECL cell histamine secretion and proliferation, the effe
32 est of the evaluated agents had no effect on ECL cell histamine secretion.
33 al and gastrin-driven enterochromaffin-like (ECL) cell histamine release.
34 rcinoids evolved from enterochromaffin-like (ECL) cell hyperplasia are usually associated with high p
35 e differentiation of serotonin-producing and ECL cells in stomach tissues of NeuroD1-cre;ROSA(tdTom),
36 istamine release from enterochromaffin-like (ECL) cells in responses to tumor extract (TE) and synthe
37                  Gene expression analysis of ECL cells indicated that they are endocrine cells of epi
38                              The response of ECL cell markers in carcinoid tissue to octreotide sugge
39     An interaction between H. pylori LPS and ECL cells may contribute to the reported abnormalities i
40              Neither serotonin-secreting nor ECL cells of the corpus arose from cells expressing Neur
41                                  Using a rat ECL cell preparation of high purity (+/-95%), basal and
42                             PACAP-stimulated ECL cell proliferation (EC50, approximately 3 x 10(-)14
43  vasoactive intestinal polypeptide (VIP), on ECL cell proliferation and characterized the receptor su
44                    H. pylori influences both ECL cell proliferation and secretion in vitro.
45 lated peptides are more potent modulators of ECL cell proliferation than gastrin, and their effect is
46  the parietal cell receptors rather then the ECL cell receptors of the oxyntic glands.
47                               Stimulation of ECL cells results in activation of chloride channels, an
48                   RNA sequencing analysis of ECL cells revealed high expression levels of many genes
49 ransciption polymerase chain reaction of the ECL cell RNA showed a galanin type I receptor subtype.
50 e-transcription polymerase chain reaction of ECL cell RNA showed that the receptor was the nontruncat
51 e, in a reciprocal way, this histamine (from ECL cells), stimulates the G-cells to produce and secret
52                     Histamine, released from ECL cells, stimulates the parietal cell directly via H2
53 tory receptor subtype present on the gastric ECL cell that inhibits gastrin-induced ECL cell histamin
54  endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell, and the somatostatin o
55    The gastrin (from G-cells) stimulates the ECL cells to produce and secrete histamine while, in a r
56 ansformation of naive enterochromaffin-like (ECL) cells to the neoplastic state and are associated pr
57 tic transformation of enterochromaffin-like (ECL) cells to tumor status.
58 gonist loxtidine for 0, 8, and 16 weeks, and ECL cell transformation was monitored by assessing gastr
59 gastrin is critical in the initiation of the ECL cell transformation, the role of other growth factor
60 owth factor (TGF) alpha in the regulation of ECL cell transformation.
61 stitute an autocrine regulatory mechanism in ECL cell tumor transformation.
62 pression of PAC1 splice variants in purified ECL cells was determined by RT-PCR.
63 ia, the proliferative effect of TGF-alpha on ECL cells was specifically amplified during the developm
64 p, enriched with smooth muscle cells but not ECL cells, was removed.
65                             PACAP effects on ECL cells were analyzed by video imaging of [Ca(2+)](i)
66                                 Purified rat ECL cells were analyzed in culture for DNA synthesis as
67                         Isolated rat gastric ECL cells were analyzed in short-term culture for histam
68                                 Isolated rat ECL cells were purified to 85% homogeneity by a combinat
69                                          The ECL cells were purified, and cell proliferation at each
70 the gastrin would stimulate cell division of ECL cells while histamine would stimulate that of G-cell