Cell-Surface Receptors. Cell-surface receptors, also known as transmembrane receptors, are cell surface, membrane-anchored, or integral proteins that bind to external ligand molecules. This type of receptor spans the plasma membrane and performs signal transduction, converting an extracellular signal into an intracellular signal.

The ECL cells have receptors on their cell membranes for the peptide hormone gastrin, and a neurotransmitter released in response to vagal stimulation. The parietal cell basal membrane carries receptors for histamine (H 2), gastrin and acetylcholine. We used to believe that the gastrin and acetylcholine receptors on the parietal cell were particularly important in acid secretion. However, current evidence suggests that the gastrin receptors on the parietal cell are more concerned with cell

The so-called enterochromaffin-like (ECL) cells constitute 65–75% of the endocrine cells in the acid-producing part of the rat stomach. They produce and secrete histamine and pancreastatin, a chromogranin A (CGA)-derived peptide, in response to gastrin. Cholecystokinin (CCK) B /gastrin receptor blockade is known to suppress their activity. TMPH inhibited both basal and gastrin driven histamine secretion with a maximal effect (34 percent) (1.78 +/- 0.08 nmol/10(3) cells) and an IC50 of > 5 x 10(-7) M. H1 receptor antagonism did not cells called enterochromaffin-like (ECL) cells. ECL cells also have receptors for gastrin and acetylcholine, which stimulate histamine release. Histamine binds to the H2 receptor on the parietal cell, resulting in activation of adenylyl cyclase, which increases intra- cellular cyclic adenosine monophosphate (cAMP) and activates protein kinases that stimulate acid secretion by the H+/K+-ATPase. Histamine, released from ECL cells, is the most impor-tant direct stimulant of acid secretion, as shown by the broad efficacy of histamine-2 receptor antagonists as full inhibitors of gastrin and partial inhibitors of vagally stimulated acid secretion (6).

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wild-type (WT) mice were investigated by immunocytochemical 2002-12-01 THE ENTEROCHROMAFFIN-LIKE (ECL) CELL 143 Pathophysiological role of the ECL cell Role in duodenal ulcer diseuse und Zollinger -Ellison syndrome Recently, D’Adda et al. (54) described an increased ECL cell density in patients with duodenal ulcer disease. 1995-08-01 1999-11-15 2005-08-01 2002-08-01 TMPH inhibited both basal and gastrin driven histamine secretion with a maximal effect (34 percent) (1.78 +/- 0.08 nmol/10(3) cells) and an IC50 of > 5 x 10(-7) M. H1 receptor antagonism did not 1996-02-01 1 The so-called enterochromaffin-like (ECL) cells constitute 65-75% of the endocrine cells in the acid-producing part of the rat stomach. They produce and secrete histamine and pancreastatin, a chromogranin A (CGA)-derived peptide, in response to gastrin, Cholecystokinin (CCK)B/gastrin receptor bloc … The ECL cells in the oxyntic mucosa of rat stomach produce histamine and chromogranin A-derived peptides such as pancreastatin. The cells respond to gastrin via cholecystokinin-2 (CCK2) receptors.

However, no depolarization was observed following stimulation with gastrin. Abstract: We previously reported that PAC1 is expressed on ECL cells resulting in stimulation of [Ca2+]i, histamine and acid secretion.

International Physicians for the Prevention of Nuclear War (IPPNW) is a European Journal of Obstetrics & Gyneclogy and Reproductive Biology 7 This study aimed to evaluate the expression of oestrogen receptor β (ERβ) in blood cells 

If this is confirmed, an increase in the ECL cell mass could partly explain the increased acid secretion in these patients since the magnitude of the gastrin-stimulated histamine release is dependent on the ECL cell mass (49, 50). Pa- receptors on ECL cells (10, 25, 49, 62, 65, 70). Gastrin Fig.1.

rar Toll-like receptor 9 (TLR9) genom att tional status in patients with chronic liver disease” Endast linjär och nodulär ECL-cells hyperplasi 

The gastric enterochromaffin-like (ECL) cell plays a major role in the regulation of gastric acid secretion. We have previously described that Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) is present on myenteric neurons in the rat and colocalizes with its high-affinity receptor, PAC1, expressed on the surface of gastric ECL cells. YF476 is a potent and highly selective cholecystokin 2 (CCK(2)) receptor antagonist of the benzodiazepine class. It inhibits gastric neuroendocrine enterochromaffin-like (ECL) cell secretion, proliferation and spontaneous formation of gastric neuroendocrine … 2003-09-26 ture variable proportions of TSHR cleavage have been reported. While complete receptor cleavage was observed in homogenates of cultured cells [6], cross-linking of TSHR with radiolabelled TSH in intact cells revealed that both single-chain and cleaved receptors coexist on the cell surface [7]. The coexistence on the cell … 2000-01-01 2017-10-04 These results have been taken as evidence for a CCK2 receptor on all or on a subpopulation of the parietal cells.

409. B Larsson  Previously, we have demonstrated that Pitx3-/- embryos lack the expression of neurons requires the combined actions of the orphan nuclear receptor Nurr1 and Parietal cell activation by arborization of ECL cell cytoplasmic projections is  tid ersatts av 68Ga-DOTATOC-PET hos patienter med somatostatinreceptorpositiv tumör. utgår från de så kallade ECL-cellerna (enterochromaffin like cells). Gastrin verkar som en trofisk faktor på ECL-cellerna, vilka i sin tur svarar med en growth in patients with metastatic neuroendocrine midgut carcinoid tumors: a  en increase in the amount of organic tissue that results from cell proliferation. Nasal bone hyperplasia has not been observed with ambrisentan in mice or dogs.
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The increase in HDC mRNA might be mediated via the auto-feedback H3 receptor on the ECL cell. By combining long-term hypergastrinemia with ECL cell density in patients with duodenal ulcer disease. If this is confirmed, an increase in the ECL cell mass could partly explain the increased acid secretion in these patients since the magnitude of the gastrin-stimulated histamine release is dependent on the ECL cell mass (49, 50). Pa- The ECL cell is the only known cell in the oxyntic mucosa with a functional gastrin receptor, and the ECL cell produces histamine in response to gastrin stimulation. Longstanding hypergastrinemia predisposes to ECL neoplasia, which is associated with conditions such as atrophic gastritis and gastrinoma.

ture variable proportions of TSHR cleavage have been reported. While complete receptor cleavage was observed in homogenates of cultured cells [6], cross-linking of TSHR with radiolabelled TSH in intact cells revealed that both single-chain and cleaved receptors coexist on the cell surface [7]. The coexistence on the cell surface In the present study, we have identified distinct cell types in the gastric epithelium expressing a bitter receptor protein; thus, confirming and extending the results of previous studies, which demonstrated the presence of mRNA for bitter receptors in epithelial cells of the stomach (Wu et al., 2002; Vegezzi et al., 2014; Liu et al., 2017; Prandi et al., 2018). The ECL cells in the oxyntic mucosa of rat stomach produce histamine and chromogranin A-derived peptides such as pancreastatin.
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Spontaneous ECL cell carcinomas in cotton rats: natural course and prevention by a gastrin receptor antagonist Tom C.Martinsen, Shiro Kawase1, Rolf Ha˚kanson2, Sverre H.Torp3, Reidar Fossmark, Gunnar Qvigstad, Arne K.Sandvik and Helge L.Waldum4 Department of …

11, 12, 13, 14 Studies using gastrin-transgenic mice 15, 16 have demonstrated the stimulatory effect of gastrin on ECL cell proliferation. YF476 is a potent and highly selective cholecystokin 2 (CCK(2)) receptor antagonist of the benzodiazepine class. It inhibits gastric neuroendocrine enterochromaffin-like (ECL) cell secretion, proliferation and spontaneous formation of gastric neuroendocrine tumors (carcinoids) in cotton rats. from enterochromaffin-like (ECL) cells due to binding of either acetylcholine or gastrin to receptors on the ECL cell. 1'2 The gastrin is released from antral G cells in response to amino acids or peptides in the antral lumen.