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The principal peptide inhibitor of gastrin release is SST. Paper-1671507.
RESULTS: G-17 stimulated growth of both AGS and SIIA cells. Paper-1155294.
However, gastrin- induced CrkII and JNK pathways are independent. Paper-9297999.
Gastrin induced membrane translocation of PKC-alpha. Paper-8812769.
Gastrin release does not seem to be under the control of GRP. Paper-8993240.
Glycine-extended gastrin regulates HEK cell growth. Paper-1982509.
Half-maximal PKD activation for both CCK-8 and gastrin was achieved at 10 nM. Paper-8715651.
These agents are useful tools to study how gastrin controls the ECL cells. Paper-1880369.
Gastrin- induced cyclooxygenase-2 expression in Barrett's carcinogenesis. Paper-10471361.
CCK-8 together with gastrin-17 inhibited gastrin-induced acid output by 67%. Paper-8003572.
Both 8-BrcAMP and TPA stimulated gastrin release in a dose-dependent fashion. Paper-5811184.
Basal and secretin- stimulated gastrin responses were suppressed but not normalized. Paper-6592071.
Here we identify the mechanisms of gastrin- induced PKD2 activation in AGS-B cells. Paper-9167970.
G-17-gly but not G-17 induced significant proliferation of the PLC/PRF/5 cell line. Paper-9032069.
CCKB-receptors mediate the effects of gastrin on the gut and the effects of CCK in the brain. Paper-7877315.
Mechanism for increase of gastrin release by secretin in Zollinger-Ellison syndrome. Paper-6461418.
The effect of gastrin on basal and aminoacid- stimulated insulin and glucagon secretion in man. Paper-3136982.
Higher values of other GI hormones, gastrin, pepsinogen I and II, CCK, GRP, and TNF-alpha. Paper-10010819.
Rat histidine decarboxylase promoter is regulated by gastrin through a protein kinase C pathway. Paper-713847.
0. After the meal, plasma gastrin rose by 57%, CCK by 177%, PP by 100%, and somatostatin by 39%. Paper-7986667.
We have shown previously that chronically elevated gastrin levels suppress somatostatin. Paper-13076943.
The effect of somatostatin on bombesin- stimulated serum gastrin and gastric acid secretion in man. Paper-3913957.
Antral gastrin- producing G-cells and somatostatin-producing D-cells in peptic ulcer. Paper-5446328.
Acute CCK2 receptor blockade inhibits gastrin-evoked but not histamine-induced acid secretion. Paper-8805419.
This motility effect of somatostatin seems to be independent of any effect on the gastrin concentration. Paper-3180556.
Background and Aim: Cholecystokinin ( CKK) and gastrin exert their influences via CKK receptors. Paper-13073233.
CCK antagonism failed to affect significantly the pH profile or the increments in plasma gastrin. Paper-267871.
Somatostatin may inhibit gastric exocrine functions independent of blockade of gastrin secretion. Paper-5819461.
The effect of somatostatin on pentagastrin- stimulated gastric secretion and on plasma gastrin in man. Paper-2909282.
We hypothesized that SMS would suppress basal and provoked gastrin and secondary peptide secretion in ZES. Paper-6577822.
Gastrin induces proliferation in Barrett's metaplasia through activation of the CCK2 receptor. Paper-9824169.
Gastrin stimulated p70 S6 kinase activity for concentrations ranging from 10 pM to 1 nM. Paper-2074444.
In case 1, VIP, gastrin and calcitonin were produced in the tumor and only plasma VIP levels were elevated. Paper-3450638.
Antral G-cells synthesize the most gastrin and express PC1/3, 2 and 5/6 in the rat and human. Paper-12930299.
In contrast, somatostatin and epidermal growth factor had no effect on either gastrin uptake or bacterial growth. Paper-2031745.
Gastrin activates paracrine networks leading to induction of PAI-2 via MAZ and ASC-1. Paper-13589946.
The human gut was the richest source, where DSIP-LI was located in gastrin/ CCK, secretin and PYY/glicentin cells. Paper-6279243.
Anti-stress ulcer and anti-secretory effect of somatostatin in rats -- failure to suppress serum gastrin. Paper-2745419.
Basal and secretin- stimulated gastrin responses were suppressed but not normalized in eight of eight patients. Paper-5811627.
Moreover, several vertebrate type peptides (such as CRF/ GRF and CCK/ gastrin) may coexist in a single neurone. Paper-4828773.
Gastrin/ CCK-like immunoreactivity in the corpus cardiacum-corpus allatum complex of the cockroach Leucophaea maderae. Paper-5634562.
The distribution of gastrin/ CCK-like immunoreactive material has been studied in the retrocerebral complex of Calliphora. Paper-4547681.
We determined which CCK receptor mediated the trophic effect of gastrin on human colon cancer cells (LoVo). Paper-8030673.
Response of circulating somatostatin, insulin, gastrin and GIP, to intraduodenal infusion of nutrients in normal man. Paper-4726234.
CCK antagonism failed to affect significantly the pH profile or the increments in plasma gastrin or CCK. Paper-267871.
In the stomach, somatostatin is secreted from D cells and is a potent inhibitor of gastrin-induced acid secretion. Paper-10226293.
Vagotomy augmented somatostatin suppression of food- stimulated gastrin release in a dose-dependent manner. Paper-2937516.
This could have been mediated by neutralization of both serum G17 and cell- associated precursor gastrin molecules. Paper-548435.
Allelic deletion of the MEN1 gene in duodenal gastrin and somatostatin cell neoplasms and their precursor lesions. Paper-13191569.
Loss of vagal stimulation results in intensification of somatostatin- induced inhibition of postprandial gastrin release. Paper-2937516.
It increased serum gastrin concentration and suppressed plasma pancreatic polypeptide response to modified sham-feeding. Paper-4496270.
Cholecystokinin is a negative regulator of gastric acid secretion and postprandial release of gastrin in humans. Paper-8003572.
CCK antagonism failed to affect significantly the pH profile or the increments in plasma gastrin in DU patients. Paper-7986667.
Positive Boots secretin stimulation tests in two of the control subjects were confirmed by a different gastrin assay kit. Paper-4315722.
Plasma gastrin levels also were measured via radioimmunoassay (RIA) in control and CGRP 8-37-stimulated animals. Paper-125874.
Controls consisting of cholecystokinin and pentagastrin inhibited gastrin uptake but did not stimulate growth. Paper-2031745.
In conclusion, human gastrin was expressed in mouse enteroendocrine cells and was regulated by somatostatin. Paper-13076943.
Synthetic secretin stimulation in two of the patients and the four control subjects showed no rise in postsecretin gastrin. Paper-4315722.
Gastrin inhibits growth and induces apoptosis in Mz-ChA-1 cells through the Ca2+-dependent PKC-alpha. Paper-8812769.
Gastrin- stimulated p70 S6 kinase activity and protein synthesis were blocked by rapamycin and wortmannin. Paper-2074444.
These results show that intake of whisky stimulates the secretion of gastrin and is associated with a later increase in CCK. Paper-9913908.
Carbachol stimulated gastrin release in a dose-dependent manner but had no effect on somatostatin release. Paper-8439542.
Secretin stimulated the rate of gastrin release from cultured GT cells in both a time- and a dose-dependent fashion. Paper-5811184.
Thus, PKD2 is likely to be a novel downstream target of specific PKCs upon the stimulation of AGS-B cells with gastrin. Paper-9167970.
H1 receptor antagonists inhibited DNA synthesis in vitro and ECL neoplasia in vivo without altering gastrin levels. Paper-587479.
The human gastrin/ cholecystokinin type B receptor gene: alternative splice donor site in exon 4 generates two variant mRNAs. Paper-101589.
PURPOSE: Gastrin is known to enhance the growth of pancreatic carcinoma via the cholecystokinin (CCK)-2/ gastrin receptor. Paper-12750103.
The D cell is activated by either gastrin or CCK and appears to be inhibited by acetylcholine and somatostatin. Paper-997051.
Gastrin-responsive DNA- binding sites in the TFF2 promoter were evaluated by electrophoretic mobility shift assay. Paper-13278687.
However, gastrin may, like cholecystokinin, potentiate the effect of secretin on pancreatic secretion of juice and bicarbonate. Paper-5255162.
BACKGROUND: Gastrin is thought to stimulate growth of the pancreas via gastrin/ cholecystokinin (CCK)-B-type receptors. Paper-633698.
In vitro studies on LES muscle showed that CCK selectively antagonized the effect of gastrin I, but not other agonists. Paper-2238915.
Gastrin and not gastric pH has been identified as the most important factor regulating the density of fundic ECL cells. Paper-7475958.
Gastrin also stimulated CREB Ser-133 phosphorylation, and abundance of cellular CREB protein levels. Paper-1693580.
Long-acting somatostatin analog controls acid and gastrin secretion in benign, not in malignant, Zollinger-Ellison syndrome. Paper-6382808.
In the antrum, gastrin secretion from G cells is inhibited in a paracrine manner by somatostatin secreted from D cells. Paper-9145611.
The tumor was found to contain gastrin, ACTH, alpha-endorphin, somatostatin and calcitonin, by the immunoperoxidase technic. Paper-3632306.
Gastrin I had no independent effect on the PV response of the gallbladder but reduced the stimulatory affect of CCK. Paper-2665445.
We have now sought to identify the response element(s) in the PAI-2 promoter targeted by paracrine mediators initiated by gastrin. Paper-13589946.
Glucagon, insulin, and gastrin levels were suppressed by somatostatin while calcium infusion caused a paradoxical increase. Paper-2551366.
Atropine abolished secretory, motor, and pancreatic polypeptide responses to sham feeding and enhanced gastrin release. Paper-7429704.
Antral gastrin- producing G-cells and somatostatin-producing D-cells in different states of gastric acid secretion. Paper-4198118.
The purpose of this study was to explore the intracellular events of colorectal cancer cells after gastrin binding to CCK2R. Paper-11536300.
Truncated GLP-1 significantly inhibited postprandial acid secretion by 43 +/- 11% in spite of unchanged plasma gastrin concentration. Paper-87003.
Recent evidence suggests that abnormalities in gastrin release and action may be influenced by participation of somatostatin. Paper-3650477.
Before treatment the celiac patients had enhanced gastrin response and normal PP response compared with normal controls. Paper-4439274.
Here we have generated G protein- coupled cholecystokinin (CCK)-B/ gastrin receptor deficient-mice by gene targeting. Paper-736898.
Gastrin significantly induced COX-2, prostaglandin E(2), and cell proliferation in biopsies and cell lines. Paper-10471361.
Competition for the gastrin effect by pentagastrin and cholecystokinin ( CCK-8) resulted in inhibition of bacterial growth. Paper-9654476.
To analyze the interaction between these different peptides, we explored the influence of EGF and gastrin on the somatostatin receptors. Paper-128673.
Similar mechanisms exist in the distal antral segment of the stomach for the paracrine regulation of gastrin release by somatostatin. Paper-6507142.
CONCLUSIONS: Blockade of CCK-A receptors converts CCK-8 into a potent acid secretagogue and augments postprandial gastrin secretion. Paper-8003572.
Plasma levels of cholecystokinin ( CCK), secretin, gastrin, and ghrelin were determined using specific enzyme immunoassays. Paper-13503676.
Thus, S-0509 has an increase in selectivity for the peripheral effects of gastrin antagonism from the central effects of CCK-B antagonism. Paper-1229205.
CONCLUSION: H. pylori infection is associated with enhanced gastrin release from human antrum and TNF-alpha produces a similar effect. Paper-1194836.
Gastrin regulates the TFF2 promoter through gastrin-responsive cis-acting elements and multiple signaling pathways. Paper-13278687.
At this dose, GRP was as effective as bombesin in releasing gastrin, although unlike bombesin its effect was enhanced by atropine. Paper-4407448.
BW-10 (10-100 nmol/kg) was equally effective at significantly inhibiting bombesin evoked gastrin release in anesthetized rats, in vivo. Paper-74473.
Both atropine and loxiglumide enhanced gastrin release whereas only loxiglumide markedly stimulated CCK release. Paper-823738.
Gastrin-recognizing CCK2 receptors are expressed in parietal cells and in so-called ECL cells in the acid-producing part of the stomach. Paper-1880369.
We evaluated if gastrin effects on Mz-ChA-1 growth and apoptosis are associated with membrane translocation of PKC-alpha. Paper-8812769.
Effect of cholecystokinin and gastrin on human peripheral blood lymphocyte functions, implication of cyclic AMP and interleukin 2. Paper-1158022.
Radioimmunological measurements of CCK may not detect all biological active forms or may have the disadvantage of crossreacting with gastrin. Paper-6361530.
The results showed that the somatostatin analogue inhibits basal as well as secretin- and calcium- stimulated gastrin secretion. Paper-5444783.
Gastrin then stimulates the cholecystokinin-B receptor on the enterochromaffin-like cell beginning a calcium signaling cascade. Paper-8246813.
Glycine-extended gastrin inhibits apoptosis in colon cancer cells via separate activation of Akt and JNK pathways. Paper-11317311.
The effects could have been controlled by insulin-like growth factor-1 but probably not by any of the cholecystokinin/ gastrin peptide family. Paper-13626228.
The effect of intravenous somatostatin on bombesin- stimulated serum gastrin and gastric acid secretion was studied in 5 healthy subjects. Paper-3913957.
Gastrin mediated cholecystokinin-2 receptor activation induces loss of cell adhesion and scattering in epithelial MDCK cells. Paper-9522336.
Here, we demonstrate that OsGSR1, a member of the GAST ( GA-stimulated transcript) gene family, is induced by GA and repressed by BR. Paper-13619789.
Role of cholecystokinin in the control of gastric acid secretion and gastrin release in dogs and healthy and duodenal ulcer subjects. Paper-7590297.
Indeed, 111In-labeled DTPA derivatives of gastrin showed excellent targeting of CCK-B receptor expressing tissues in animals and patients. Paper-9028847.
Indeed, 111In-labeled DTPA derivatives of gastrin showed excellent targeting of CCK-B receptor expressing tissues in animals and patients. Paper-2028078.
Cholecystokinin ( CCK) has been implicated in the feedback control of gastrin release and gastric acid secretion in healthy subjects. Paper-423407.
Identification of gastrin- secreting cells and cholecystokinin-secreting cells in the gastrointestinal tract of the human fetus and adult man. Paper-2581052.
The integrity of the paracrine feedback loop inhibiting gastrin release was tested by concurrent administration of cholecystokinin ( CCK). Paper-1194836.
Pituitary adenylate cyclase-activating polypeptide ( PACAP), somatostatin, and gastrin receptor expression was determined by real-time RT-PCR. Paper-12262848.
Serotonin and gastrin/ cholecystokinin-like immunoreactive neurons in the larval retrocerebral complex of the blowfly Calliphora erythrocephala. Paper-5916354.
These antibodies have to be exquisitely specific for the 0-sulfated C-terminal heptapeptide amide of CCK without binding the similar gastrin epitope. Paper-1773511.
G protein- coupled cholecystokinin-B/ gastrin receptors are responsible for physiological cell growth of the stomach mucosa in vivo. Paper-736898.
Low-level distention of the antrum activates, preferentially, VIP neurons that stimulate somatostatin secretion and thus inhibit gastrin secretion. Paper-106120.
SRIF inhibits TSH-induced cAMP accumulation in human thyroid cell, while CCK, gastrin and substance P do not modify cAMP response to TSH. Paper-4830601.
Radioimmunoassay with a carboxyl-terminal CCK-antibody fully cross-reacting with gastrin did not reveal additional molecular forms of CCK. Paper-4405649.
However, the specific gastrin binding was not inhibited by glucagon, insulin, acetylcholine, atropine, histamine, or cimetidine. Paper-4804208.
Somatostatin potently suppressed forskolin- and bombesin- mediated gastrin release but did not significantly alter basal gastrin levels. Paper-11316.
Gastrin increases mcl-1 expression in type I gastric carcinoid tumors and a gastric epithelial cell line that expresses the CCK-2 receptor. Paper-13028999.
It is concluded that G-17- stimulated proliferation is mediated via the CCK-B receptor and G-17-gly via a separate, as yet uncharacterized, receptor. Paper-9032069.
In vitro, using isolated ECL cells, SRIF inhibits both gastrin-stimulated ECL cell histamine secretion and DNA synthesis. Paper-806899.
Initially, using growth assays, we determined that the human CRC cell line DLD-1 expressed both functional PPARgamma and gastrin receptors. Paper-12012624.
Basal and postprandial plasma concentrations of gastrin, cholecystokinin, and peptide YY were measured with sensitive and specific radioimmunoassays. Paper-9646914.
In AR4-2J cells, gastrin stimulated Reg mRNA abundance; this was eliminated by the gastrin/ cholecystokinin B antagonist L-740,093 (10(-9) mol/L). Paper-1883203.
There was no correlation between acid secretion and mucosal gastrin- releasing polypeptide or SS concentrations in any part of the stomach and duodenum. Paper-5751791.
Higher levels of distention activate predominantly cholinergic neurons that suppress antral somatostatin secretion and thus stimulate gastrin secretion. Paper-106120.
Using COOH-terminal-specific antisera raised to gastrin and/or CCK, the distribution of CCK neurones has been described with immunohistochemical techniques. Paper-3648385.
Distinct CCK and gastrin peptides were identified in two shark species, the spiny dogfish ( Squalus acanthias) and the porbeagle ( Lamna cornubica). Paper-1176815.
In dogs with gastric fistulas and Heidenhain pouches, the lowest dose of CCK that inhibited gastrin-stimulated acid secretion was 674 pmol kg-1 h-1. Paper-3241454.
BW-10 (1 and 10 nM) significantly inhibited the gastrin response to 1 nM bombesin, from isolated rat stomach, in vitro, in a dose-dependent fashion. Paper-74473.
Altered concentrations of gastrin- releasing polypeptide and somatostatin in fundic and duodenal bulb mucosa of patients with duodenal ulcer disease. Paper-5751791.
The principal findings of the dynamic perifusion experiments were that hCGRP exerted a dual or biphasic effect on ACh discharge and gastrin release. Paper-58059.
Five patients with hypochlorhydria, chronic gastritis, and high serum gastrin levels and four control subjects underwent secretin stimulation testing. Paper-4315722.
Activation of its gastrin/ CCKB receptor results in histamine synthesis and release with consequent activation of the fundic parietal cell H2 receptor. Paper-1671507.
The circulating pancreastatin concentration is raised, was lowered when the action of gastrin on the ECL cells was blocked by the CCK2 receptor antagonists. Paper-1880369.
After successful eradication, improvement of histological inflammation and an increase in BAO, basal and gastrin- stimulated somatostatin output were observed. Paper-9896686.
The proliferation of pancreatic tumor AR42J cells has been shown to be stimulated by Epidermal growth factor ( EGF) and gastrin and inhibited by somatostatin. Paper-128673.
Thus, the gastrin receptors on the parietal cells and the brain appear to be encoded by the same gene as those on the ECL carcinoid tumor in Mastomys. Paper-7822546.
By use of immunocytochemistry, a gastrin/ CCK-like material has been demonstrated in the corpus cardiacum-corpus allatum complex of the cockroach Leucophaea maderae. Paper-5634562.
Significant changes in cell size (cross-sectional area) were also demonstrated in the somatostatin and gastrin cells which were smaller in the celiac biopsies. Paper-4727046.
BACKGROUND & AIMS: Gastrin ( G-17) stimulates the growth of certain gastric and colon cancers mostly through gastrin/ cholecystokinin (CCK)-B receptors. Paper-1155294.
In conclusion: Gastric acidification in man stimulates plasma release of somatostatin in parallel to suppressing gastrin release and gastric acid secretion. Paper-6504786.
Synaptophysin immunoreactivity occurred in the serotonin cells throughout the gastrointestinal tract, and in the antral gastrin and somatostatin cells. Paper-1778212.
Somatostatin 14 inhibited secretin, bombesin, and gastrin-releasing peptide stimulated gastrin release but did not alter basal release. Paper-6569337.
The interaction of the novel CCK analogs JMV-180, JMV-320, and JMV-332 with CCK-B/ gastrin receptors on small cell lung cancer ( SCLC) cells was investigated. Paper-7219354.
Gastric acid stimulated by gastrin I at the physiological post-prandial concentration of 150 pg/ml was inhibited by secretin at 40 pg/ml by approximately 80%. Paper-776438.
PURPOSE: Radiolabelled cholecystokinin ( CCK) and gastrin-derived peptides potentially can be used for peptide receptor radionuclide therapy ( PRRT). Paper-12698423.
Glycine-extended gastrin inhibits apoptosis in Barrett's oesophageal and oesophageal adenocarcinoma cells through JAK2/ STAT3 activation. Paper-13675174.
This indirectly supports the hypothesis that SMS 201-995 acts in gastrinoma cells to inhibit gastrin secretion by inhibition of adenylate cyclase activity. Paper-5444783.
Secretin inhibits gastric secretion of acid and gastrin in dog and a physiological role of secretin as an enterogastrone has been suggested in this species. Paper-5466252.
Attenuation of peroxisome proliferator-activated receptor gamma (PPARgamma) mediates gastrin-stimulated colorectal cancer cell proliferation. Paper-12012624.
Effects of Dexlansoprazole MR, a Novel Dual Delayed Release Formulation of a Proton Pump Inhibitor, on Plasma Gastrin Levels in Healthy Subjects. Paper-13682679.
It appears that somatostatin release is the mechanism through which prostaglandin can simultaneously inhibit acid secretion and release plasma gastrin. Paper-6928090.
The somatostatin analogue, somatostatin-(201-995), did not alter basal gastrin release but inhibited secretin, carbachol, and bombesin stimulation. Paper-5872144.
Somatostatin inhibits insulin- stimulated gastrin release and gastric secretion of acid, pepsin, and intrinsic factor (IF) in duodenal ulcer patients. Paper-2576801.
The results suggest that an abnormal somatostatin- mediated inhibition of gastrin release and/or gastric acid secretion does not exist in duodenal ulcer patients. Paper-7974806.
Present observations indicate that glucagon and HNBB may inhibit serum PGI level, whereas the former has the additional effect of inhibiting serum gastrin level. Paper-7916874.
The Ca(2+)-mobilizing effects of gastrin and CCK-8 were prevented by proglumide, benzotript, and the specific gastrin/ CCKB receptor antagonist L365260. Paper-7530409.
Cholecystokinin-B/ Gastrin receptor- targeting peptides for staging and therapy of medullary thyroid cancer and other cholecystokinin-B receptor-expressing malignancies. Paper-9439051.
During alkaline gastric perfusion, indomethacin increased circulating somatostatin (p less than 0.05) levels without affecting plasma gastrin or gastric acid. Paper-6504786.
Somatostatin levels were significantly higher and oxytocin levels lower in patients than in controls and gastrin levels tended to be higher in patients than in controls. Paper-6981257.
Static incubation studies indicated that hCGRP (10(-10) to 10(-7) M) stimulated somatostatin and inhibited gastrin release in a dose-dependent manner. Paper-58059.
BACKGROUND: Alpha-amidated gastrin promotes the growth of nontransfected pancreatic cell lines expressing the gastrin/ cholecystokinin (CCK)-B receptor. Paper-8417202.
Inhibition of somatostatin release would explain stimulation of gastrin release and gastric acid secretion with co-infusion of bethanechol and loxiglumide. Paper-223039.
CCKB-antagonists can also inhibit the growth of some gastrin-dependent tumours, including certain human colonic cancer cell lines which produce gastrin. Paper-7877315.
Moreover, food-stimulated gastric acid secretion and gastrin release were inhibited by intravenous somatostatin to the same extent in ulcer patients and controls. Paper-4725632.
The selective CCKB/ gastrin antagonist blocked the increase in [Ca2+]i induced by CCK-8 (half-maximal inhibitory concentration = 80 pM) in H510 but not in GLC19 cells. Paper-7613530.
Transcriptional regulation of gastrin mRNA synthesis is positively regulated by transforming growth factor-alpha ( TGF-alpha) and inhibited by somatostatin ( SST). Paper-1671507.
These data indicate that JMV-320 and JMV-332 function as CCK-B/ gastrin receptor agonists while JMV-180 functions as a CCK-B/ gastrin receptor antagonist in H345 cells. Paper-7219354.
In addition, we measured plasma gastrin levels in both the renal artery and renal vein in six patients with normal renal function before and during glucagon infusion. Paper-4289884.
Helicobacter pylori infection has been found to decrease the expression of antral somatostatin and to increase the release of the acid- stimulating hormone gastrin. Paper-9389894.
Finally, both CCK-8 and gastrin induced DNA synthesis in Rat1 cells transfected with the human CCKB/ gastrin receptor through a pertussis toxin-insensitive pathway. Paper-275169.
The importance of the C-terminal Phe of gastrin and structural requirements at position 17 for binding to the human CCK2 receptor were assessed using analogs of [Leu15]G(11-17). Paper-8887093.
Glycine-extended gastrin induces matrix metalloproteinase-1- and -3-mediated invasion of human colon cancer cells through type I collagen gel and Matrigel. Paper-10303822.
Administration of loxiglumide resulted in a significant increase in plasma gastrin and CCK responses to GRP, whereas plasma somatostatin was not significantly altered. Paper-267871.
Endocrine cells containing bombesin-, met-enkephalin-, gastrin/ CCK-, neurotensin-, somatostatin- or substance P- like immunoreactivity were present in the mucosa. Paper-5110642.
The fully active gastrin and CCK analogues [ Nle 15]-gastrin-17 and [ Nle, Thr]-CCK-9 were analysed for their Ca2+ and Tb3+ affinities in various membrane mimetic conditions. Paper-1144581.
According to current hypothesis, the lack of inhibition by somatostatin allows excessive release of gastrin, which stimulates acid secretion and thus causes duodenal ulcers. Paper-1703907.
These results identify gastrin as a potent trophic peptide that actively stimulates growth of human pancreatic cancer and does so through a CCK-B/ gastrin-like receptor. Paper-156738.
High basal levels of activated PKB/Akt were linked to endogenous gastrin expression and were reduced by treatment with a cholecystokinin-type 2 receptor (CCK-2R) antagonist. Paper-10207489.
CaBP is colocalized in endocrine cells containing gastrin, glucagon, somatostatin and neurotensin, but not glucose dependent insulinotrophic peptide ( GIP). Paper-7209993.
Global expression analysis of ECL cells in Mastomys natalensis gastric mucosa identifies alterations in the AP-1 pathway induced by gastrin-mediated transformation. Paper-11432015.
These studies indicate that, in addition to its established effect on peptide release, somatostatin exerts inhibitory effects on antral gastrin cells at the pretranslational level. Paper-6358898.
In the duodenal ulcer patients, however, there was no correlation between gastrin release and somatostatin release from antral mucosa ( r = 0.09; p greater than 0.2). Paper-5439746.
When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Paper-2270424.
Early diagnosis of pancreatic endocrine tumours in MEN-1 is enhanced by the use of a standardized meal stimulation test with measurements of serum PP and gastrin response. Paper-1509246.
The secretion and expression of gastrin are under the paracrine control of somatostatin, produced by D cells situated in close contact with gastrin-producing G cells. Paper-2157455.
These data suggest that the effect of PCS upon gastrin levels is associated with the impaired appetite while the effect upon glucagon is the result of diversion past the liver. Paper-3332283.
CONCLUSIONS: G-17 stimulates proliferation of AGS cells through the CCK-B receptor; however, G-17- mediated growth of SIIA acts through a CCK-A-like receptor. Paper-1155294.
SMS may be useful in ZES by suppressing basal and provoked gastrin and secondary peptide secretion and may occasionally give palliation by yielding temporary tumor registration. Paper-6577822.
Exogenous gastrin-releasing peptide stimulates a greater increase in plasma gastrin concentrations in patients infected with Helicobacter pylori than in uninfected controls. Paper-1067289.
Overexpression of an inhibitory mutant of Shc completely blocked gastrin- stimulated Shc.Grb2 complex formation but partially inhibited ERK-1 activation by this peptide. Paper-1940917.
We found that gastrin regulates TFF2 transcription through a GC-rich DNA-binding site and a PKC-, MEK1- and PI 3-kinase-dependent but EGFR-independent pathway. Paper-13278687.
Two receptors for cholecystokinin ( CCK) have been isolated which also bind gastrin: CCK-A type and CCK-B type, both are coupled to phospholipase C (PLC) activation. Paper-8030673.
GRP stimulated the secretion of gastrin, pancreatic polypeptide, insulin, glucagon, and glucose-dependent insulinotropic polypeptide in a dose-dependent manner. Paper-4805323.
The rank order of CCK-related peptides was CCK8-sulfated greater than or equal to Gastrin 17 greater than or equal to CCK33 greater than CCK4 greater than or equal to CCK8-desulfated. Paper-4909761.
OBJECTIVE: To characterise the cholecystokinin ( CCK) receptor subtypes in medullary thyroid cancer by measuring the expression of CCK-A and CCK-B/ gastrin receptor mRNA. Paper-1993373.
We compared the effects of intraduodenally perfused saline, medium-chain and long-chain triglycerides on gastrin- stimulated gastric acid secretion and cholecystokinin release. Paper-859100.
RESULTS: L-NMMA delayed the recovery of intragastric pH to the pre-meal value, and suppressed postprandial gastrin release while increasing the plasma somatostatin level. Paper-2087041.
Furthermore, most recent data indicate that ebrotidine has the ability to reverse the impairment caused by H. pylori in feedback inhibition of gastrin release by somatostatin. Paper-1096103.
Our data lead us to conclude that the trophic actions of gastrin are mediated by ERK2- induced c-fos gene expression via PKC-dependent and -independent pathways. Paper-1213938.
This study examined whether gastrin modulates endothelial cell activity via heparin- binding epidermal growth factor-like growth factor ( HB-EGF) expression. Paper-11395113.
BACKGROUND: Mature amidated gastrin ( G17 amide) mediates its effects in the gastrointestinal tract by activating G protein- coupled CCK-B/ gastrin receptors. Paper-8959737.
Cholecystokinin in the control of gastric acid secretion and gastrin release in response to a meal at low and high pH in healthy subjects and duodenal ulcer patients. Paper-416001.
SOM is a key component of the gastrin-acid feedback loop as luminal acid releases SOM, which in turn has inhibitory effects on both gastrin and gastric acid. Paper-7949559.
CONCLUSIONS: The results do not support the hypothesis that K-ras and B-raf gene mutations have an impact on gastrin- and CCK-receptor mRNA expression in colorectal tumour tissues. Paper-10384578.
In the presence of 3-isobutyl-1-methylxanthine, secretin significantly stimulated gastrin release from dispersed gastrinoma cells, which was inhibited by somatostatin. Paper-6461418.
The findings of this study show that postprandial gastrin secretion is influenced by CCK and support the concept of a negative feedback control of gastrin secretion by CCK. Paper-7481819.
Although this inhibition appears to occur in part at the gene transcriptional level, the results also indicate that somatostatin may affect posttranscriptional processing of gastrin mRNA. Paper-6358898.
SMS 201-995 blocks acid secretion and secretin- and calcium- stimulated gastrin release, indicating that SMS 201-995 inhibits peptide secretion by postreceptor mechanisms. Paper-5241266.
Cholecystokinin receptor antagonist loxiglumide modulates plasma levels of gastro-entero-pancreatic hormones in man. Feedback control of cholecystokinin and gastrin secretion. Paper-7028074.
In man, endogenous stimulation of CCK had no effect on gastrin release; however, when CCK was given exogenously (10% pure form), serum gastrin levels were significantly increased. Paper-2463031.
Results of these studies identify enhanced gastrin release in response to stimulation and decreased release of somatostatin from antral mucosa of duodenal ulcer patients. Paper-5439746.
Boots secretin was found to contain substantial quantities of gastrin, immunoreactive cholecystokinin, vasoactive intestinal peptide, gastric inhibitory peptide, and somatostatin. Paper-5436661.
METHODS: The ability of muscarinic agonists to stimulate or inhibit gastrin release was assessed with or without an immunoneutralizing somatostatin antibody or an m3 receptor antagonist. Paper-902049.
The great majority of the cells expressing CD133 also expressed gastrin precursors in both DLD-1 cells, which retain a stem cell-like subpopulation, and human CRC specimens. Paper-13683808.
These results provide the first identification of a CCK-B/ gastrin receptor in human pancreatic cancer cells and tumors and explain the effects of CCK on the growth of this malignancy. Paper-7928889.
There was an increased release of pancreatic polypeptide but the difference in the post-prandial hormone profile between patients and controls for gastrin did not reach statistical significance. Paper-4847408.
Both the N- and C-terminal halves of the GBP bind gastrin, but the affinity of the N-terminal half for gastrin is 7.2-fold higher than the affinity of the C-terminal half. Paper-9144500.
We also demonstrated that Src family kinases and the phosphatidylinositol-3-kinase ( PI-3-kinase) pathway play a crucial role in the expression of beta1-integrin induced by gastrin. Paper-12155440.
Furthermore, pertussis toxin pretreatment reversed the ability of somatostatin to inhibit secretin- induced increase in gastrin release and activation of adenylate cyclase. Paper-6461418.
Gastric acid secretion was stimulated 15 min after the increase in gastrin secretion, suggesting that GRP stimulated gastric acid secretion via release of gastrin. Paper-4805323.
We conclude that sucrose polyester, in contrast with digestible fat, does not inhibit gastrin- stimulated gastric acid secretion or stimulate release of cholecystokinin. Paper-937424.
The problem of false-positive results in SRS resulting from inflammatory disease might be overcome by the use of new radiopeptides such as cholecystokinin-B receptor- binding gastrin analogues. Paper-10143106.
Our previous research has demonstrated that activation of cholecystokinin-2 receptor ( CCK2R) by gastrin stimulates a rapid activation of FAK pathway in human colon cancer cells. Paper-12299297.
The effect os somatostatin (0.6 mg/hour) on insulin- stimulated gastrin release and gastric secretion of acid, pepsin, and IF has been examined in 6 unoperated patients with duodenal ulcer. Paper-2576801.
The immunohistological demonstration of somatostatin- producing cells apposite to antral G-cells suggest a physiological role of somatostatin in the regulation of gastrin secretion in man. Paper-2622522.
The antibodies were of an affinity high enough to compete with the cholecystokinin B/ gastrin receptor for G17 binding with adequate capacity to neutralize postprandial gastrin surges. Paper-8557508.
This finding suggests that the action of secretin on LES pressure may be independent on endogenous gastrin, while the glucagon effect on LES tone may be mediated through gastrin. Paper-2426345.
CCKB/ gastrin receptor- stimulated protein synthesis likely results from an enhancement of mRNA translation and involves phosphatidyl inositol 3-kinase and p70 S6 kinase. Paper-2074444.
Gastrin, histamine, acetylcholine, and ghrelin stimulate whereas somatostatin, cholecystokinin, atrial natriuretic peptide, and nitric oxide inhibit acid secretion. Paper-12563871.
The levels of immunoreactive substances of plasma CGRP, somatostatin and gastrin were measured by enzyme immunoassay, and the amount of peptide release was calculated by the trapezoidal method. Paper-12161403.
A CCK- mediated stimulation of paracrine somatostatin secretion from antral and fundic D cells represents a candidate mechanism for the inhibition of the parietal and gastrin cell in humans. Paper-8003572.
The two groups were similar in their morning thyroxin, triiodothyronine, TSH, estradiol, cortisol, gastrin, cholecystokinin, somatostatin, oxytocin, insulin and IGF-1 levels. Paper-1815847.
Aim To identify VR1- expressing endocrine-like cells in human antral glands and to examine whether stimulation with capsaicin causes release of gastrin, somatostatin, and serotonin. Paper-13529820.
Our results suggest that activation of CCK2R by gastrin stimulates heterotrimeric G-protein Gq and G(12/13) mediated intracellular signal transduction pathway in colon cancer cells. Paper-11536300.
Endocytosis of gastrin has been demonstrated in tumour cell lines expressing cholecystokinin-B/gastrin receptor ( CCK-BR); this has raised the possibility of receptor targeted therapy. Paper-12304914.
Receptor binding assays as well as transcriptional and growth studies provide evidence that gastrin- stimulated growth of human gastric cancer is mediated by CCK-B/ gastrin-like receptors. Paper-11661207.
This finding indicates an inhibitory effect of somatostatin on insulin- induced gastrin release and gastrin secretion in addition to the already known effects of somatostatin. Paper-2576801.
We conclude that the postprandial release of GIP and somatostatin increases and that the release of gastrin decreases when the intestinal mucosa is regenerated in celiacs on a gluten-free diet. Paper-4439274.
The postprandial gastrin release was suppressed during the first 60 minutes of glucagon infusion and occurrence of the postprandial increment in the serum gastrin concentration was delayed. Paper-6172771.
The human cholecystokinin (CCK)B/ gastrin receptor was stably transfected into Rat1 fibroblasts to examine the signaling pathways mediated by this seven-transmembrane, G protein-linked receptor. Paper-275169.
These results suggest that post cibum, CCK is an inhibitor of acid secretion by regulating gastrin through local somatostatin; they support the hypothesis that CCK acts as an enterogastrone. Paper-8000920.
BACKGROUND: It has been assumed that gastrin stimulates the growth of pancreatic cancer in an autocrine way through co-expression of gastrin and the cholecystokinin-B receptor ( CCK-BR). Paper-9100933.
Gastrin stimulates gastric acid secretion through direct activation of CCK-B/ gastrin receptors on parietal cells and indirectly through release of histamine from ECL cells. Paper-10679040.
The observation of distinct deletion patterns in small synchronous tumours supports the concept that each gastrin- producing tumour in an individual MEN1 patient arises from an independent cell clone. Paper-13191569.
Somatostatin- induced inhibition of postprandial gastrin, cholecystokinin, pancreatic polypeptide, and insulin release was not influenced by indomethacin pretreatment in healthy subjects. Paper-5121439.
CONCLUSIONS: Glycine-extended gastrin receptors are present on human colon cancer cells that mediate glycine-extended gastrin's trophic effects via a MEK-independent mechanism. Paper-1923432.
These results clearly demonstrated that the G protein- coupled CCK-B/ gastrin receptor is essential for the physiological as well as pathological proliferation of gastric mucosal cells in vivo. Paper-736898.
To explore the role of cholecystokinin ( CCK) in regulating gastrin secretion in humans, the effect of a CCK antagonist ( loxiglumide) on meal-stimulated hormone responses was investigated. Paper-7481819.
In addition, somatostatin binding to cytosol from gastric (fundus and antrum) mucosa and fasting serum gastrin levels and serum gastrin response to a standard breakfast were also studied. Paper-7950673.
Somatostatin is a potent inhibitor of gastrin release; its secretion is regulated predominantly by the cholinergic pathway, which inhibits somatostatin and thus stimulates gastrin release. Paper-5447675.
The trophic effect of gastrin is specific for ECL cells and its sensitivity is enhanced by the female sex and by the genetic background of the multiple endocrine neoplasia type 1 ( MEN-1) syndrome. Paper-237231.
The hypergastrinemia and hyperacidity associated with Helicobacter pylori infection has been explained by either a primary excess of gastrin or a lack of inhibitory influence by somatostatin ( SOM). Paper-8613428.
CONCLUSION: CCK/ gastrin analogs may be a useful new class of receptor- binding peptides for diagnosis and therapy of CCK-B receptor-expressing tumors, such as MTC or small cell lung cancer. Paper-1956646.
In all subjects studied, the cyclic GIF inhibited gastrin secretion during basal conditions as well as during a standard food stimulus, with immediate rebound after the infusion was stopped. Paper-2290017.
Immunocytochemical staining of tumour tissue showed that 9/13 (69%) of insulin producing tumours, 4/14 (29%) of non-functioning tumours and 1/9 (11%) of gastrin producing tumours were IAPP immunoreactive. Paper-236531.
TNF-alpha treatment of H. pylori-negative fragments significantly enhanced bombesin- stimulated gastrin release (by 82%, P < 0.01) and diminished inhibitory feedback by CCK (by 53%, P < 0.05). Paper-1194836.
Chromogranin A ( CgA) is a multifunctional acidic protein that in the stomach is expressed predominantly in enterochromaffin-like cells ( ECL cells) where it is regulated by gastrin. Paper-1693580.
In patients with non-ulcer dyspepsia the absence of the cagA gene and the presence of vacA alleles s2 and m2 were associated with higher values of tryptase and to a lesser extent of gastrin. Paper-1949060.
The unlabeled antibody enzyme method was used for the detection of insulin, glucagon, somatostatin, pancreatic polypeptide, corticotropin, beta-lipotropin, calcitonin, parathyroid hormone, and gastrin. Paper-3899185.
The present study demonstrates that the elevated gastrin concentrations associated with H. pylori infection may be due to a reduction in the paracrine inhibitory effect of SOM on antral gastrin release. Paper-8613428.
Gastrinoma cells were prepared in cell culture to study the effect of SMS 201-995 on gastrin secretion stimulated by secretin and by post-receptor increases in adenosine cyclic nucleotide. Paper-5444783.
Northern analysis and reverse transcription PCR showed, that the human gastric carcinoma cell line ( AGS) expresses both a gastrin mRNA of 0.7 kb and a cholecystokinin transcript of 0.8 kb. Paper-7271182.
The gastrin/ CCK receptor antagonist dibutyryl cGMP inhibited the proliferation of two human colon carcinoma cell lines HCT 116 (EC50 = 1.3 mM) and CBS (EC50 = 2.5 mM) in a dose-dependent manner. Paper-6600654.
Fat in healthy subjects significantly increased and prolonged intragastric pH after the meal while reducing the increments in plasma gastrin and enhancing plasma CCK without alteration of plasma somatostatin. Paper-267871.
Four gastrin/ cholecystokinin-like peptides (G/ CCK) which cross-react with a specific C-terminal gastrin/ CCK antiserum have been isolated from the stomach of the marine crustacean Nephrops norvegicus. Paper-6854541.
In conclusion, these results might indicate that the pharmacological action of Sho-hange-ka-bukuryo-to is closely related to changes in gastrin-, somatostatin-, CGRP- and substance P-IS levels in human plasma. Paper-10894882.
One was identified as a putative MAZ site, mutation of which dramatically reduced both basal and gastrin- stimulated responses of the PAI-2 promoter by a mechanism involving PGE(2) and the small GTPase RhoA. Paper-13589946.
Cholecystokinin in the control of gastric acid and plasma gastrin and somatostatin secretion in healthy subjects and duodenal ulcer patients before and after eradication of Helicobacter pylori. Paper-267871.
OBJECTIVES: Helicobacter pylori infection is associated with an exaggeration of gastrin release following meals or bombesin stimulation attributed to a defect of somatostatin secretion of antral D-cells. Paper-1068837.
In 3 subjects, 337 pmol kg-1 h-1 of CCK slightly stimulated acid secretion when given alone and tended to reduce acid secretion in response to gastrin, but each of the subjects experienced cramping abdominal pain. Paper-3241454.
The effect of gastrin neutralization was evaluated on the in vivo growth of the rat colon line, DHDK12, which expressed cholecystokinin B/ gastrin receptors and secreted glycine-extended gastrin-17 ( G17). Paper-548435.
In vitro studies with Fas- expressing RGM1 cells showed that gastrin stimulation alone directly induced apoptosis via gastrin/ CCK-2 receptor and synergized with FasL stimulation. Paper-12234722.
In AGS cells, gastrin/ CCK-B receptor antagonists inhibited the effect of G-17 and competitively antagonized 125I- G-17 binding, whereas the CCK-preferring (CCK-A) receptor antagonists had no effect. Paper-1155294.
The inhibitory action of gastrazole, was in a similar range as that of SOM implying that physiological acid- induced inhibition of gastric acid may primarily be exerted through inhibition of gastrin endocrine secretion. Paper-13494718.
This daily shows that gastrin releases somatostatin and pancreatic polypeptide in a dose-dependent fashion, and since this release was not acid mediated, it appears likely to be a direct action of gastrin. Paper-3647778.
Expression of Csk, which inactivates Src-family kinases, totally inhibited gastrin- induced Src-like activity detected in anti-Src and anti-Shc precipitates but diminished by 50% Shc phosphorylation and ERK-1 activation. Paper-1940917.
In addition, G-17- mediated increase in cyclin D1 transcription was significantly attenuated by axin or dominant-negative (dn) T-cell factor 4(TCF4), suggesting crosstalk of G-17 with the Wnt-signaling pathway. Paper-10207133.
This study was designed to determine the involvement of leptin in the control of basal, CCK- and meal- induced gastric H+ secretion and plasma gastrin and CCK levels in humans before and after an eradication of H. pylori. Paper-9139204.
Immunohistochemistry was performed using antibodies to Ki-67 and pancreatic hormones (insulin, glucagon, gastrin, somatostatin, pancreatic polypeptide, vasoactive intestinal polypeptide, and corticotropin). Paper-9706576.
CCK and gastrin have close relationships with other peptides like oxytocin, CRF, vasopressin, and the enkephalins; these relationships vary in different projecting areas and in different types of hypothalamic neurons. Paper-4860116.
The area under the drug concentration-time curve ( AUC) from 0 to 4 h after administration correlated well with the Delta- CGRP and Delta- somatostatin release but not with total amount of gastrin released. Paper-12161403.
Human stomach expressed both transcripts of delta CCK-B and entire CCK-B/ gastrin receptor ( CCK-BR), whereas human stomach cancer cell line AGS exclusively expressed delta CCK-B transcripts. Paper-179992.
In vitro, SMS 201-995 inhibits basal gastrin secretion from gastrinoma prepared in acute cell dispersion, but not gastrinoma in cell culture, probably due to differences in basal secretory rates. Paper-5444783.
Somatostatin and gastrin inhibit basal and/or secretin- stimulated bicarbonate excretion by down-regulating the secretin receptor and decreasing cAMP intracellular levels induced by secretin. Paper-1536628.
Endogenous prostanoids participate to regulate antral hormone interactions and may have dual actions on antral somatostatin, as negative modulators of release and as mediators of somatostatin effects on the gastrin cell. Paper-6504786.
The enkephalin-like immunoreactive material of certain neurons identified within the brain and thoracic ganglion shows a complex pattern of co-existence with pancreatic polypeptide- and gastrin/ cholecystokinin-like peptides. Paper-5883127.
Since mature, amidated gastrin ( G-17) can induce cyclin D1, we determined whether G-17- mediated induction of cyclin D1 transcription involved Wnt signaling and CRE- binding protein ( CREB) pathways. Paper-10207133.
The induction of PAI-2 by H. pylori was mediated by release of interleukin-8 and activation of cyclooxygenase-2, and interestingly, gastrin stimulated PAI-2 expression by similar paracrine pathways. Paper-10370276.
Also, there was an increase in basal and gastrin- stimulated somatostatin-containing cell activity accompanied by improved antral neutrophil infiltration in the early phase after H. pylori eradication in gastric ulcers. Paper-9896686.
In Hp positive DU patients, the postprandial acid secretion (measured by continuous intragastric pH monitoring) was accompanied by a pronounced increment in plasma gastrin with negligible increase of intraluminal release of S-S. Paper-630809.
Inhibition of PKC by GF109203X completely blocked the effect of PMA on Shc tyrosine phosphorylation and its subsequent association with Grb2, but had a partial inhibitory effect on the response to gastrin. Paper-1110072.
Gastrin and tryptase were increased in patients with H pylori infection, although the variations were statistically significant only for gastrin; somatostatin and histamine were not influenced by H pylori infection. Paper-1949060.
The release of human pancreatic polypeptide, gastrin, gastric inhibitory polypeptide, and somatostatin in celiac disease related to the histological appearance of jejunal mucosa before and 1 year after gluten withdrawal. Paper-4439274.
The effects of a cholecystokinin (CCK)-A receptor antagonist and a CCK-B receptor antagonist on insulin- induced or gastrin-induced relaxation of the proximal stomach and on plasma glucose and gastrin were also determined. Paper-12270514.
These data indicate that stimulation of the CCK-B/ gastrin receptor activates the rat HDC promoter in a time- and dose-dependent fashion and that this effect is primarily mediated via a PKC-dependent signaling pathway. Paper-713847.
GRP was not able to induce a parietal cell response, a finding that is in accord with the assumption that the stimulatory effect of GRP on gastric acid secretion in vivo is by releasing gastrin from antral G-cells. Paper-27992.
Levels of endogenous progastrin-derived peptides were modified by stable transfection of NRK cells with tetracycline-repressible plasmids containing sequences encoding human gastrin in either the sense or antisense orientation. Paper-1853953.
A more complex genetic background, independent of gastrin and possibly implicating altered function or mutation of p53 and other genes is highly suspected for the development of aggressive type III ECL cell carcinomas and PDECs. Paper-2186436.
These results indicate that the neuropeptides gastrin and CCK can activate multiple signal transduction pathways and act as sole mitogens by binding to the CCKB/ gastrin receptor transfected into Rat1 fibroblasts. Paper-275169.
The relative potencies of CCK-related peptides in inhibiting radioligand binding were caerulein greater than gastrin II approximately equal to CCK-8 approximately equal to CCK-33 greater than CCK-8-DS approximately equal to gastrin I. Paper-5827730.
Zollinger-Ellison syndrome was excluded by reduction in acid secretion and serum gastrin during the observation period as well as by the effect on gastric secretion and serum gastrin after injections of secretin and glucagon. Paper-2905878.
The peptide-betaCD conjugate displays a binding affinity and activation profile comparable to those of HG[11-17] at the cholecysokinin 2 (CCK(2)) receptor, the G protein-coupled receptor responsible for the gastrointestinal function of gastrin. Paper-10288554.
Having recently cloned the rat CCKB receptor, we used it's cDNA to isolate the human CCKB receptor homologue from brain and stomach which encodes a 447 amino acid protein with 90% identity to both rat CCKB and canine gastrin receptors. Paper-7328294.
PKD2 can be activated by phorbol esters both in vivo and in vitro but also by gastrin via the cholecystokinin/CCK(B) receptor in human gastric cancer cells stably transfected with the CCK(B)/gastrin receptor (AGS-B cells). Paper-9167970.
The gastroduodenal segment, although containing several proposed insulinotropic hormones ( gastrin, secretin, and cholecystokinin), had no effect on serum glucose of glucagon and stimulated only small insulin and GIP responses. Paper-3135501.
Previous studies performed in this laboratory have demonstrated somatostatin-containing cells in close proximity to gastrin cells in antral mucosa and have shown that somatostatin exerts a local regulatory effect on gastrin release. Paper-6358898.
Cimetidine (300 mg, as an iv bolus), given 40 min after the beginning of the second infusion, did not affect gastrin- stimulated release of somatostatin and pancreatic polypeptide, whereas acid output was completely abolished. Paper-3647778.
We have shown that gastrin and cholecystokinin octapeptide ( CCK-8) are differently coupled to G protein (GTP- binding protein) through type B cholecystokinin receptors in guinea-pig brain membranes and Jurkat cells. Paper-492903.
In addition, we observed that in response to gastrin, beta1-integrin is tyrosine phosphorylated by Src family kinases and associates with paxillin, a scaffold protein involved in focal adhesion and integrin signalling. Paper-12155440.
Indomethacin given against intravenously infused somatostatin (0.1 microgram.kg-1.h-1) partially reversed the inhibited gastrin response to vagal stimulation without affecting somatostatin-suppressed gastric acid secretion. Paper-6504786.
These studies suggest that duodenal ulcer patients release normal amounts of somatostatin into the circulation and that target cells controlling acid secretion and gastrin release are normally sensitive to somatostatin in these patients. Paper-4725632.
Previous studies have demonstrated that gastrin induces PAI-2 both in gastric epithelial cells expressing the gastrin (CCK-2) receptor and, via activation of paracrine networks, in adjacent cells that do not express the receptor. Paper-13589946.
The gastrin receptor pharmacology on LoVo cells and the lack of appropriate transcripts suggest that gastrin stimulated growth of these cells by a receptor other than CCK-A or CCK-B type and there likely exists another receptor for gastrin. Paper-8030673.
Here, we studied the effects of metoclopramide on human plasma gastrin-, somatostatin-, motilin-, and CCK-like immunoreactive substances (ISs) and ACTH-IS and cortisol under stress conditions using repetitive blood sampling in healthy subjects. Paper-11802284.
Gastrin has the ability to stimulate cell growth in some colorectal cancer cells and some of these cells also express gastrin/ CCKB receptors, suggesting that gastrin and its autocrine loop are involved in their proliferation. Paper-9700109.
A lower and more physiological dose of SS-14 (75 pmol/kg-h) reduced gastric acid and PP responses but failed to affect the serum gastrin response to a meal; whereas a larger, pharmacological dose (500 pmol/kg-h) also suppressed serum gastrin responses. Paper-4995328.
Gastrin acts on CCK2 receptors to control the synthesis of ECL-cell histamine, accelerating the expression of the histamine-forming enzyme histidine decarboxylase ( HDC) at both the transcription and the translation/posttranslation levels. Paper-8805419.
The data are consistent with the suggestions that the intraluminal administration of somatostatin inhibits antral gastrin release in a paracrinic manner and inhibits acid secretion indirectly by inhibiting lumina gastrin-mediated acid secretory activity. Paper-3649258.
Somatostatin inhibits gastrin-stimulated histamine release via a paracrine mechanism, and a prostaglandin E1 analogue ( misoprostol) has been shown to be a potent inhibitor of base-line and gastrin-stimulated histamine release. Paper-6928089.
Strong potentiation between histamine and either gastrin or acetylcholine reflects postreceptor interaction between the distinct pathways as well as the ability of acetylcholine and gastrin to release histamine from mucosal ECL cells. Paper-7215420.
In cells pretreated with EGF or gastrin, the potency of somatostatin for inhibiting vasoactive intestinal peptide- stimulated cAMP content was increased 2-fold as that of somatostatin analog, SMS, for inhibiting cell proliferation. Paper-128673.
However, the findings of an active carboxypeptidase E ( CpE) enzyme and the normal amidated forms of gastrin and cholecystokinin octapeptide ( CCK-8) in Psammomys tissues were inconsistent with CpE-related aberrant processing of insulin. Paper-1029158.
In conclusion, results of these studies indicate that CGRP is capable of exerting both stimulatory and inhibitory effects on ACh release from mucosal-submucosal neurons and gastrin release from antral mucosal G cells in in vitro studies. Paper-58059.
Depletion of the intracellular Ca2+ pools by treatment with thapsigargin blocked the increase in intracellular free calcium concentration induced by gastrin and diminished the ability of the peptide to stimulate Shc phosphorylation and recruitment of Grb2. Paper-1110072.
According to their relative frequency and secretion products the antral gastrin producing G cell and somatostatin producing D cell and the fundic histamine producing ECL cell are the best characterized cell types. Paper-7475958.
Thyrotropin-releasing hormone, somatostatin, arginine vasopressin, angiotensin II, substance P, vasoactive intestinal polypeptide, beta-endorphin, gastrin, and cholecystokinin are all present in assayable quantities in human CSF. Paper-3990332.
No VMAT2 immunoreactivity was observed in five gastrin, four somatostatin and three enteroglucagon/peptideYY tumors of the gastrointestinal tract, in six gastric PDECs, in three adrenocortical growths, and two parathyroid and two lung neuroendocrine tumors. Paper-2192217.
Glucagon used in a standard dose of 25 mug per kg-hr produced about 50% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in the serum gastrin level measured by radioimmunoassay. Paper-2249786.
Neuron-specific enolase ( NSE) as a common marker of neurons and NEC, as well as gastrin ( G-) and somatostatin (D-) immunoreactive cells served for evaluation of volume density, which proved to be the most convenient method for quantitative analysis of NEC. Paper-7006851.
Synergistic interaction between an H2-receptor antagonist and enprostil on 24-hour intragastric pH, serum gastrin concentration, and tissue immunoperoxidase staining for gastrin, somatostatin, and serotonin in a patient with metastatic gastrinoma. Paper-5442747.
We conclude that in man and dog 95% pure CCK weakly stimulates gastric acid secretion and inhibits gastrin- stimulated acid secretion but these actions occur only with doses of CCK that are maximal or supramaximal for pancreatic enzyme secretion. Paper-3241454.
Gastric and intestinal samples contained dense populations of fibers containing vasoactive intestinal peptide, neuropeptide Y, substance P, and enkephalin in the equivalent layers, but somatostatin- and gastrin-releasing peptide-immunoreactive fibers were scarce. Paper-5759497.
The data suggest that gastrin/ CCK receptor antagonists warrant further investigation as therapeutic agents for the control of gastrin-responsive tumours derived from outside, as well as inside, the gastrointestinal tract, including tumours derived from the kidney. Paper-8251733.
In vitro studies showed that Z-360 significantly inhibited gastrin- induced proliferation of human CCK-2 receptor-expressing cells, and also significantly reduced gastrin- induced PKB/Akt phosphorylation to the level of untreated controls. Paper-12750103.
Although GRP is known to participate in meal- stimulated acid secretion by releasing gastrin in a variety of laboratory animals, recent studies were unable to demonstrate a role for endogenous GRP in meal- stimulated gastrin secretion in humans. Paper-12264322.
Using semithin-thin sections five types of endocrine cells (serotonin-, somatostatin-, gastrin/ CCK-, glucagon- and bombesin-immunoreactive cells) have been characterized according to their immunocytochemical reaction and the ultrastructure of the secretory granules. Paper-100786.
CONCLUSIONS: This study demonstrates that 1) gastrin stimulates the gene and protein expression of COX-2 and HGF in human cultured gastric cancer cells and 2) gastrin shows antiapoptotic activity through the upregulation of Bcl-2 and survivin. Paper-10013279.
RNase protection assay detected the RNA for the gastrin/ CCK-B receptor in 11% of the carcinomas investigated, whereas the RNA for the gastrin/ CCK- C receptor was demonstrated in 75% and the RNA for gastrin in 86% of the carcinomas investigated. Paper-403942.
This effect was blocked by the specific CCK-B receptor antagonist D2 but not by the specific CCK-A receptor antagonist L-364,718 or by pertussis toxin, indicating that gastrin targets the SRE via specific CCK-B receptors through a mechanism independent of Gi. Paper-1213938.
Preclinical studies, initiated to identify biological functionality of G17DT-induced antibodies, confirmed that the antibodies both reduced G17 stimulated gastric acid secretion and inhibited gastrin from interacting with the CCK-2 receptor. Paper-9096573.
Double-tailed lipo-tetragastrin derivatives of increasing fatty acid chain length were used to identify the minimum size of the fatty acid moieties (> or = C10) that restricts the access to the CCK-B/ gastrin ( CCK: cholecystokinin) receptor via a membrane-bound pathway. Paper-991751.
It has been assumed that mutations in the K-ras gene induce gastrin gene expression and that gastrin stimulates the growth of colorectal cancer in an autocrine fashion by coexpressing gastrin and cholecystokinin (CCK)2 receptors. Paper-10384578.
A kinase-inactive mutant PAK1(K299A) blocked the gastrin- stimulated dissociation of beta-catenin from E-cadherin, translocation of beta-catenin from the cell membrane to the nucleus, and association of beta-catenin with the transcription factor TCF4. Paper-12991725.
I conclude that the 78-kDa gastrin-binding protein is (i) a member of the hydratase/dehydrogenase family of fatty acid oxidation enzymes, (ii) the gastrin/ CCK- C receptor, and (iii) the target for the antiproliferative action of two gastrin/ CCK receptor antagonists. Paper-8203454.
Cholecystokinin (CCK)-8 and human gastrin I ( gastrin) were found to be almost equipotent in displacing the specific binding of not only 125I-CCK-8 but also 125I-gastrin to both ECL carcinoid tumor and parietal cell membranes of Mastomys natalensis. Paper-7822546.
Endogenous PG generated at ulcer margin appear to be involved in ulcer healing promoted by growth factors and gut hormones such as gastrin or CCK and melatonin acting, at least in part, through increase of induction of COX-2 and local release of PGE(2) in the ulcer area. Paper-11534567.
While CCK appears to be a negative regulator of gastric acid secretion and postprandial release of gastrin in the normal human gastrointestinal tract, its impact on the pathogenesis of acid hypersecretion in Helicobacter pylori-infected individuals remains uncertain. Paper-10679040.
CONCLUSIONS: These results suggest the therapeutic usefulness of inhibitors of gastrin expression and release such as powerful somatostatin analogs ( Sandostatin) or blockers of COX-2 (coxibs) in the control of GC development and progression as chemopreventive agents. Paper-9964684.
G-17- induced degradation of PPARgamma appeared to be mediated through phosphorylation of PPARgamma at serine 84 by a process involving the biphasic phosphorylation of ERK1/2 and activation of the epidermal growth factor receptor ( EGFR). Paper-12012624.
The results of these studies demonstrate that the trophic properties of gastrin in CRC may be mediated in part by transactivation of the EGFR and phosphorylation of ERK1/2, leading to degradation of PPARgamma protein and a decrease in PPARgamma activation. Paper-12012624.
Inappropriate expression of hGH occurred in a high percentage (greater than 80%) of secretin, gastrin, cholecystokinin, and gastric inhibitory peptide producing enteroendocrine cells present in the intact jejunum of 4-6-wk-old L-FABP-596 to +21/ hGH transgenics. Paper-7114661.
Our data support the concept that gastrin stimulates gastric acid secretion directly via CCK-B receptors on parietal cells and indirectly by inducing histamine release from histamine-containing ECL cells, which contributes to acid secretion by parietal cells. Paper-8487177.
Gastrin/ cholecystokinin (G/CCK)-like peptides cross-reacting with an antiserum specific for the carboxyamide terminal pentapeptide of gastrin and CCK have been detected in the eyestalks and in the stomach of the prawn Palaemon serratus using immunocytochemical methods. Paper-5502498.
CEB also presents effective healing action in chronic gastric disease (1.90+/-0.55 vs. 6.86+/-0.46 mm(2) in the control) and its action mechanisms consisted of increasing the PGE(2) (40%) and somatostatin levels (269%) while decreasing the gastrin level in rat plasma (79%). Paper-13573023.
We conclude that the major gastrin17gly binding site on the human colorectal carcinoma cell line DLD-1 is clearly distinct from the cholecystokinin-A and gastrin/cholecystokinin-B receptors, but is similar in some respects to the gastrin/ cholecystokinin- C receptor. Paper-8943130.
Nevertheless the observed receptor interaction of the deliberately membrane-anchored gastrin offers interesting constraints for computational docking experiments on a modelled CCK-B/ gastrin receptor by additionally taking into account information derived from mutagenesis studies. Paper-1112737.
The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. Paper-2270424.
There was a shift in the distribution of the molecular species, so that 6 hours after SMS treatment nearly 50% of total gastrin activity was accounted for by BBG and component I. SMS seems to have a different potency to inhibit release of the various gastrin molecular species. Paper-5464643.
It is proposed that gastrin acting in an autocrine and endocrine manner via a CCK-2R isoform may activate PKB/Akt and that with expression of gastrin and CCK-2R isoforms increasing in BM samples, gastrin may aid progression of BM through amplification of antiapoptotic pathways. Paper-10207489.
CONCLUSIONS: While sst2A receptors on antral gastrin cells presumably mediate somatostatin inhibition of gastrin secretion, the effects of somatostatin on motility and ion transport in the lower gastrointestinal tract may be mediated by sst2A receptors in the neural plexus. Paper-10622771.
Exocytosis of histamine following gastrin stimulation and Ca(2+) entry across the plasma membrane is catalyzed by synaptobrevin and synaptosomal-associated protein of 25 kDa, both characterized as a soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein. Paper-8317674.
In contrast, in acute cell dispersion, the somatostatin analogue inhibited gastrin secretion (basal medium gastrin, 12.8 +/- 1.3 ng/ml; with SMS 201-995 10(-9) M, 9.0 +/- 0.1 ng/ml; with SMS 201-995 10(-8) M, 8.4 +/- 1.5 ng/ml; and with SMS 201-995 10(-7) M, 7.9 +/- 0.2 ng/ml). Paper-5444783.
The observations that the peptide hormone gastrin interacts with transferrin in vitro and that circulating gastrin concentrations are increased in the iron-loading disorder hemochromatosis suggest a possible link between gastrin and iron homeostasis. Paper-13037659.
Gastrin and cholecystokinin ( CCK) octapeptide equipotently stimulated the transcriptional activity of the rat HDC promoter three- to fourfold, and deletion analysis revealed the presence of a gastrin response element within 201 nucleotides upstream of the translational start site. Paper-713847.
The addition of somatostatin inhibited the rate of acid secretion as compared with placebo alone in the control subjects (p < 0.025) without altering the concentration of immunoreactive gastrin in the serum but reducing the concentration of immunoreactive gastrin in gastric juice (p < 0.02). Paper-3649258.
Lipidation with long-chain di-fattyacyl-glycerol moieties was used to anchor gastrin in CCK peptides irreversibly to lipid bilayers lipopeptide transfer to model phospholipid bilayers is fast and quantitative, leading to a different mode of insertion of lipo- gastrin and lipo- CCK in lipid layers. Paper-1112737.
We conclude that inhibition of gastrin- stimulated acid secretion by partially pure cholecystokinin preparations can be explained by their cholecystokinin content and that previously reported differences in inhibitory potencies may be explained by nonspecific adsorption to glass from protein-free solutions. Paper-4054125.
Cholecystokinin (CCK)-A and CCK-B/ gastrin receptors were evaluated with in vitro receptor autoradiography in 406 human tumors of various origins using a sulfated 125I- labeled CCK decapeptide analogue 125I-(D-Tyr-Gly, Nle28,3l)-CCK 26-33 and 125I-labeled Leu15-gastrin as radioligands. Paper-951706.
The expression of the CCK-A receptor in esophageal, gastric and colon cancers and of the CCK-B/ gastrin receptor in the majority of gastric adenocarcinomas screened may be an important indicator of the influence of CCK and gastrin of local or systemic origin on the growth of these cancers. Paper-1200794.
Enterochromaffin-like (ECL) cells play a pivotal role in the peripheral regulation of gastric acid secretion as they respond to the functionally important gastrointestinal hormones gastrin and somatostatin and neural mediators such as pituitary adenylate cyclase- activating peptide and galanin. Paper-8317674.
Basal and post-prandial plasma concentrations of the gut regulatory peptides pancreatic glucagon, motilin, pancreatic polypeptide, gastric inhibitory polypeptide, enteroglucagon, gastrin and peptide YY were suppressed up to 5 hours after subcutaneous administration of a single dose of SMS 201-995. Paper-5742776.
The production of hormones and local messengers such as 5-hydroxytryptamine, gastrin, cholecystokinin, somatostatin, secretin, gastric inhibitory peptide ( GIP), enteroglucagon (glicentin, GLI), motilin, neurotensin, substance P and the enkephalins, by these cells, has been established. Paper-3920159.
Because somatostatin ( SS) inhibits basal and stimulated gastric acid secretion and gastrin release, it is conceivable that decreased gastric SS concentration may be one of the factors responsible for hypergastrinemia found in patients formerly operated on for hypertrophic pyloric stenosis (HPS). Paper-634460.
Moreover, sst2A cells were found abundantly in the neural plexus. sst2A receptors on antral gastrin cells could mediate somatostatin inhibition on gastrin secretion, whereas those in the neural plexus could mediate somatostatin effects on motility and ion transport in the lower gastrointestinal tract. Paper-10255848.
This review discusses the consequences of disrupting genes that are important for ECL cell histamine release and synthesis ( HDC, gastrin, and CCK(2) receptor genes) and genes that are important for "cross-talk" between H(2) receptors and other receptors on the parietal cell (CCK(2), M(3), and sst(2) receptors). Paper-12214488.
In order to define the gastrin- binding sites of the GBP in greater detail, we have constructed a truncation mutant lacking residues 221-318 of the N-terminal domain and a series of point mutants in which the lysine residues in the first 220 residues of the N-terminal domain were mutated to arginine residues. Paper-9144500.
Gastrin secretion is regulated by a cholinergic neuron that causes inhibition of somatostatin secretion and thus stimulation of gastrin secretion (disinhibition) and a noncholinergic neuron that causes direct stimulation of gastrin secretion by releasing the neurotransmitter, bombesin (or gastrin-releasing peptide). Paper-6602459.
The cholecystokinin receptor antagonist loxiglumide did not attenuate pancreatic enzyme response but diminished antral motor response by 72% (P less than 0.05) and release of pancreatic polypeptide by 91% (P less than 0.05); it enhanced gastrin release and abolished retardation of reappearance of phase III with sham feeding. Paper-7429704.
In the liver, 10 types of peptidergic nerve fibers were detected: glucagon-, glucagon-like peptide- ( GLP), somatostatin-, neuropeptide Y- ( NPY), vasoactive intestinal polypeptide-, neurotensin-, gastrin/ cholecystokinin C-terminus-, substance P-, serotonin-, and galanin-immunoreactive nerve fibers. Paper-7874950.
Our data demonstrate that gastrin- stimulated PKD2 activation involves a heterotrimeric G alpha(q) protein as well as the activation of phospholipase C. Furthermore, we show that PKD2 can be activated by classical and novel members of the protein kinase C (PKC) family such as PKC alpha, PKC epsilon, and PKC eta. Paper-9167970.
Two structurally-related guanine nucleotide-binding protein-coupled receptors for two related peptides, cholecystokinin ( CCK) and gastrin, have evolved to exhibit substantial diversity in specificity of ligand recognition, in their molecular basis of binding these ligands, and in their mechanisms of biochemical and cellular regulation. Paper-12877728.
Glycine-extended gastrin induced a dose-dependent increase in [3H]thymidine uptake in LoVo (143 +/- 8% versus control at 10(-10) M) and HT 29 (151 +/- 11% versus control at 10(-10) M) cells that was not inhibited by PD 134308 or by a mitogen- activated protein (MAP) or ERK kinase ( MEK) inhibitor (PD 98509). Paper-1923432.
Since somatostatin inhibits basal and stimulated gastric acid secretion and gastrin release, it is conceivable that decreased gastric somatostatin concentration may be one of the factors responsible for gastric hypersecretion found in patients who have undergone long-term pylorotomy for hypertrophic pyloric stenosis. Paper-7950673.
CONCLUSION: In the present study, we have shown that Z-360 combined with gemcitabine can inhibit pancreatic tumor growth and prolong survival in a pancreatic carcinoma xenograft model, on a possible mode of action being the inhibition of gastrin- induced PKB/Akt phosphorylation through blockade of the CCK-2 receptor. Paper-12750103.
Immunocytochemical examination revealed a fourfold increase in insulin-positive cells in the human pancreatic cell grafts in GLP-1 plus gastrin-treated mice, and most of this increase was accounted for by the appearance of cytokeratin 19-positive pancreatic duct cells expressing insulin. Paper-12953476.
It is concluded that (a) there is a distinct cephalic phase of gastropancreatic secretion, antroduodenal motility, and pancreatic polypeptide release in humans that is primarily under cholinergic control and that (b) endogenous cholecystokinin is involved in antral motor, gastrin, and pancreatic polypeptide responses to sham feeding. Paper-7429704.
Another derivative of cyclic GMP, 8-Bromo cGMP used as control due to its considerably weaker affinity for the gastrin/ CCK receptor, did not compete with radiolabeled gastrin for binding to HCT 116 cells and had no effect on the morphology or proliferation in monolayer cultures of HCT 116 or CBS cells at concentrations up to 10 mM. Paper-6600654.
These data indicate that endogenous cholecystokinin inhibits gastric acid secretion under basal conditions and gastrin release and gastric acid secretion during infusion of bombesin in humans and suggest that the augmented effect of loxiglumide on bombesin-stimulated gastric acid secretion may be explained largely by enhanced gastrin release. Paper-7295741.
These include wingless-type MMTV ( mouse mammary tumor virus) integration site family member 7A ( WNT7A) induced by IFNT, as well as galectin, proteases, protease inhibitors, transporters for glucose and amino acids, gastrin releasing polypeptide, insulin-like growth factor binding protein 1 and a hypoxia inducible factor. Paper-13510589.
CONCLUSIONS: These results indicate that endogenous CCK released by a fatty meal delays gastric emptying and inhibits gastric acid and plasma gastrin responses in healthy subjects, but in DU patients the inhibitory effect of CCK is less pronounced, suggesting a defect in the action of this hormone on gastrin release and gastric acid secretion. Paper-7986667.
To investigate whether the effects of progastrin observed in hGAS colon require the presence of other forms of circulating gastrin, we have crossed hGAS ( hg(+/+)) with gastrin knockout ( G(-/-)) mice to generate mice that express progastrin and no murine gastrin (G(-/-)hg(+/+)). Paper-11195737.
These synonyms are used for gene GAST (gastrin): Gastrin, GAS.
These accession numbers are used for gene GAST: P78464 (UNIPROT__AC), P78463 (UNIPROT__AC), CAA25006 (NCBI_GENBANK__AC), AAA52520 (NCBI_GENBANK__AC).
GAST is a homologue of GAST (gastrin) from Bos taurus.
GAST is a homologue of GAST (gastrin) from Pan troglodytes.
GAST is a homologue of Gast (gastrin) from Mus musculus.
GAST is a homologue of Gast (gastrin) from Rattus norvegicus.
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iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.