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1 sphorylation and cell motility stimulated by gastrin.
2 ity to the regulation of G-cell secretion of gastrin.
3 TFF1, which can be suppressed by the hormone gastrin.
4 , gastric acid content, and plasma levels of gastrin.
5 eptor for cholecystokinin (CCK) and amidated gastrin.
6 ccurring forms and extensive similarities to gastrin.
7 een associated with elevated levels of serum gastrin.
8 otection against injury by administration of gastrin.
9 MKN45 cells were cocultured with IFNgamma or gastrin.
10 y reduced fundic expression of both Pdx1 and gastrin.
11 ion of STAT3 in the MKN45 cell line, but not gastrin.
12 timulates the G-cells to produce and secrete gastrin.
13 f the antral gastric mucosa does not require gastrin.
14 cells, to assess proliferative responses to gastrin.
15 ecificity, phytaspase was shown to hydrolyze gastrin-1 and cholecystokinin at the predicted sites in
16 e normal, except for the elevation of plasma gastrin (1031 pg/ml; reference value <108) and chromogra
17 f pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneo
28 and HDAC7 with HDC promoter, suggesting that gastrin activates HDC gene expression at least partly by
30 erum inflammatory mediators, antibodies, and gastrin among germfree and H pylori-monoinfected INS-GAS
31 letion of the pentaglutamate sequence in the gastrin analogs lowered the tumor uptake by a factor of
32 ognized for decades as potent stimulants for gastrin and acid secretion, although the molecular basis
33 pecific calcimimetic, cinacalcet, stimulated gastrin and acid secretion, whereas the calcilytic, NPS
38 wth factor gastrin, and mice mutant for both gastrin and Hip1r exhibited normalization of both prolif
39 L cells are coupled by the couplet molecules gastrin and histamine and by a prior asymmetrical cell d
41 tric cancer in INS-GAS mice that overexpress gastrin and IL-8Tg mice infected with Helicobacter felis
42 one has led to new research into the role of gastrin and its receptor (cholecystokinin-2 receptor) in
46 cells from C57BL/6 mice were incubated with gastrin and separated into nuclear and cytoplasmic fract
52 centages of circulating intact somatostatin, gastrin, and bombesin radiopeptides in mouse models, res
54 ased expression of the gastric growth factor gastrin, and mice mutant for both gastrin and Hip1r exhi
55 red that membrane-associated ANX II binds PG/gastrins, and partially mediates growth factor effects o
57 rming growth factor-alpha, amphiregulin, and gastrin; and activation of extracellular signal-regulate
59 cted of possibly having ZES, the appropriate gastrin assay to use, the role of surgery in patients wi
60 2 receptor mRNA abundance and increased 125I-gastrin binding was demonstrated in IEC-6 cells followin
61 d earlier reported the presence of 33-36 kDa gastrin-binding proteins on cellular membranes of colon
62 e combination of epidermal growth factor and gastrin, can stimulate regeneration of beta-cells in viv
64 expressed in antral mucosal cells including gastrin cells and TFF2-expressing deep glandular mucous
69 , nitric oxide, and galanin), hormonal (e.g. gastrin, cholecystokinin, and ghrelin), paracrine (e.g.
74 had increases in glucagon-like peptide-1 and gastrin concentrations that were expected with treatment
75 fibrillary acidic protein (GFAP+) expressed gastrin de novo through a mechanism that required PKA.
76 nd histology of 12-month-old wild-type (WT), gastrin-deficient (G-/-) and somatostatin-deficient (SOM
77 investigated in hypergastrinemic (INS-GAS), gastrin-deficient (GAS(-/-)), Tff1-deficient (Tff1(+/-))
83 rophic gastritis from hypochlorhydria in the gastrin-deficient mouse predisposes the stomach to gastr
89 in in mice is expressed in insulin(+) cells, gastrin expression in humans with T2D occurs in both ins
90 In vivo and in vitro experiments show that gastrin expression is rapidly eliminated upon exposure o
91 netic lineage tracing in mice indicates that gastrin expression is turned on in a subset of different
96 roduct of the gastrin gene (glycine-extended gastrin (G-gly)) as a new ligand for the F(1)-ATPase.
97 identified a peptide hormone product of the gastrin gene (glycine-extended gastrin (G-gly)) as a new
98 igated how menin regulates expression of the gastrin gene and induces generation of submucosal gastri
100 recent developments in the biology of other gastrin gene products, including the precursor progastri
102 onstrate a novel mechanism for regulation of gastrin gene transcription and support a concept that p5
103 ed and incompletely processed product of the gastrin gene, has been shown to induce colonic hyperprol
104 cyclase-activating peptide), hormonal (e.g., gastrin, ghrelin, and apelin), and paracrine (e.g., hist
105 y cilia on gastric endocrine cells producing gastrin, ghrelin, and somatostatin (Sst), hormones regul
106 rum chromogranin A, neuron-specific enolase, gastrin, glucagon, vasoactive intestinal peptide, pancre
107 ease of enteroendocrine cell types including gastrin-, glucagon/GLP-1-, CCK-, secretin-producing cell
110 nsforming growth factor-alpha, and endocrine gastrins have been implicated in the tumorigenic potenti
112 actor, and neuromedin U) and peripheral (eg, gastrin, histamine, acetylcholine, somatostatin, cholecy
116 se results support an important role for the gastrin-histamine axis in Helicobacter-induced gastric c
117 R, revealing similar up-regulation of Sox-2, Gastrin, HoxA5, GATA4/5/6, Villin and Forkhead 6 (Foxl1)
118 (CCKS) and doubly protonated Tyr12-sulfated gastrin II (GST) resulted in complete loss of SO3 from a
119 meal-stimulated acid secretion by releasing gastrin in a variety of laboratory animals, recent studi
121 s demonstrate that the trophic properties of gastrin in CRC may be mediated in part by transactivatio
126 focus on the role of endocrine and autocrine gastrins in colon cancer and review recent advances that
127 udies also provide support for the idea that gastrin, in concert with other hormones, could potential
128 ew we consider important additional roles of gastrin, including regulation of genes encoding proteins
131 n-positive cells; increased levels of plasma gastrin; increased expression of transforming growth fac
133 colon carcinoma cells depleted of Galpha13, gastrin-induced FAK Tyr(P)-397 and paxillin Tyr(P)-31 ph
140 d in transgenic mice overexpressing amidated gastrin (INS-GAS) and mice in which hypergastrinemia was
145 e gastric corpus and antrum, suggesting that gastrin is an essential cofactor for gastric corpus carc
149 e that express a human progastrin transgene, gastrin knockout mice, and C57BL/6 mice (controls); the
151 owed lower cilia numbers and acid but higher gastrin levels than mice fed a standard diet, suggesting
153 gastrin (INS-GAS) mice have high circulating gastrin levels, and develop spontaneous atrophic gastrit
155 inhibits acid secretion and increases serum gastrin levels, factors strongly associated with cancer
159 aging studies had lower preoperative fasting gastrin levels; had a longer delay before surgery; more
163 both wild-type and hypergastrinemic insulin-gastrin mice, using immunohistochemistry and flow cytome
167 These results point to a distinct effect of gastrin on carcinogenesis of both the gastric corpus and
168 We therefore investigated the effects of gastrin on intestinal regeneration following a range of
169 amma expression might mediate the effects of gastrin on the proliferation of colorectal cancer (CRC).
170 nd gastrin-receptor knockout mice as well as gastrin-overexpressing and cAMP-overexpressing mice deve
171 -tetraacetic acid (DOTA)-conjugated divalent gastrin peptides based on the C-terminal sequence of min
172 ynthesized and screened a series of divalent gastrin peptides for improved biochemical and biologic c
174 ow markedly reduced gastrin mRNA, many fewer gastrin-producing (G) cells in the stomach antrum, hypog
176 d with Helicobacter felis and given the CCK2/gastrin receptor antagonist YF476 and/or the histamine H
177 (400 ppm in drinking water) alone, the CCK2/gastrin receptor antagonist YM022 (45 mg/kg/wk) alone, a
178 is unclear how FAK receives signals from the gastrin receptor or other G-protein-coupled receptors th
179 e variants of the cholecystokinin-2 (CCK(2))/gastrin receptor; however, their relative contributions
181 ported the presence of novel progastrin (PG)/gastrin receptors on normal and cancerous intestinal cel
183 te with gastric atrophy, we examined whether gastrin regulates Shh expression in parietal cells.
187 hanical strain stimulated (2-fold to 8-fold) gastrin release, and decreasing pH from 7.4 to 5.5 inhib
192 says are in high demand, and analysis of pro-gastrin releasing peptide (ProGRP) as a small cell lung
194 into tumor cells, their affinity toward the gastrin releasing peptide receptor (GRPr), metabolic sta
195 e been proposed for diagnosis and therapy of gastrin releasing peptide receptor (GRPR)-expressing tum
197 483 cells with siRNA causes an inhibition of gastrin-releasing peptide (GRP) -induced phosphorylation
198 halocyanine-peptide conjugates targeting the gastrin-releasing peptide (GRP) and integrin receptors i
200 for the oncogenic transformations induced by gastrin-releasing peptide (GRP) and its receptor, GRP-R,
201 of a cohort of itch-sensing genes, including gastrin-releasing peptide (GRP) and MAS-related GPCR mem
202 NeuroD2 that contribute to these processes: gastrin-releasing peptide (GRP) and the small conductanc
204 only vasoactive intestinal polypeptide (VIP)/gastrin-releasing peptide (GRP) cells located ventrally
205 ctions of spinal opioid-related peptides and gastrin-releasing peptide (GRP) in awake, behaving monke
206 Brief light pulses or microinjection of gastrin-releasing peptide (GRP) into the third ventricle
211 ning the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR).
213 tides have demonstrated high affinity toward gastrin-releasing peptide (GRP) receptors in vivo that a
216 epolarization and a second SCN neuropeptide, gastrin-releasing peptide (GRP), can acutely enhance and
217 hetamine-related transcript (CART), galanin, gastrin-releasing peptide (GRP), neuropeptide Y (NPY), n
219 oxide, vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP), substance P, and calcit
220 a subset of spinal interneurons, labeled by gastrin-releasing peptide (Grp), that receive direct syn
223 ied 5-HT1A as a key receptor in facilitating gastrin-releasing peptide (GRP)-dependent scratching beh
228 Normally, levels of mammalian bombesin (gastrin-releasing peptide [GRP]) drop postnatally, but t
230 ed release of the pruritogenic neuropeptides gastrin-releasing peptide and atrial natriuretic peptide
232 ropeptides of the bombesin family, including gastrin-releasing peptide and neuromedin B, which are fo
233 ranscription that regulate these parameters: gastrin-releasing peptide and the small conductance, cal
234 ry adenylate cyclase-activating peptide, and gastrin-releasing peptide have shown how these peptides
236 ed by activation of cholinergic and bombesin/gastrin-releasing peptide neurons, acts mainly by releas
238 ed by cells expressing the G-protein-coupled gastrin-releasing peptide receptor (GRP-R) and is curren
239 imilar rationale, radioligands targeting the gastrin-releasing peptide receptor (GRP-R) might offer a
242 e treatment of prostate cancer, radiolabeled gastrin-releasing peptide receptor (GRPr) antagonists ha
246 Although our previous study suggested that gastrin-releasing peptide receptor (GRPR) is an itch-spe
251 A growing body of evidence suggests that gastrin-releasing peptide receptor (GRPR) might be a val
254 he Trpv1-Cre population, depends on CGRP and gastrin-releasing peptide receptor (GRPR) transmission b
257 BBN) is a peptide with high affinity for the gastrin-releasing peptide receptor (GRPr), a receptor th
260 peptide that binds with high affinity to the gastrin-releasing peptide receptor (GRPR), which is over
263 is and to use bombesin analogs to target the gastrin-releasing peptide receptor for the diagnosis and
264 icals, such as prostate-specific membrane or gastrin-releasing peptide receptor ligands for the imagi
265 BON cells or BON cells stably expressing the gastrin-releasing peptide receptor treated with either p
266 between an agonist and an antagonist for the gastrin-releasing peptide receptor were found to have ex
271 ded to understand the expression of PSMA and gastrin-releasing peptide receptors in different types o
273 ied two TMs (neuron-specific enolase and pro-gastrin-releasing peptide) that differentiate the risk o
274 g neurons respond to histamine and coexpress gastrin-releasing peptide, a peptide involved in itch se
275 uitary adenylate cyclase-activating peptide, gastrin-releasing peptide, and substance P is reviewed.
277 expressing cells, but a second neuropeptide, gastrin-releasing peptide, still induced strong response
278 ve agonist stimulated scratching behavior by gastrin-releasing peptide- and opioid-dependent mechanis
280 e compounds demonstrated that antagonists of gastrin-releasing peptide/neuromedin B receptors (BB/BB)
285 These studies of nutrient-regulated G-cell gastrin secretion and growth provide definitive evidence
288 tion of FAK activity, is sufficient to block gastrin-stimulated paxillin phosphorylation, cell motili
293 lls, Rgnef forms a complex with FAK and upon gastrin stimulation, FAK translocates to newly-forming f
294 s that bombesin causes release of endogenous gastrin that activates sensory neurons located in the ga
296 nker was used for crosslinking radio-labeled gastrins to membrane proteins from gastrin/PG responsive
298 and particularly in neurons, elevated plasma gastrin, vacuolization in parietal cells, and retinal de
300 les would also stimulate cell division - the gastrin would stimulate cell division of ECL cells while
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