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1 cells, to assess proliferative responses to gastrin.
2 sphorylation and cell motility stimulated by gastrin.
3 ity to the regulation of G-cell secretion of gastrin.
4 TFF1, which can be suppressed by the hormone gastrin.
5 , gastric acid content, and plasma levels of gastrin.
6 eptor for cholecystokinin (CCK) and amidated gastrin.
7 ccurring forms and extensive similarities to gastrin.
8 een associated with elevated levels of serum gastrin.
9 otection against injury by administration of gastrin.
10 timulates the G-cells to produce and secrete gastrin.
11 ecificity, phytaspase was shown to hydrolyze gastrin-1 and cholecystokinin at the predicted sites in
12 e normal, except for the elevation of plasma gastrin (1031 pg/ml; reference value <108) and chromogra
13 f pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneo
24 and HDAC7 with HDC promoter, suggesting that gastrin activates HDC gene expression at least partly by
25 erum inflammatory mediators, antibodies, and gastrin among germfree and H pylori-monoinfected INS-GAS
26 letion of the pentaglutamate sequence in the gastrin analogs lowered the tumor uptake by a factor of
29 ognized for decades as potent stimulants for gastrin and acid secretion, although the molecular basis
30 pecific calcimimetic, cinacalcet, stimulated gastrin and acid secretion, whereas the calcilytic, NPS
35 wth factor gastrin, and mice mutant for both gastrin and Hip1r exhibited normalization of both prolif
36 L cells are coupled by the couplet molecules gastrin and histamine and by a prior asymmetrical cell d
38 tric cancer in INS-GAS mice that overexpress gastrin and IL-8Tg mice infected with Helicobacter felis
39 one has led to new research into the role of gastrin and its receptor (cholecystokinin-2 receptor) in
43 cells from C57BL/6 mice were incubated with gastrin and separated into nuclear and cytoplasmic fract
48 centages of circulating intact somatostatin, gastrin, and bombesin radiopeptides in mouse models, res
50 ased expression of the gastric growth factor gastrin, and mice mutant for both gastrin and Hip1r exhi
51 red that membrane-associated ANX II binds PG/gastrins, and partially mediates growth factor effects o
52 rming growth factor-alpha, amphiregulin, and gastrin; and activation of extracellular signal-regulate
54 cted of possibly having ZES, the appropriate gastrin assay to use, the role of surgery in patients wi
55 2 receptor mRNA abundance and increased 125I-gastrin binding was demonstrated in IEC-6 cells followin
56 d earlier reported the presence of 33-36 kDa gastrin-binding proteins on cellular membranes of colon
66 had increases in glucagon-like peptide-1 and gastrin concentrations that were expected with treatment
67 fibrillary acidic protein (GFAP+) expressed gastrin de novo through a mechanism that required PKA.
68 investigated in hypergastrinemic (INS-GAS), gastrin-deficient (GAS(-/-)), Tff1-deficient (Tff1(+/-))
80 in in mice is expressed in insulin(+) cells, gastrin expression in humans with T2D occurs in both ins
81 In vivo and in vitro experiments show that gastrin expression is rapidly eliminated upon exposure o
82 netic lineage tracing in mice indicates that gastrin expression is turned on in a subset of different
87 roduct of the gastrin gene (glycine-extended gastrin (G-gly)) as a new ligand for the F(1)-ATPase.
88 identified a peptide hormone product of the gastrin gene (glycine-extended gastrin (G-gly)) as a new
89 igated how menin regulates expression of the gastrin gene and induces generation of submucosal gastri
91 recent developments in the biology of other gastrin gene products, including the precursor progastri
93 onstrate a novel mechanism for regulation of gastrin gene transcription and support a concept that p5
94 ed and incompletely processed product of the gastrin gene, has been shown to induce colonic hyperprol
95 cyclase-activating peptide), hormonal (e.g., gastrin, ghrelin, and apelin), and paracrine (e.g., hist
96 y cilia on gastric endocrine cells producing gastrin, ghrelin, and somatostatin (Sst), hormones regul
97 rum chromogranin A, neuron-specific enolase, gastrin, glucagon, vasoactive intestinal peptide, pancre
98 ease of enteroendocrine cell types including gastrin-, glucagon/GLP-1-, CCK-, secretin-producing cell
100 nsforming growth factor-alpha, and endocrine gastrins have been implicated in the tumorigenic potenti
104 (CCKS) and doubly protonated Tyr12-sulfated gastrin II (GST) resulted in complete loss of SO3 from a
105 meal-stimulated acid secretion by releasing gastrin in a variety of laboratory animals, recent studi
107 s demonstrate that the trophic properties of gastrin in CRC may be mediated in part by transactivatio
112 focus on the role of endocrine and autocrine gastrins in colon cancer and review recent advances that
113 udies also provide support for the idea that gastrin, in concert with other hormones, could potential
114 ew we consider important additional roles of gastrin, including regulation of genes encoding proteins
117 n-positive cells; increased levels of plasma gastrin; increased expression of transforming growth fac
119 colon carcinoma cells depleted of Galpha13, gastrin-induced FAK Tyr(P)-397 and paxillin Tyr(P)-31 ph
126 d in transgenic mice overexpressing amidated gastrin (INS-GAS) and mice in which hypergastrinemia was
127 , was determined in transgenic FVB/N insulin-gastrin (INS-GAS) mice and Mongolian gerbils as models o
132 e gastric corpus and antrum, suggesting that gastrin is an essential cofactor for gastric corpus carc
136 e that express a human progastrin transgene, gastrin knockout mice, and C57BL/6 mice (controls); the
138 owed lower cilia numbers and acid but higher gastrin levels than mice fed a standard diet, suggesting
140 gastrin (INS-GAS) mice have high circulating gastrin levels, and develop spontaneous atrophic gastrit
142 inhibits acid secretion and increases serum gastrin levels, factors strongly associated with cancer
145 aging studies had lower preoperative fasting gastrin levels; had a longer delay before surgery; more
148 both wild-type and hypergastrinemic insulin-gastrin mice, using immunohistochemistry and flow cytome
152 These results point to a distinct effect of gastrin on carcinogenesis of both the gastric corpus and
153 We therefore investigated the effects of gastrin on intestinal regeneration following a range of
154 amma expression might mediate the effects of gastrin on the proliferation of colorectal cancer (CRC).
155 nd gastrin-receptor knockout mice as well as gastrin-overexpressing and cAMP-overexpressing mice deve
156 -tetraacetic acid (DOTA)-conjugated divalent gastrin peptides based on the C-terminal sequence of min
157 ynthesized and screened a series of divalent gastrin peptides for improved biochemical and biologic c
159 ow markedly reduced gastrin mRNA, many fewer gastrin-producing (G) cells in the stomach antrum, hypog
161 (400 ppm in drinking water) alone, the CCK2/gastrin receptor antagonist YM022 (45 mg/kg/wk) alone, a
162 is unclear how FAK receives signals from the gastrin receptor or other G-protein-coupled receptors th
163 e variants of the cholecystokinin-2 (CCK(2))/gastrin receptor; however, their relative contributions
165 ported the presence of novel progastrin (PG)/gastrin receptors on normal and cancerous intestinal cel
167 te with gastric atrophy, we examined whether gastrin regulates Shh expression in parietal cells.
170 hanical strain stimulated (2-fold to 8-fold) gastrin release, and decreasing pH from 7.4 to 5.5 inhib
174 says are in high demand, and analysis of pro-gastrin releasing peptide (ProGRP) as a small cell lung
177 , we show that the spinal neurons expressing gastrin releasing peptide receptor (GRPR) primarily comp
178 into tumor cells, their affinity toward the gastrin releasing peptide receptor (GRPr), metabolic sta
179 e been proposed for diagnosis and therapy of gastrin releasing peptide receptor (GRPR)-expressing tum
181 483 cells with siRNA causes an inhibition of gastrin-releasing peptide (GRP) -induced phosphorylation
182 halocyanine-peptide conjugates targeting the gastrin-releasing peptide (GRP) and integrin receptors i
184 for the oncogenic transformations induced by gastrin-releasing peptide (GRP) and its receptor, GRP-R,
185 of a cohort of itch-sensing genes, including gastrin-releasing peptide (GRP) and MAS-related GPCR mem
186 NeuroD2 that contribute to these processes: gastrin-releasing peptide (GRP) and the small conductanc
187 al horn excitatory interneurons that express gastrin-releasing peptide (GRP) are part of the circuit
189 only vasoactive intestinal polypeptide (VIP)/gastrin-releasing peptide (GRP) cells located ventrally
191 ctions of spinal opioid-related peptides and gastrin-releasing peptide (GRP) in awake, behaving monke
192 Brief light pulses or microinjection of gastrin-releasing peptide (GRP) into the third ventricle
198 ning the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR).
200 tides have demonstrated high affinity toward gastrin-releasing peptide (GRP) receptors in vivo that a
205 epolarization and a second SCN neuropeptide, gastrin-releasing peptide (GRP), can acutely enhance and
206 hetamine-related transcript (CART), galanin, gastrin-releasing peptide (GRP), neuropeptide Y (NPY), n
208 oxide, vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP), substance P, and calcit
209 a subset of spinal interneurons, labeled by gastrin-releasing peptide (Grp), that receive direct syn
211 ied 5-HT1A as a key receptor in facilitating gastrin-releasing peptide (GRP)-dependent scratching beh
216 Normally, levels of mammalian bombesin (gastrin-releasing peptide [GRP]) drop postnatally, but t
218 ed release of the pruritogenic neuropeptides gastrin-releasing peptide and atrial natriuretic peptide
220 ropeptides of the bombesin family, including gastrin-releasing peptide and neuromedin B, which are fo
221 ranscription that regulate these parameters: gastrin-releasing peptide and the small conductance, cal
222 ry adenylate cyclase-activating peptide, and gastrin-releasing peptide have shown how these peptides
224 r support for a critical role of dorsal horn gastrin-releasing peptide neurons in itch circuits, but
225 e in pain.SIGNIFICANCE STATEMENT Dorsal horn gastrin-releasing peptide neurons serve a well-establish
226 ed by activation of cholinergic and bombesin/gastrin-releasing peptide neurons, acts mainly by releas
229 ed by cells expressing the G-protein-coupled gastrin-releasing peptide receptor (GRP-R) and is curren
230 imilar rationale, radioligands targeting the gastrin-releasing peptide receptor (GRP-R) might offer a
233 e treatment of prostate cancer, radiolabeled gastrin-releasing peptide receptor (GRPr) antagonists ha
234 e spinal cord to establish that NK1R and the gastrin-releasing peptide receptor (GRPR) are coexpresse
238 These NK1R neurons comprise a subset of gastrin-releasing peptide receptor (GRPR) interneurons a
240 Although our previous study suggested that gastrin-releasing peptide receptor (GRPR) is an itch-spe
245 A growing body of evidence suggests that gastrin-releasing peptide receptor (GRPR) might be a val
249 he Trpv1-Cre population, depends on CGRP and gastrin-releasing peptide receptor (GRPR) transmission b
252 BBN) is a peptide with high affinity for the gastrin-releasing peptide receptor (GRPr), a receptor th
255 peptide that binds with high affinity to the gastrin-releasing peptide receptor (GRPR), which is over
260 is and to use bombesin analogs to target the gastrin-releasing peptide receptor for the diagnosis and
261 icals, such as prostate-specific membrane or gastrin-releasing peptide receptor ligands for the imagi
262 BON cells or BON cells stably expressing the gastrin-releasing peptide receptor treated with either p
263 between an agonist and an antagonist for the gastrin-releasing peptide receptor were found to have ex
264 different neuropeptides for itch, including gastrin-releasing peptide receptor, natriuretic peptide
270 ded to understand the expression of PSMA and gastrin-releasing peptide receptors in different types o
274 ied two TMs (neuron-specific enolase and pro-gastrin-releasing peptide) that differentiate the risk o
275 g neurons respond to histamine and coexpress gastrin-releasing peptide, a peptide involved in itch se
276 uitary adenylate cyclase-activating peptide, gastrin-releasing peptide, and substance P is reviewed.
278 expressing cells, but a second neuropeptide, gastrin-releasing peptide, still induced strong response
279 ve agonist stimulated scratching behavior by gastrin-releasing peptide- and opioid-dependent mechanis
281 e compounds demonstrated that antagonists of gastrin-releasing peptide/neuromedin B receptors (BB/BB)
286 These studies of nutrient-regulated G-cell gastrin secretion and growth provide definitive evidence
289 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
295 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