ライフサイエンスコーパス: cholecystokinin

1 al Ca(2+) spiking evoked by acetylcholine or cholecystokinin.

2 concentrations of caerulein, an ortholog of cholecystokinin.

3 ed pancreatic fluid secretion in response to cholecystokinin.

4 ssion of calcitonin-gene-related peptide and cholecystokinin.

5 os responses to peripheral administration of cholecystokinin.

6 stimulation of pancreatic acinar cells with cholecystokinin.

7 tides substance P, dynorphin, enkephalin and cholecystokinin.

8 oop of the receptor for the peptide hormone, cholecystokinin.

9 e obtained at 30-minute intervals for plasma cholecystokinin.

10 astrointestinal peptide hormones gastrin and cholecystokinin.

11 one functions, with perhaps the exception of cholecystokinin.

12 cells stimulated with the intestinal hormone cholecystokinin.

13 imulation via the vagal nerve or the hormone cholecystokinin.

14 -3-yl]-2-m-tolyl propionic acid, a selective cholecystokinin 1 (CCK 1) receptor antagonist, is descri

15 Cholecystokinin-1 receptor agonist A-71623 [Boc-Trp-Lys(

16 Pegylated (PEG)-CCK9A, A70104 (a cholecystokinin-1 receptor antagonist), and chlorisondam

17 Blockage of the cholecystokinin-1 receptor or the nicotinic acetylcholin

18 Stimulation of the cholecystokinin-1 receptor-dependent vagal anti-inflamma

19 e inflammation and reduce organ damage via a cholecystokinin-1 receptor-mediated vagovagal reflex in

20 than 1000-fold selectivity over the related cholecystokinin-1 receptor.

21 Because the cholecystokinin 2 receptor (CCK2R) is overexpressed in v

22 proliferation and carcinogenesis through the cholecystokinin 2 receptor (CCK2R)-partly by increasing

23 Cholecystokinin 2 receptor antagonists encompass a wide

24 ined on in vitro colonic crypt cultures from cholecystokinin 2 receptor knockout and wild-type mice.

25 vation of Group I metabotropic glutamate and cholecystokinin 2 receptors in neurons of the amygdala.

26 Group I metabotropic glutamate receptors and cholecystokinin 2 receptors, respectively.

27 ally express multiple splice variants of the cholecystokinin-2 (CCK(2))/gastrin receptor; however, th

28 The gastrin/cholecystokinin-2 (CCK-2) receptor has been identified a

29 eptide to the cells expressing both hMC4 and cholecystokinin-2 (CCK-2) receptors.

30 approach to the identification of selective cholecystokinin-2 receptor (CCK-2R) ligands resulted in

31 Cholecystokinin-2 receptor (CCK2R) is the primary recept

32 or) in carcinogenesis and the development of cholecystokinin-2 receptor antagonists.

33 he development of novel medications, such as cholecystokinin-2 receptor antagonists.

34 ormation in a manner dependent upon upstream cholecystokinin-2 receptor expression.

35 n gastric cancer cell line stably expressing cholecystokinin-2 receptor was treated with amidated gas

36 h into the role of gastrin and its receptor (cholecystokinin-2 receptor) in carcinogenesis and the de

37 Gastrin, acting via cholecystokinin-2 receptors on enterochromaffin-like cel

38 We compared the abilities of cholecystokinin-33 (CCK-33) and CCK-8 to reduce food int

39 uronide (E17betaG), prostaglandin E2 (PGE2), cholecystokinin 8 (CCK8), and vasopressin displayed an i

40 xcitability in vitro and in vivo, as well as cholecystokinin 8-stimulated secretion of pancreatic enz

41 spinothalamic (STT) neurons that co-contain cholecystokinin-8 (CCK) and galanin (GAL) are sexually d

42 physiologic and pathologic concentrations of cholecystokinin-8 (CCK).

43 f the cellular uptake of the known substrate cholecystokinin-8 in the presence of the insulinotropic

44 2 along the apical plasma membrane following cholecystokinin-8 stimulation.

45 lume; gallbladder contraction in response to cholecystokinin-8 was normal.

46 ying in response to exogenously administered cholecystokinin-8 was significantly reduced in MUC1.Tg m

47 at the synergistic interaction between vagal cholecystokinin-A receptors (CCKARs) and leptin receptor

48 show that certain variants of mu-opioid and Cholecystokinin-A receptors could lead to altered or adv

49 r postprandial incremental AUC for GLP-1 and cholecystokinin (all P < 0.05).

50 ponse to injury due to administration of the cholecystokinin analogue cerulein and interfered with ac

51 Two photolabile cholecystokinin analogues were developed and characteriz

52 elease of gut hormones and mediators such as cholecystokinin and 5-HT.

53 Compared with NP, HP increased insulin and cholecystokinin and decreased ghrelin and glucose-depend

54 al and isolated pyloric pressures and plasma cholecystokinin and GLP-1 concentrations, and greater su

55 Cholecystokinin and GLP-1 release and pyloric stimulatio

56 ated gastric emptying, enhanced postprandial cholecystokinin and glucagon-like peptide 1 concentratio

57 concentrations and higher early postprandial cholecystokinin and glucagon-like peptide 1 peaks than d

58 o superfusion with the satiety neuropeptides cholecystokinin and glucagon-like peptide 1.

59 .05) but not obese men, and lipid-stimulated cholecystokinin and peptide YY and the desire to eat wer

60 ult duodenum, Nkx2.2 becomes dispensable for cholecystokinin and secretin production.

61 Mechanisms for the regulation of cholecystokinin and secretin release by releasing factor

62 sent on acinar cells, particularly those for cholecystokinin and secretin, have been better character

63 sent on acinar cells, particularly those for cholecystokinin and secretin, have been better character

64 al fat absorption, secretion of the peptides cholecystokinin and secretin, regulation of hepatic lipo

65 uction of gallbladder contraction by food or cholecystokinin and that movement of bacteria through th

66 egulation to diet and hormones, particularly cholecystokinin, and in the regeneration that occurs aft

67 stinal peptide (VIP), calretinin, calbindin, cholecystokinin, and somatostatin.

68 ion of long-chain fatty acyl-CoA, release of cholecystokinin, and subsequent neuronal signaling.

69 fibers sensitive to satiety signals such as cholecystokinin, and that MC4R signaling in vagal effere

70 mediator of ethanol-induced sensitization of cholecystokinin- and carbachol-regulated Ca(2+) signalin

71 vented the sensitizing effects of ethanol on cholecystokinin- and carbachol-stimulated Ca(2+) signali

72 s we reveal that in the mouse basal amygdala cholecystokinin- and parvalbumin-containing basket cells

73 norepinephrine reuptake inhibitors, opioids, cholecystokinin antagonists, neurokinin-antagonists, chl

74 e intestinal polypeptide, neuropeptide Y, or cholecystokinin (antigens commonly co-expressed by subsp

75 induced by the anorectic hormones amylin and cholecystokinin, as well as by lithium chloride and lipo

76 a decreased GB ejection fraction induced by cholecystokinin at cholescintigraphy and after disappear

77 taspase was shown to hydrolyze gastrin-1 and cholecystokinin at the predicted sites in vitro, thus de

78 and ghrelin stimulate whereas somatostatin, cholecystokinin, atrial natriuretic peptide, and nitric

79 Gastrin-induced nuclear export of menin via cholecystokinin B receptor (CCKBR)-mediated activation o

80 Recent information suggests that the cholecystokinin B receptor has a role in pancreatic amyl

81 Gastrin, acting via gastrin/cholecystokinin-B (CCK-B), now termed CCK2, receptors on

82 onstrated clear differences in mechanisms of cholecystokinin binding and activation of these structur

83 release ACh after stimulation with sulfated cholecystokinin but not norepinephrine.

84 New data suggest that cholecystokinin can stimulate neurons located in the dor

85 , vesicular glutamate transporter 3 (VGLUT3)/cholecystokinin/CB(1) cannabinoid receptor(+) and neurop

86 ramidal neurons from basket cells expressing cholecystokinin (CCK(b) cells) and parvalbumin (PV(b) ce

87 veal that a subset of NTS neurons containing cholecystokinin (CCK(NTS)) is responsive to nutritional

88 ) that coexpress leptin receptor (LepRb) and cholecystokinin (CCK) (PBN LepRb(CCK) neurons), which pr

89 Cholecystokinin (CCK) acts on vagal afferent neurons to

90 receptor (CCK2R) is the primary receptor for cholecystokinin (CCK) and amidated gastrin.

91 The distributions of cholecystokinin (CCK) and CCK receptors in the central n

92 Separate studies have implicated the cholecystokinin (CCK) and endocannabinoid systems in fea

93 Gut hormones, such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1

94 ls evoked by anorexigenic molecules, such as cholecystokinin (CCK) and leptin, to stimulate feeding.

95 ls evoked by anorexigenic molecules, such as cholecystokinin (CCK) and leptin, to stimulate feeding.

96 Here we identify cholecystokinin (CCK) and noradrenergic, dopamine beta-h

97 tide (GIP), glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK) and oxyntomodulin (OXM) as treatme

98 endin-4, a glucagon-like peptide 1 analogue, cholecystokinin (CCK) and pancreatic polypeptide (PP).

99 ignaling influences FA-mediated secretion of cholecystokinin (CCK) and secretin, peptides released by

100 Cholecystokinin (CCK) and the different molecular forms

101 Cholecystokinin (CCK) can stimulate exocrine secretion b

102 The combination of gastric distension and cholecystokinin (CCK) enhances both suppression of food

103 Glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) exert important complementary bene

104 Animals infused with high doses of cholecystokinin (CCK) exhibit hyperamylasemia, pancreati

105 ll subtypes, presumably parvalbumin (PV) and cholecystokinin (CCK) expressing basket interneurons.

106 ediating the secretion of the fat-stimulated cholecystokinin (CCK) hormone in the small intestine, wh

107 the gene for the classic intestinal hormone cholecystokinin (CCK) in amounts similar to those in the

108 as under the curve for total GLP-1, GIP, and cholecystokinin (CCK) in plasma.

109 artly due to increased intestinal release of cholecystokinin (CCK) in rat pups as a result of increas

110 matodendritic release of the satiety peptide cholecystokinin (CCK) in the brain.

111 Cholecystokinin (CCK) in the nervous system has effects

112 Cholecystokinin (CCK) increased the activity of CTSB, ca

113 5-HT and cholecystokinin (CCK) induced dose-dependent increases i

114 Here, we show that a non-biased agonist, cholecystokinin (CCK) induces conformational states of t

115 e we show that serotonin 5-HT1B receptors in cholecystokinin (CCK) inhibitory interneurons of the mam

116 has demonstrated that one mechanism by which cholecystokinin (CCK) inhibits food intake through activ

117 Cholecystokinin (CCK) interacts with two types of G prot

118 Here, we find that cholecystokinin (Cck) is a direct transcriptional target

119 Cholecystokinin (CCK) is a neuropeptide expressed in neu

120 Cholecystokinin (CCK) is a peptide hormone that induces

121 Cholecystokinin (CCK) is a potent regulator of visceral

122 Cholecystokinin (CCK) is a satiation peptide released du

123 Cholecystokinin (CCK) is a satiety hormone produced by d

124 dant and functionally important neuropeptide cholecystokinin (CCK) is able to selectively depolarize

125 The gene encoding cholecystokinin (Cck) is abundantly expressed in the mam

126 Cholecystokinin (CCK) is an abundant neuropeptide involv

127 Cholecystokinin (CCK) is an important satiety factor, ac

128 Cholecystokinin (CCK) is released in response to lipid i

129 V), somatostatin (SOM), calretinin (CR), and cholecystokinin (CCK) label four distinct chemical class

130 administration of an opioid and intravenous cholecystokinin (CCK) on gallbladder ejection fraction.

131 the present study we examined the actions of cholecystokinin (CCK) on layer 6b neocortical neurons us

132 This report examines the effect of cholecystokinin (CCK) on plasma cholesterol level and in

133 entified based on their expression of either cholecystokinin (CCK) or parvalbumin.

134 c htMVLs that contain melanocortin (MSH) and cholecystokinin (CCK) pharmacophores that are connected

135 t of rapamycin (mTOR) pathway by the hormone cholecystokinin (CCK) plays an important role in normal

136 nique small molecule ligand that is a type 1 cholecystokinin (CCK) receptor agonist and type 2 CCK re

137 Oligomerization of the G protein-coupled cholecystokinin (CCK) receptor has been demonstrated, bu

138 In addition, T2R stimulation of cholecystokinin (CCK) secretion was enhanced directly by

139 nase A (PKA) is sufficient and necessary for cholecystokinin (CCK) signaling to trigger vagal afferen

140 Cholecystokinin (CCK) stimulates the type 1 CCK receptor

141 The effect of cholecystokinin (CCK) was also seen in intact acini usin

142 i) the proportion of DMV neurones excited by cholecystokinin (CCK) was unaltered but the proportion o

143 , we have utilized full agonist analogues of cholecystokinin (CCK) with Aladan distributed throughout

144 Cholecystokinin (CCK), a neuropeptide originally discove

145 I cells in the intestine secrete cholecystokinin (CCK), a peptide hormone that stimulates

146 ility from signal-transduction decoupling of cholecystokinin (CCK), a physiological agonist for small

147 d and amphetamine-related transcript (cart), cholecystokinin (cck), calcitonin gene-related peptide (

148 Stimulation with cholecystokinin (CCK), carbachol, and vasoactive intesti

149 Another satiety hormone, cholecystokinin (CCK), has also been linked to activatio

150 at two key intestinal hormones, secretin and cholecystokinin (CCK), in physiologic doses, act through

151 Cholecystokinin (CCK), one of the most abundant neuropep

152 luding amylin, secreted by the pancreas, and cholecystokinin (CCK), secreted by the small intestine.

153 ected CREB target based on previous reports, cholecystokinin (Cck), was not controlled by CREB in str

154 terneurons containing the anxiogenic peptide cholecystokinin (CCK), we also examined whether the PCP-

155 essing either nitric oxide synthase (NOS) or cholecystokinin (CCK), which are known to be physiologic

156 One such satiation signal is cholecystokinin (CCK), whose effects on food intake are

157 auses a decrease in presynaptic release from cholecystokinin (CCK)- but not parvalbumin-containing in

158 utamic acid decarboxylase 1 (GAD1) in either cholecystokinin (CCK)- or neuropeptide Y (NPY)-expressin

159 posure of pancreatic acini to ethanol blocks cholecystokinin (CCK)-8-stimulated apical exocytosis and

160 hese effects partly through induction of the cholecystokinin (CCK)-B receptor: CCKB blockade in mPFC

161 Q-type Ca(2+) channels, whereas release from cholecystokinin (CCK)-containing interneurons is generat

162 nduced suppression of inhibition-expressing, cholecystokinin (CCK)-containing, hippocampal interneuro

163 Parvalbumin- and cholecystokinin (CCK)-expressing basket cells provide tw

164 tor-expressing (CB1R+) interneurons - mainly cholecystokinin (CCK)-expressing cells.

165 naptic inhibitory interactions exist between cholecystokinin (CCK)-expressing hilar commissural assoc

166 es SC-associated perisomatic inhibition from cholecystokinin (CCK)-expressing interneurons.

167 n mice, selective loss of TrkB signalling in cholecystokinin (CCK)-GABAergic neurons induces glucocor

168 by GW reduced acetylcholine (ACh)-, but not cholecystokinin (CCK)-induced Ca(2+) oscillations in a c

169 ted mice exhibited increased spontaneous and cholecystokinin (CCK)-induced contractions of longitudin

170 Cholecystokinin (CCK)-induced pancreatic growth in mice

171 pe-3 (5-HT3) receptor antagonist, attenuates cholecystokinin (CCK)-induced suppression of food intake

172 f basket cells that express the neuropeptide cholecystokinin (CCK).

173 the cannabinoid type 1 receptor (CB(1)R) and cholecystokinin (CCK).

174 ulated by gastrointestinal hormones, notably cholecystokinin (CCK).

175 V), somatostatin (SST), calretinin (CR), and cholecystokinin (CCK).

176 Several of the gut hormones (cholecystokinin (CCK); peptide YY3-36 (PYY3-36); glucago

177 ork has demonstrated robust brain changes in cholecystokinin (CCK-8) following social defeat.

178 ction of acinar pancreatitis by supramaximal cholecystokinin (CCK-8) stimulation inhibits VAMP8-media

179 the cholinergic agonist carbachol (Cch) and cholecystokinin (CCK-8), including 1) amylase secretion,

180 ogic stimulation with the intestinal hormone cholecystokinin (CCK-8).

181 he dichotomy of the two basket cell classes, cholecystokinin- (CCK) and parvalbumin (PV)-containing b

182 Both mu-opioid (MOP) and type 2 cholecystokinin (CCK2) receptors are present in areas of

183 ECD of doubly protonated Tyr2-sulfated cholecystokinin (CCKS) and doubly protonated Tyr12-sulfa

184 ein, which are expressed most heavily in the cholecystokinin class of gamma-aminobutyric acid (GABA)

185 ere no differences in fasting or incremental cholecystokinin concentrations.

186 PSCs but never in neighbouring PACs, whereas cholecystokinin, consistently evoking Ca(2+) signals in

187 its gamma-aminobutyric acid release from the cholecystokinin-containing population of interneurons; a

188 Chlorpyrifos evoked robust upregulation of cholecystokinin, corticotropin releasing hormone, galani

189 ns demonstrate that several peptide markers (cholecystokinin, corticotropin-releasing hormone, and ta

190 ofiling identified off-target effects at the cholecystokinin, dopamine D2, histamine H1 and H2, melan

191 ciated with increased circulating leptin and cholecystokinin, elevated fatty acid oxidation, and 3-be

192 rans as fluid phase tracers and observed the cholecystokinin-elicited formation and translocation of

193 One subtype of interneuron, the cholecystokinin-expressing basket cell (CCKBC), is parti

194 g neurons possess the characteristics of the cholecystokinin-expressing basket cells (CCK-BC).

195 apses formed by hippocampal parvalbumin- and cholecystokinin-expressing basket cells onto pyramidal n

196 decays evoked by axo-axonic, parvalbumin- or cholecystokinin-expressing basket cells were found to be

197 erneuron cohorts, including parvalbumin- and cholecystokinin-expressing basket cells.

198 apses, we recorded unitary IPSCs (uIPSCs) at cholecystokinin-expressing interneuron-pyramidal cell co

199 hippocampal interneurons largely focusing on cholecystokinin-expressing interneurons (CCK-INTs), a pr

200 umin-, but not somatostatin-, calbindin-, or cholecystokinin-expressing interneurons were preferred s

201 tivation of CB1 endocannabinoid receptors on cholecystokinin-expressing interneurons, CA2 ITDP result

202 r types of GABAergic cells, parvalbumin- and cholecystokinin-expressing interneurons.

203 They received GABAergic synapses from cholecystokinin-expressing mossy fiber-associated cells

204 ACs, whereas the physiological PAC stimulant cholecystokinin failed to evoke Ca(2+) signals in PSCs.

205 Cholecystokinin failed to modulate the miniature IPSCs r

206 neither dose affected glucagon, GLP-1, GIP, cholecystokinin, gastric emptying, or energy intake.

207 concentrations [insulin, glucagon, ghrelin, cholecystokinin, gastric inhibitory polypeptide (GIP), g

208 ease in concentrations of insulin, glucagon, cholecystokinin, GIP, GLP-1, and PYY, and an increase in

209 ession of energy intake after adjustment for cholecystokinin, GLP-1, and insulin was related inversel

210 No change in cholecystokinin, GLP-1, or PYY concentrations was observ

211 a concentrations of the gut-derived peptides cholecystokinin, GLP-1, or PYY.

212 samples were drawn at regular intervals for cholecystokinin, glucagon-like peptide 1 (GLP-1), and pe

213 the use of 3-dimensional ultrasound), plasma cholecystokinin, glucagon-like peptide 1, glucose-depend

214 ntropyloroduodenal motility, plasma ghrelin, cholecystokinin, glucagon-like peptide 1, peptide YY, in

215 Antropyloroduodenal motility, cholecystokinin, glucagon-like peptide-1 (GLP-1), insuli

216 t on acinar cells, especially muscarinic and cholecystokinin, have been better identified and charact

217 ze migration of synaptically interconnected, cholecystokinin-immunopositive [CCK(+)] interneurons in

218 Recent studies have elucidated a role for cholecystokinin in the regulation of bicarbonate and flu

219 ed receptors (beta-adrenergic, secretin, and cholecystokinin) induces translocation of Gbeta2 to the

220 orm a meta-analysis for ghrelin, peptide YY, cholecystokinin, insulin, and pancreatic polypeptide.

221 GABA transmission from perisomatic-targeting cholecystokinin interneurons with impaired GABA synthesi

222 endent insulinotropic polypeptide (GIP), and cholecystokinin (leucine study only) were measured for 6

223 of nutrition significantly increased plasma cholecystokinin levels throughout the lipopolysaccharide

224 We developed three cholecystokinin-like probes with Aladan situated at the

225 Here, we demonstrate that cholecystokinin-like receptor (CCKLR) and drosulfakinin

226 kinase) signaling and significantly enhances cholecystokinin-mediated pancreatic amylase secretion.

227 rge effect), peptide YY (medium effect), and cholecystokinin (medium effect for ED, large effect for

228 those in glutamic acid decarboxylase 67 and cholecystokinin mRNA levels.

229 g approximately 40% of PV neurons and 65% of cholecystokinin neurons, increased spontaneous and amphe

230 tons, and specifically in those that express cholecystokinin, not parvalbumin.

231 o receive an intravenous injection of either cholecystokinin octapeptide (200 mug/kg in 0.3 mL saline

232 peridol (HAL-0.12 mg/kg, i.p.), and sulfated cholecystokinin octapeptide (CCK-0.05 and 0.1 mg/kg, i.p

233 ith OATP1B1, OATP1B3 specifically transports cholecystokinin octapeptide (CCK-8).

234 rat model of cardiopulmonary resuscitation, cholecystokinin octapeptide induced mild hypothermia, at

235 Gallbladder emptying in response to cholecystokinin octapeptide was measured gravimetrically

236 nal discharges in response to 30 and 60 pmol cholecystokinin octapeptide were significantly lower in

237 After injection of cholecystokinin octapeptide, blood temperature decreased

238 of survival were significantly better in the cholecystokinin octapeptide-treated animals when compare

239 idence suggests a direct secretory action of cholecystokinin on human acinar cells.

240 ed DBS, unaffected by DPPIV inhibition or by cholecystokinin or 5-HT3 receptor antagonists, but was i

241 activation of fast-spiking interneurons with cholecystokinin or channelrhodopsin-2.

242 NeuN-IR does not co-localize with either cholecystokinin- or vasoactive intestinal polypeptide, b

243 pressures but also slightly increased plasma cholecystokinin (P < 0.05).

244 The postprandial rise in plasma cholecystokinin, peptide YY (PYY), glucagon-like peptide

245 res, plasma glucagon-like peptide 1 (GLP-1), cholecystokinin, peptide YY, ghrelin, blood glucose, ser

246 facing Cav2.1 (i.e. parvalbumin) or Cav2.2 (cholecystokinin) positive presynaptic active zones are c

247 ally targeting parvalbumin-positive (PV+) or cholecystokinin-positive (CCK+) basket cells (BCs), we t

248 Cholecystokinin-positive (CCK+) basket cells are a major

249 diated by the selective muting of inhibitory cholecystokinin-positive basket cells (CCK(+) BCs), thro

250 ncy action potentials in post hoc identified cholecystokinin-positive CA1 basket cells elicited IPSCs

251 ry synapses originating from parvalbumin and cholecystokinin-positive interneurons.

252 We show that two types of cholecystokinin-positive local circuit inhibitory intern

253 n, choline acetylatransferase, and G6-Gly, a cholecystokinin precursor.

254 The satiety peptide, cholecystokinin, presynaptically facilitated glutamate t

255 uding those encoding the anti-opioid peptide cholecystokinin, pronociceptive Substance P (SP), Neurok

256 ffers substantially, with higher peak plasma cholecystokinin, PYY, GLP-1, and GLP-2 concentrations be

257 The type 1 cholecystokinin receptor (CCK1R) has multiple physiologi

258 f a new antagonist radioligand of the type 1 cholecystokinin receptor (CCK1R), (2-fluorophenyl)-2,3-d

259 urable binding to the closely related type 2 cholecystokinin receptor (CCK2R).

260 r 1 (NTSR1), neuropeptide S receptor (NPSR), cholecystokinin receptor A (CCKAR), and the kappa-opioid

261 tely 20% of GFP-positive neurons coexpressed cholecystokinin receptor A.

262 within the second extracellular loop of the cholecystokinin receptor interacts with a specific acidi

263 , the position 33 probe docked at the type A cholecystokinin receptor was more easily quenched in the

264 whereas the same probe docked at the type B cholecystokinin receptor was more easily quenched in the

265 e were built into two homology models of the cholecystokinin receptor, based on the recent crystal st

266 iod, inducible/reversible forebrain-specific cholecystokinin receptor-2 transgenic (IF-CCKR-2 tg) mic

267 ily A G protein-coupled receptor, the type 1 cholecystokinin receptor.

268 new molecular model of the agonist-occupied cholecystokinin receptor.

269 alpha13 downstream of gastrin and the type 2 cholecystokinin receptor.

270 rminants for this pocket within type 1 and 2 cholecystokinin receptors (CCK1R and CCK2R), we prepared

271 Although both type A and B cholecystokinin receptors bind cholecystokinin with high

272 ndependent risk factor for gallstone disease.Cholecystokinin receptors may be responsible for the alt

273 ative pain-facilitating neurons, or block of cholecystokinin receptors prevented or significantly att

274 mass and protein content was independent of cholecystokinin receptors, associated with a rapid incre

275 l sequencing of labeled wild-type and mutant cholecystokinin receptors.

276 udied in solution and docked at type A and B cholecystokinin receptors.

277 Cholecystokinin reduced the amplitude of the after-hyper

278 Increased cholecystokinin, reduced insulin, leptin, adiponectin, T

279 -terminal EF-hand calcium-binding protein 1, cholecystokinin, reelin, or a combination of these molec

280 onstrated significantly greater postprandial cholecystokinin release compared with participants with

281 ts of eating disorder severity, postprandial cholecystokinin response, and subjective responses to te

282 cy of endogenous glucagon-like peptide-1 and cholecystokinin satiation were significantly increased i

283 neous EPSCs) onto TH-EGFP neurons, including cholecystokinin-sensitive neurons, an effect blocked by

284 proximately 13%, P < 0.05), increased plasma cholecystokinin, slightly reduced blood glucose and incr

285 ubpopulations were distinguished by peptide (cholecystokinin, somatostatin) or calcium-binding protei

286 ry protein phosphorylation, sensitization of cholecystokinin-stimulated Ca(2+) signaling, and potenti

287 Cholecystokinin-stimulated endoscopic pancreatic functio

288 ignaling, and potentiation of both basal and cholecystokinin-stimulated extracellular signal-regulate

289 rom pancreatic duct cells and suggested that cholecystokinin stimulation of human pancreatic acinar c

290 ells transfected to stably express the human cholecystokinin subtype 2 receptor) in mice at 4 h after

291 Gastrin/cholecystokinin subtype 2 receptors (CCK-2Rs) are overex

292 ted by a bolus injection of the neuropeptide cholecystokinin-tetrapeptide (CCK-4) in 16 healthy male

293 mber of inhibitory synapses and the ratio of cholecystokinin to parvalbumin-positive inhibitory input

294 o-expression of mu opioid receptor (MOR) and cholecystokinin type 2 receptor (CCK2).

295 The porcine cholecystokinin type A receptor (CCKAR) is a candidate g

296 ro as high affinity selective antagonists at cholecystokinin types 1 and 2 (CCK(1) and CCK(2)) recept

297 R1 signaling induced increased expression of cholecystokinin, vasoactive intestinal peptide, peptide

298 On day 5, fasting cholecystokinin was less, and ghrelin was higher, in lea

299 and T3 remained low, whereas adiponectin and cholecystokinin were normal.

300 type A and B cholecystokinin receptors bind cholecystokinin with high affinity, resulting in fully e