ライフサイエンスコーパス: cholecystokinin

1 one functions, with perhaps the exception of cholecystokinin.

2 imulation via the vagal nerve or the hormone cholecystokinin.

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

4 concentrations of caerulein, an ortholog of cholecystokinin.

5 ed pancreatic fluid secretion in response to cholecystokinin.

6 os responses to peripheral administration of cholecystokinin.

7 stimulation of pancreatic acinar cells with cholecystokinin.

8 tides substance P, dynorphin, enkephalin and cholecystokinin.

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

10 cells stimulated with the intestinal hormone cholecystokinin.

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

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

13 astrointestinal peptide hormones gastrin and cholecystokinin.

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

15 based, long-acting, stable, highly selective cholecystokinin 1 receptor (CCK-1R) agonists with the po

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

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

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

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

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

21 8, very high selectivity for CCK-1R over the cholecystokinin 2 receptor (CCK-2R), strong reduction of

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

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

24 Cholecystokinin 2 receptor antagonists encompass a wide

25 e than 2 decades, it has been known that the cholecystokinin 2 receptor is a promising target for the

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

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

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

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

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

31 es, known for their high potential to target cholecystokinin-2 receptor (CCK2R) expressing tumors, ha

32 f radiolabeled gastrin analogs targeting the cholecystokinin-2 receptor (CCK2R) is an attractive appr

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

34 and targeted radiotherapy with radiolabeled cholecystokinin-2 receptor (CCK2R) targeting peptide pro

35 ith high affinity and specificity toward the cholecystokinin-2 receptor (CCK2R), which is overexpress

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

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

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

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

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

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

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

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

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

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

46 2 along the apical plasma membrane following cholecystokinin-8 stimulation.

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

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

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

50 in, glucagon-like peptide 1, peptide YY, and cholecystokinin after RYGB, whereas levels of ghrelin we

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

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

53 Two photolabile cholecystokinin analogues were developed and characteriz

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

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

56 including food cues, intragastric nutrients, cholecystokinin and ghrelin.

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

58 Cholecystokinin and GLP-1 release and pyloric stimulatio

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

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

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

62 e peptide 1 [GLP-1], total peptide YY [PYY], cholecystokinin and insulin), and subjective feelings of

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

64 showed no changes in response to capsaicin, cholecystokinin and potassium chloride in TNX-deficient

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

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

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

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

69 ally excited by the anorectic neuromodulator cholecystokinin, and inhibited by orexigenic neuromodula

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

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

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

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

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

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

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

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

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

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

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

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

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

83 ; they were excited by the anorectic peptide cholecystokinin, but inhibited by orexigenic neuropeptid

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 Cholecystokinin (CCK) and leptin are satiety-controlling

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

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

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

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

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

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

101 Cholecystokinin (CCK) and the different molecular forms

102 Glucagon-like peptide 1 (GLP-1) and cholecystokinin (CCK) are gut-derived peptide hormones k

103 Cholecystokinin (CCK) can stimulate exocrine secretion b

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

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 evealed dramatically increased expression of cholecystokinin (CCK) in regenerating muscle from Trim33

111 beta cell expression of the peptide hormone cholecystokinin (Cck) in response to obesity and show th

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

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

114 5-HT and cholecystokinin (CCK) induced dose-dependent increases i

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

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

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

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 Cholecystokinin (Cck) mRNA and protein expression in the

131 Cholecystokinin (CCK) neurons located deeper within the

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

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

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

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

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

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

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 pendent TRPV4 pathway was independent of the cholecystokinin (CCK) stimulation pathway.

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 sures were measured continuously, and plasma cholecystokinin (CCK), ghrelin, and glucagon-like peptid

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

151 -dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), peptide YY (PYY), and neurotensin

152 e report the role of endogenous neuropeptide cholecystokinin (CCK), released from dentate CCK interne

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

154 , which exclusively express the neuropeptide cholecystokinin (CCK), to two groups of spatially segreg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Cholecystokinin (CCK)-induced pancreatic growth in mice

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

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

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

176 utamatergic neurons that express the peptide cholecystokinin (CCK).

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

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

179 We first show that cholecystokinin (CCK+), parvalbumin (PV+), and somatosta

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

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

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

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

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

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

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

187 ere no differences in fasting or incremental cholecystokinin concentrations.

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

189 responsive to pharmacological inhibition of cholecystokinin-containing interneurons.

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

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

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

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

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

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

196 eral biological satiation signals, including cholecystokinin, exendin-4 (a glucagon-like peptide-1 re

197 of vesicular glutamate transporter three and cholecystokinin expressing cortical interneurons (CCK(+)

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

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

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

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

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

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

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

205 enhanced, whereas perisomatic inhibition by cholecystokinin-expressing interneurons is weakened.

206 As parvalbumin- and cholecystokinin-expressing interneurons mediate distinct

207 k development, a connectivity preference for cholecystokinin-expressing interneurons to target calbin

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

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

210 eceives enhanced inhibitory drive from local cholecystokinin-expressing interneurons, the activity of

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

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

213 Fructose malabsorption induces cholecystokinin expression in the ileum and cecum by cha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 of nutrition significantly increased plasma cholecystokinin levels throughout the lipopolysaccharide

230 Here, we identify the Cholecystokinin-like peptide Drosulfakinin (DSK) that fu

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

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

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

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

235 5 receptor, GFRAL, is located in a subset of cholecystokinin neurons which span the area postrema and

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

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

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

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

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

241 Gallbladder emptying in response to cholecystokinin octapeptide was measured gravimetrically

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

243 After injection of cholecystokinin octapeptide, blood temperature decreased

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

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

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

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

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

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

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

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

252 peptide-1 (GLP-1), polypeptide YY (PYY), and cholecystokinin peptides were measured.

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

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

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

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

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

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

259 The satiety peptide, cholecystokinin, presynaptically facilitated glutamate t

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

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

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

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

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

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

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

267 l hypothalamic nucleus (VMN), we studied the cholecystokinin receptor B-expressing (CCKBR-expressing)

268 neuromuscular junction activity through the cholecystokinin receptor homolog on motor axons, setting

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

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

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

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

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

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

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

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

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

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

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

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

281 onstrated significantly greater postprandial cholecystokinin release compared with participants with

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

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

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

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

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

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

288 Cholecystokinin-stimulated endoscopic pancreatic functio

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

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 Administration of cholecystokinin to mice resulted in acute release of BAs

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

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

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 Tgr5(ISC-/-) mice were given cholecystokinin; we measured the effects of BA release i

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