ライフサイエンスコーパス: CCK-8

1 us protease that degrades cholecystokinin-8 (CCK-8).

2 n E2 (PGE2) and cholecystokinin octapeptide (CCK-8).

3 titis caused by cholecystokinin octapeptide (CCK-8).

4 agonist (Sp-cAMPS) or CCK1 receptor agonist (CCK-8).

5 ally transports cholecystokinin octapeptide (CCK-8).

6 e cholescintigraphy with octapeptide of CCK (CCK-8).

7 with the intestinal hormone cholecystokinin (CCK-8).

8 ivity (Fos-LI) induced by cholecystokinin-8 (CCK-8).

9 al tumor, process pro-CCK mainly to amidated CCK 8.

10 CCK-58, whereas the brain primarily produces CCK-8.

11 st dose on the effects of the second dose of CCK-8.

12 ger with fatty meal than with either dose of CCK-8.

13 Binding studies were performed using (125)I-CCK-8.

14 et sensitizes rats to pancreatitis caused by CCK-8.

15 rmal responsiveness to intrabrain PGE(2) and CCK-8.

16 eased only in rats treated with ethanol plus CCK-8.

17 s and inhibits currents evoked by leptin and CCK-8.

18 is resulting from repeated administration of CCK-8.

19 tiating effect of intraperitoneally injected CCK-8.

20 ton-Hunter-CCK-8 binding by gastrin-17-I and CCK-8.

21 pM, 2200 Ci/mmol) and 0.1-100 nM unlabelled CCK-8.

22 olites (1-3 mmol/L) and then stimulated with CCK-8.

23 rs both the basal and postprandial levels of CCK-8.

24 cial for recognition and/or translocation of CCK-8.

25 d intake, but CCK-33 was more effective than CCK-8.

26 fied residues might form hydrogen bonds with CCK-8.

27 combination partially reversed the effect of CCK-8.

28 ns but OLETF expressed Fos-LI in response to CCK-8.

29 ated myenteric but not DVC Fos-LI induced by CCK-8.

30 d no response to either high or low doses of CCK-8.

31 or =50% as normal with a 10-min infusion of CCK-8.

32 -free saline with 0.5% ethanol (5 microl) or CCK-8 (0 or 1.6 microg) in artificial cerebro-spinal flu

33 Serotonin (7.75 microg) or CCK-8 (0.12 microg) injected in the PVN significantly de

34 ffect in the brain is anatomically specific, CCK-8 (0.8, 4, 20, 100, 500 pmol) was microinjected into

35 ncubation of ghrelin (10(-11)-10(-7) M) with CCK-8 (10(-10) M) demonstrated no inhibition of CCK-stim

36 of low doses of cholecystokinin octapeptide (CCK-8; 10-60 pmol); group B neurones responded only to h

37 CCK-8 (100 nmol/kg, i.p.) significantly (P < 0.001) redu

38 p B neurones responded only to high doses of CCK-8 (120-240 pmol), and were also activated by duodena

39 denum following intraperitoneal injection of CCK-8 (20 microg/kg).

40 Each subject received 2 sequential doses of CCK-8 (3 ng/kg/min for 10 min) on day 1, followed by, on

41 tions of leptin (120 microg/kg) and sulfated CCK-8 (3.5 microg/kg) in male lean mice (C57BL/6) fasted

42 The CCK-8 (300 ng)-induced hyperthermia was blocked by pretr

43 ther alone or with 3H-labelled propionylated CCK-8 (3H-pCCK-8) and plasma samples were taken at vario

44 le intraperitoneally (IP), and injected with CCK-8 (40 microg/kg) or saline IP.

45 ivo, pancreatic protein output stimulated by CCK-8 (400 pmol kg(-1) h(-1)) was dose-dependently inhib

46 , in response to sulfated cholecystokinin-8 (CCK-8) (5, 10, 20, 40 mug/kg), among Sprague-Dawley (SD)

47 ce that paraventricular nucleus injection of CCK-8 (500 pmol) did not increase plasma CCK-levels suff

48 Supramaximal CCK-8 (60 min) caused a 60% reduction in the expression

49 Changes in levels of one form, CCK-8, a naturally occurring eight amino acid peptide of

50 istration of the peptides, except (pGlu-Gln)-CCK-8 alone, in combination with glucose significantly l

51 pGlu-Gln)-CCK-8/exendin-4 hybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu-Gln)-CCK-8 in combination with exe

52 ane input resistance compared with leptin or CCK-8 alone.

53 293 cells, and determined rates of uptake of CCK-8 along with surface expression of the proteins.

54 8c(+/-) mice after hyperstimulation with the CCK-8 analog caerulein.

55 ues that were >100-fold more potent than the CCK-8 analogues and >10-fold selective for PTP1B over tw

56 l lines resulted in a selective depletion of CCK 8 and a comparative sparing of CCK 22.

57 cells results in production and secretion of CCK 8 and CCK 22.

58 Furthermore, CCK-8 and -12 are likely derived from cleavage of CCK-33

59 PVN injections of CCK-8 and 3H-pCCK-8 produced estimated peak increases in

60 +/- 16.3% (P < 0.01) with the first dose of CCK-8 and 71.3% +/- 17.4% (P < 0.05) with the second dos

61 CK(A)-R(329-357), and also the structures of CCK-8 and CCK(A)-R(1-47) previously determined, extensiv

62 e mutant CCK-BRs were assessed for peptides (CCK-8 and CCK-4) and for peptoids (PD-135,158 and PD-136

63 t, the functional activity of both peptides, CCK-8 and CCK-4, was not affected by any of the CCK-BR m

64 eas were treated with CCK receptor agonists, CCK-8 and gastrin, and an agonist for m3 muscarinic acet

65 ned positive cAMP responses to both sulfated CCK-8 and gastrin-17 with EC50 values of 8.5 +/- 1 nM an

66 ion and intermolecular NOEs (Trp30, Met31 of CCK-8 and P371, F374 of CCK2-R) indicated the formation

67 Both regular CCK-8 and pharmacy-compounded CCK-8 produce similar, but

68 fused for 10 min with 3 ng/kg/min of regular CCK-8 and pharmacy-compounded CCK-8, sequentially, with

69 hanced secretion in response to supramaximal CCK-8 and prevented accumulation of activated trypsin.

70 CCK-8 and SP increased only Galpha(q/11), and CPA increa

71 phospholipase C-beta (PLC-beta) response to CCK-8 and SP, but not CPA, was decreased; conversely, af

72 Thus, the effects of both CCK-8 and SST on Tb appear to involve the endogenous opi

73 However, GTP gamma S binding induced by CCK-8 and vasoactive intestinal polypeptide and the bind

74 olecular NOEs between Tyr(27) and Met(28) of CCK-8 and W39 of CCK(A)-R(1-47).

75 the octapeptide of cholecystokinin (regular CCK-8) and pharmacy-compounded CCK-8 produce similar res

76 ) injections of cholecystokinin-octapeptide (CCK-8) and somatostatin (SST) and the interactions of th

77 Cholecystokinin octapeptide (CCK-8) and substance P (SP) were used to activate G(q/11

78 tant to secretory inhibition by supramaximal CCK-8, and despite a 4.5-fold increase in total cellular

79 es a much more prolonged satiety action than CCK-8; and (3) the myenteric plexus and DVC may play rol

80 sts (acetylcholine [ACh], cholecystokinin 8 [CCK-8], and KCl) that occurs after BDL.

81 ion binding experiments were run using [125I]CCK-8 (approximately 40 pM, 2200 Ci/mmol) and 0.1-100 nM

82 ificant reduction of the cellular content of CCK 8 as measured by radioimmunoassay.

83 -8 functions much similar to that of regular CCK-8 as long as an interval of at least 30 min is allow

84 eal-time PCR, western blots, scratch assays, CCK-8 assays and tubule formation assays.

85 , differ from previous structural studies of CCK-8 association with CCK1-R, in which the ligand forme

86 In female controls, CCK-8 at 1 micromol/L caused increased [35S]GTPgammaS bi

87 CCK-8 at 500 pmol significantly suppressed intake during

88 en infused for 6 hours with either saline or CCK-8 at a dose of 3000 pmol.kg(-1).h(-1), which by itse

89 (125)I-CCK-8 binding and [(35)S]guanosine triphosphate gamma S

90 e displacement of 125I-labeled Bolton-Hunter-CCK-8 binding by gastrin-17-I and CCK-8.

91 125I-labeled Bolton-Hunter-CCK-8 binding displacement by L365,260 (a CCKBR selectiv

92 These findings suggest that CCK-8 binds to CCK(A) with the C-terminus within the sev

93 Cch and CCK-8 both dose-dependently stimulated secretory respons

94 contact points, extensive MD simulations of CCK-8 bound to the CCK2 receptor were carried out.

95 yr in CCK 8 reduced the quantity of secreted CCK 8 by 50%, and when all the sulfated Tyr were mutated

96 CCK-8, carbachol, and bombesin, but not VIP/secretin, de

97 dies showed that a combination of leptin and CCK-8 caused a significant increase in membrane input re

98 HGF but not CCK-8 caused c-Met ubiquitination.

99 CCK-8 caused rapid and potent c-Met down-regulation and

100 CCK-8 caused rapid formation of a p130(Cas)-Crk complex.

101 7]-betaCD-CCK(2)-R complex is similar to the CCK-8-CCK(2)-R complex determined previously, providing

102 ensive molecular dynamics simulations of the CCK-8/CCK(A)-R complex were carried out.

103 Using the CCK-8 cell proliferation assay, cell cycle analysis, and

104 to A/K, CCK 22 cleavage site K/N to A/N, and CCK 8 cleavage site R/D to A/D, did not inhibit pro-CCK

105 responses to systemic (IP) administration of CCK-8 compared to diet-induced obese resistant (OR) rats

106 CCK-8 did not decrease cell viability or overall respons

107 The i.v. injections of 600 and 4800 pmol of CCK-8 did not suppress feeding.

108 VN injection of an anorexic 500-pmol dose of CCK-8 does not increase plasma CCK-8 levels sufficiently

109 The i.v. infusion of CCK-8 doses (0.2 and 1 nmol/kg h) that bracketed the thr

110 nal amidated cholecystekinin fragment 26-33 (CCK-8), DY(PO3H2)MGWMDF-NH2 versus DY(SO3H)MGWMDF-NH2) o

111 Rats received PVN injections of CCK-8 either alone or with 3H-labelled propionylated CCK

112 h-evoked responses did not affect any of the CCK-8-evoked responses, indicating that rather than acti

113 a prevented ghrelin inhibition of leptin- or CCK-8-evoked vagal firing.

114 HbA1c was reduced in the (pGlu-Gln)-CCK-8/exendin-4 hybrid and combined parent peptide treat

115 nd therapeutic utility of a novel (pGlu-Gln)-CCK-8/exendin-4 hybrid peptide compared with the stable

116 daily administration of the novel (pGlu-Gln)-CCK-8/exendin-4 hybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu

117 ted robust brain changes in cholecystokinin (CCK-8) following social defeat.

118 significantly reduced feeding compared with CCK-8 from 60 to 120 min (P < 0.01).

119 and identified and characterized endogenous CCK-8 from hamster plasma.

120 Pharmacy-compounded CCK-8 functions much similar to that of regular CCK-8 as

121 xtensively cleaved at other sites to produce CCK 8 GAA or larger peptides.

122 Monoglycated cholecystokinin octapeptide (CCK-8) (glucitol-Asp1 adduct) modified at the NH2-termin

123 Endogenous CCK-8 has not been well characterized in Syrian Golden h

124 e C-terminal octapeptide of cholecystokinin (CCK-8) have been determined by high-resolution NMR and c

125 Further, a subthreshold dose of CCK-8 (i.e. 5 pmol) produced no measurable electrophysio

126 hlorate decreased the secretion of processed CCK 8 in CCK-expressing endocrine cells in culture.

127 for PC1 endoprotease in the biosynthesis of CCK 8 in vivo.

128 The results, with CCK-8 in close proximity to TM7, differ from previous st

129 ybrid, (pGlu-Gln)-CCK-8 alone, or (pGlu-Gln)-CCK-8 in combination with exendin-4 for 21 days to high-

130 to determine increases of endogenous plasma CCK-8 in hamsters challenged with a high-fat meal.

131 ood intake, CCK-33 produced more Fos-LI than CCK-8 in nearly every section of the sampled sites.

132 zoate (EB) increases the satiating effect of CCK-8 in ovariectomized rats.

133 in vivo and in vitro gallbladder response to CCK-8 in patients with AGD.

134 -Asp-Phe-NH2, were full agonists relative to CCK-8 in stimulating intracellular calcium mobilization

135 estigated the interaction between leptin and CCK-8 in the short-term regulation of food intake induce

136 intake and blocked the effects of peripheral CCK-8 in wild-type F344.Cck1r(+/+) rats.

137 al intravenous infusions of cholecystokinin (CCK-8) in a paired study of healthy subjects.

138 The cholecystokinin-8 (CCK-8)-inactivating peptidase is a serine peptidase that

139 agonist carbachol (Cch) and cholecystokinin (CCK-8), including 1) amylase secretion, 2) exocytosis, 3

140 i.c.v.), suggesting that the higher doses of CCK-8 increase Tb through the interaction with mu-recept

141 ntravenous administration of 2 micrograms/kg CCK-8 increased the single unit activity of 54% of hepat

142 nstrate that activation of CCKA receptors by CCK-8 increases hepatic vagal afferent activity and supp

143 hetic nervous system in the pathway by which CCK-8 increases myenteric Fos-LI.

144 In both febrile and afebrile rats, CCK-8 induced dose-dependent skin vasodilatation and dec

145 the membrane fraction, and stimulation with CCK-8 induced total p130(Cas) translocation from the cyt

146 rats with a F344 background, CCK-1R mediates CCK-8-induced inhibition of food intake and Fos activati

147 Gallbladder ejection fraction and CCK-8-induced paradoxical filling were calculated.

148 After CCK-8 infusion, gallbladder ejection fraction was low in

149 received an opioid before cholecystokinin-8 (CCK-8) infusion in one study but not in the other study.

150 ous intravenous cholecystokinin octapeptide (CCK-8) infusion was determined by ultrasonography in con

151 As expected, intraperitoneal injections of CCK-8 inhibited intake of chow and Ensure Plus and induc

152 entire pro-CCK, C-terminal S9S was deleted, CCK 8 is processed and secreted normally.

153 This study demonstrated that CCK-8 is a potent short-term inhibitor of food intake, a

154 Hamster CCK-8 is composed of eight amino acid residues which are

155 The carboxy terminal octapeptide (CCK-8) is fully active in this regard, but is lacking in

156 Application of this approach to CCK-8 led to Abu-Phe-NHBu (37), but this only had Ki = 9

157 holecystokinin (CCK)-8 could increase plasma CCK-8 levels sufficiently to suppress feeding by a perip

158 -pmol dose of CCK-8 does not increase plasma CCK-8 levels sufficiently to suppress feeding by a perip

159 wever, when stimulated with supraphysiologic CCK-8 levels to mimic pancreatitis, Munc18c-depleted (Mu

160 Plasma CCK-8 levels were estimated from measurements of both to

161 Elevation of cAMP during supramaximal CCK-8 mitigates third-phase secretory inhibition and aci

162 ine residues, one of which is present in the CCK 8 moiety and two additional residues present in the

163 This association is specific for CCK-8; no association was observed upon titration of CCK

164 produced estimated peak increases in plasma CCK-8 of 15+/-11 and 22+/-3 pM, respectively.

165 ut inhibited the effect of the high doses of CCK-8 on group B neurones.

166 e abolished the synergistic action of leptin/CCK-8 on neuronal firing.

167 mpounds based on the C-terminal sequences of CCK-8 or minigastrin was constructed.

168 Similarly, after treatment with CCK-8 or SP, the PLC-beta response mediated by G(q/11) o

169 onist, the PLC-beta response to CPA, but not CCK-8 or SP, was decreased.

170 injections of 1, 3, or 5 nMol/kg of CCK-33, CCK-8, or the vehicle control.

171 resent assay enables determination of active CCK-8 over a concentration range from 0.05 to 2.5 ng/mL

172 hCCK-A receptors and a potent antagonist of CCK-8 (pA2 = 9.1) on CHO K1 cells expressing hCCK-B rece

173 modulator of downstream signals activated by CCK-8, possibly involved in regulating numerous cellular

174 ing posttranslational processing to generate CCK 8, pro-cholecystokinin (CCK) undergoes endoproteolyt

175 r lifetime and anisotropy were lower for the CCK-8 probe bound to the type B receptor than for this p

176 probe (Alexa488-Gly-[(Nle(28,31))CCK-26-33]; CCK-8 probe) bound to the type A CCK receptor.

177 inin (regular CCK-8) and pharmacy-compounded CCK-8 produce similar results with regard to gallbladder

178 Both regular CCK-8 and pharmacy-compounded CCK-8 produce similar, but not identical, results with c

179 CCK-8 produced a normal gallbladder ejection fraction in

180 CCK-8 produced short-lasting (15-60 min), dose-related i

181 gram, i.c.v.), alone and in combination with CCK-8, produced hyperthermia.

182 Titration with CCK-8 produces a stable complex with a number of intermo

183 ter, however, CCK-33 was more effective than CCK-8, producing much more sustained reductions.

184 y, we show in rat dispersed pancreatic acini CCK-8 rapidly stimulates tyrosine phosphorylation of p13

185 Substitution of Phe to Tyr in CCK 8 reduced the quantity of secreted CCK 8 by 50%, and

186 Glycated CCK-8 reduced food intake at 30-120 min (P < 0.01 to P <

187 h supraphysiologic doses of cholecystokinin (CCK-8), remain poorly understood.

188 -1 and CCK mimetics exendin-4 and (pGlu-Gln)-CCK-8, respectively.

189 The combined action of ethanol and CCK-8 results in NF-kappaB activation and up-regulation

190 JMV-180 ( 1) and CCK-8(s) are high affinity ligands at the CCK 1 receptor

191 les are compared to available models of 1 or CCK-8(s) bound to the CCK 1 receptor.

192 we calculate the tertiary structure of 1 or CCK-8(s) in the presence of dodecylphosphocholine micell

193 The NMR derived 3D structures of 1 and CCK-8(s) share a common type I beta-turn around residues

194 min of regular CCK-8 and pharmacy-compounded CCK-8, sequentially, with a 30-min interval between the

195 ty for the human CCK-A receptor, relative to CCK-8, some of these compounds are equipotent to CCK as

196 Titration of CCK(A)-R(1-47) with CCK-8 specifically affects the NMR signals of W39 of the

197 e, ethyl palmitate, and ethyl oleate reduced CCK-8-stimulated apical exocytosis and formation of apic

198 of the same pathologic effects of ethanol on CCK-8-stimulated exocytosis in pancreatic acini.

199 Acetaldehyde and ethyl oleate redirected CCK-8-stimulated exocytosis to the basal and lateral pla

200 K-8 were examined by quantifying CCK-33- and CCK-8-stimulated Fos-like immunoreactivity (Fos-LI) in e

201 Treatment with tyrphostin B44 inhibited CCK-8-stimulated p130(Cas) phosphorylation, but it had n

202 etwork with colchicine, completely inhibited CCK-8-stimulated p130(Cas) phosphorylation.

203 ses in [Ca2+]i or PKC activity did not alter CCK-8-stimulated p130(Cas) phosphorylation; however, sim

204 to acetaldehyde and ethyl oleate followed by CCK-8 stimulation mildly perturbed the actin cytoskeleto

205 ancreatitis by supramaximal cholecystokinin (CCK-8) stimulation inhibits VAMP8-mediated mid- and late

206 Here the authors analyzed brain regional, CCK-8, substance P, corticotropin releasing factor (CRF)

207 reases in hepatic vagal activity produced by CCK-8 suggests that the latter effect was not secondary

208 It cleaves the neurotransmitter CCK-8 sulfate at the Met-Gly bond to give Asp-Tyr(SO3H)-

209 Leptin/CCK-8 synergistically stimulated a 7.7-fold increase in

210 PC2 knockout mouse brains had less CCK 8 than wild-type, although a substantial amount of C

211 hin the hypothalamus, suggest that spread of CCK-8 to adjacent brain sites, and (or) to the periphery

212 ions and forces important for the binding of CCK-8 to CCK(A)-R.

213 abilities of cholecystokinin-33 (CCK-33) and CCK-8 to reduce food intake and to activate feeding-rela

214 duodenal PKA blocked the ability of duodenal CCK-8 to reduce glucose production in control rats, wher

215 Upon titration of CCK-8 to the receptor domain, chemical shift perturbatio

216 c experiments showed that the K m values for CCK-8 transport in the TM10 replacement and triple mutan

217 acid residues found in OATP1B1, the level of CCK-8 transport was similarly low as for the replacement

218 resulted in a dramatically reduced degree of CCK-8 transport, indicating that TM10 is crucial for rec

219 0) in TM10 of OATP1B3 that are important for CCK-8 transport.

220 uated by a CCK-A receptor agonist, sulphated CCK-8 (up to 0.17 microg kg-1 min-1, 120 min, I.V.).

221 While the 0-dose of either PGE2 or CCK-8 (vehicle alone) induced no thermal response, all t

222 In vitro muscle cell contraction induced by CCK-8 was also lower in AGD than in pigment stones.

223 This potentiation effect of CCK-8 was eliminated by CR 1409.

224 ated rats as compared with nondefeated rats: CCK-8 was reduced in frontal cortex and cortex overlying

225 GTPgammaS binding to Galphai3 induced by CCK-8 was reduced in gallbladder muscle from pregnant gu

226 degradation studies indicated that glycated CCK-8 was resistant to the normal rapid enzymatic conver

227 In vivo gallbladder contraction induced by CCK-8 was significantly lower in AGD (29.4%) and cholest

228 crease in hepatic vagal activity produced by CCK-8 was significantly reduced by i.v. administration o

229 hermal responsiveness of the rats to PGE2 or CCK-8 was tested.

230 s of wild-type F344.Cck1r(+/+) rats, whereas CCK-8 was without effect on food intake or Fos induction

231 entification and characterization of hamster CCK-8, we have developed a highly specific and sensitive

232 Where the GRR residues on the C-terminus of CCK 8 were mutated to GAA, no amidated CCK was produced.

233 e differential satiety effects of CCK-33 and CCK-8 were examined by quantifying CCK-33- and CCK-8-sti

234 ry responses and exocytotic events evoked by CCK-8 were mediated by CCK-A and not CCK-B receptors.

235 high level of nonspecific binding of (125)I-CCK-8 were observed.

236 ral analogues of cholecystokinin(26)(-)(33) (CCK-8) were found to be surprisingly potent inhibitors o

237 ternative method to intravenous injection of CCK-8 when the hormone is no longer available for clinic

238 es only CCK 33; 33A/K and 22A/N produce only CCK 8, whereas 8A/D produces CCK 12 and some CCK 22.

239 relin inhibits currents evoked by leptin and CCK-8, which operate through independent ionic channels.

240 in expression, and the specific depletion of CCK 8 with comparative sparing of CCK 22.

241 e C-terminal octapeptide of cholecystokinin, CCK-8, with the N-terminus of the CCK(A)-receptor, CCK(A

242 e C-terminal octapeptide of cholecystokinin, CCK-8, with the third extracellular loop of human cholec

243 , as well as the widespread effectiveness of CCK-8 within the hypothalamus, suggest that spread of CC