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1 al epithelial cell line transfected with the CCK-B receptor.
2 ent binding affinity and selectivity for the CCK-B receptor.
3 bilization in a cell line that expresses the CCK-B receptor.
4 oked by CCK-8 were mediated by CCK-A and not CCK-B receptors.
5 denoviral-mediated gene transfer of CCK-A or CCK-B receptors.
6 in-coupled receptors in the brain: CCK-A and CCK-B receptors.
7 or antagonist L365260, indicating a role for CCK(B) receptors.
8 cers mostly through gastrin/cholecystokinin (CCK)-B receptors.
9 y sought to determine the roles of CCK-A and CCK-B receptor activation in the PAG in modulating defen
10 ions of CCK8S were mimicked by the selective CCK(B) receptor agonist CCK4, and attenuated by the sele
11  a direct coupling between the G proteins of CCK-B receptors and I(K(Ca)).
12 ions in both the central nervous system (via CCK-B receptors) and the periphery (via CCK-A receptors)
13 gonist CCK4, and attenuated by the selective CCK(B) receptor antagonist L365260, indicating a role fo
14  which was not blocked by a cholecystokinin (CCK)-B receptor antagonist.
15                              We injected the CCK-B receptor antagonist PD 135,158 into the PVTh befor
16 , a CCK-A receptor antagonist but not by the CCK-B receptor antagonist, L-365,260.
17             Microinjections of the selective CCK-B receptor antagonist, LY288513 (1.05, 4.2, 17.0 nmo
18 ts were pretreated with antigastrin serum or CCK-B receptor antagonist, the acid secretion by TE was
19 and biological activity of a novel series of CCK-B receptor antagonists (1) which incorporate a tetra
20           We have designed a novel series of CCK-B receptor antagonists by combining key pharmacophor
21 latory effect of G-17 in SIIA cells, whereas CCK-B receptor antagonists had no effect.
22                        In AGS cells, gastrin/CCK-B receptor antagonists inhibited the effect of G-17
23  mg/kg) and is one of the most potent acidic CCK-B receptor antagonists yet described.
24 thesized and evaluated as cholecystokinin-B (CCK-B) receptor antagonists.
25                  Cholecystokinin (CCK)-A and CCK-B receptors are highly homologous members of the sev
26                                 Both CCK and CCK-B receptors are widely distributed in the hippocampa
27 referred topography of the Trp30 residue for CCK-B receptor binding may be the 2S,3S (erythro-L) conf
28 monstrates the specificity of the effects of CCK-B receptor blockade upon hissing.
29  moderately increased affinity for the human CCK-B receptor but was a potent full agonist on the GPGB
30  ECL function is determined by activation of CCK-B receptors, by gastrin, and by activation of beta-a
31 were constructed by replacing exons of human CCK-B receptor (CCK-BR), from the second to the fifth (l
32 ly through induction of the cholecystokinin (CCK)-B receptor: CCKB blockade in mPFC induces a resilie
33 ockout of Cck gene (Cck(-/-)) or blockade of CCK-B receptor (CCKBR) showed defective motor learning a
34  via CCK(A) receptors and gastrin acting via CCK(B) receptors exert trophic effects on a variety of n
35 ate the presence of a misspliced form of the CCK-B receptor having its fourth intron retained in thre
36 lates proliferation of AGS cells through the CCK-B receptor; however, G-17-mediated growth of SIIA ac
37                                   Acting via CCK-B receptors in pPVTh, CCK then constrains facilitate
38       Overall, the findings demonstrate that CCK-B receptors in the PAG potentiate defensive rage beh
39      Our results indicate that activation of CCK-B receptors initially and transiently increased spon
40 neurons innervate CCKBR cells in the BLA and CCK-B receptor knockout (CCKBR-KO) mice impaired LTP in
41 e, the relative amount of missplicing of the CCK-B receptor mini-gene in the pancreatic cancer cell l
42                                 In addition, CCK-B receptor mRNA expression in the pPVTh was not alte
43 h receptor and insulin mRNA but not CCK-A or CCK-B receptor mRNAs in adult human pancreas.
44 mine the effects of activation of CCK(A) and CCK(B) receptors on the growth of human pancreatic cance
45       Our data indicate that CCK, acting via CCK(B) receptors, produces a long-lasting excitation of
46 liced form of the cholecystokinin-B/gastrin (CCK-B) receptor recently was reported to be present in c
47            Binding affinity for the CCK-A vs CCK-B receptor showed little dependence on the structure
48 f Gs coupling to cholecystokinin (CCK)-A and CCK-B receptor subtypes, we examined cAMP responses in t
49 oc-CCK-4, which is 70-fold selective for the CCK-B receptor, the modified lysine-bearing tetrapeptide
50 nhanced binding affinity and selectivity for CCK-B receptors, thus providing several compounds with s
51                                Expression of CCK-B receptors was detected in all tissues arising from
52 oderate binding affinity and selectivity for CCK-B receptors, whereas its higher and lower homologues
53 re approximately 30-fold lower than those of CCK-B receptors, which were approximately 10-fold lower
54 identify the signaling pathways coupling the CCK-B receptor with up-regulation of COX-2 expression.
55 WT) CCK-A receptor (WT CCKAR) and the rat WT CCK-B receptor (WT CCKBR) were truncated after amino aci