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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
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
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
27 referred topography of the Trp30 residue for CCK-B receptor binding may be the 2S,3S (erythro-L) conf
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 via CCK(A) receptors and gastrin acting via CCK(B) receptors exert trophic effects on a variety of n
34 ate the presence of a misspliced form of the CCK-B receptor having its fourth intron retained in thre
35 lates proliferation of AGS cells through the CCK-B receptor; however, G-17-mediated growth of SIIA ac
39 e, the relative amount of missplicing of the CCK-B receptor mini-gene in the pancreatic cancer cell l
42 mine the effects of activation of CCK(A) and CCK(B) receptors on the growth of human pancreatic cance
44 liced form of the cholecystokinin-B/gastrin (CCK-B) receptor recently was reported to be present in c
46 f Gs coupling to cholecystokinin (CCK)-A and CCK-B receptor subtypes, we examined cAMP responses in t
47 oc-CCK-4, which is 70-fold selective for the CCK-B receptor, the modified lysine-bearing tetrapeptide
48 nhanced binding affinity and selectivity for CCK-B receptors, thus providing several compounds with s
50 oderate binding affinity and selectivity for CCK-B receptors, whereas its higher and lower homologues
51 re approximately 30-fold lower than those of CCK-B receptors, which were approximately 10-fold lower
52 identify the signaling pathways coupling the CCK-B receptor with up-regulation of COX-2 expression.
53 WT) CCK-A receptor (WT CCKAR) and the rat WT CCK-B receptor (WT CCKBR) were truncated after amino aci
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