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1  GPCR subgroups (e.g., the ancestral gastrin/cholecystokinin receptor).
2 ily A G protein-coupled receptor, the type 1 cholecystokinin receptor.
3  new molecular model of the agonist-occupied cholecystokinin receptor.
4 antagonist and agonist ligands of the type A cholecystokinin receptor.
5 alpha13 downstream of gastrin and the type 2 cholecystokinin receptor.
6 udied in solution and docked at type A and B cholecystokinin receptors.
7 l sequencing of labeled wild-type and mutant cholecystokinin receptors.
8 iod, inducible/reversible forebrain-specific cholecystokinin receptor-2 transgenic (IF-CCKR-2 tg) mic
9 r 1 (NTSR1), neuropeptide S receptor (NPSR), cholecystokinin receptor A (CCKAR), and the kappa-opioid
10     Similarly, peptides mimicking the TMs of cholecystokinin receptor A, were found to abolish ligand
11 tely 20% of GFP-positive neurons coexpressed cholecystokinin receptor A.
12 n-releasing peptide and carbachol but not to cholecystokinin-receptor agonists.
13 emonstrate that antagonist occupation of the cholecystokinin receptor also results in receptor intern
14                   Two physical models of the cholecystokinin receptor and ligand binding have been pr
15  mass and protein content was independent of cholecystokinin receptors, associated with a rapid incre
16 e were built into two homology models of the cholecystokinin receptor, based on the recent crystal st
17                   Although both type A and B cholecystokinin receptors bind cholecystokinin with high
18 red Ca2+ signaling with up-regulation of the cholecystokinin receptor but minimal effect upon express
19 titative autoradiography was used to analyze cholecystokinin receptor (CCK-R) binding in the ventrome
20                                   The type 1 cholecystokinin receptor (CCK1R) has multiple physiologi
21 f a new antagonist radioligand of the type 1 cholecystokinin receptor (CCK1R), (2-fluorophenyl)-2,3-d
22 rminants for this pocket within type 1 and 2 cholecystokinin receptors (CCK1R and CCK2R), we prepared
23 urable binding to the closely related type 2 cholecystokinin receptor (CCK2R).
24 ssessment of sites of phosphorylation of the cholecystokinin receptor (CCKR) in its native milieu in
25  within the second extracellular loop of the cholecystokinin receptor interacts with a specific acidi
26 ndependent risk factor for gallstone disease.Cholecystokinin receptors may be responsible for the alt
27 ative pain-facilitating neurons, or block of cholecystokinin receptors prevented or significantly att
28 ype animals and mice lacking the other known cholecystokinin receptor subtype, cholecystokinin-B/gast
29 surface and within the helical bundle of the cholecystokinin receptor to the amino terminus of a full
30         A chimeric protein consisting of the cholecystokinin receptor type A (CCKAR) and the green fl
31 , the position 33 probe docked at the type A cholecystokinin receptor was more easily quenched in the
32  whereas the same probe docked at the type B cholecystokinin receptor was more easily quenched in the

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