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1 expressing functional recombinant rat type A CCK receptor.
2 address small molecule interactions with the CCK receptor.
3 o the type B CCK receptor than to the type A CCK receptor.
4 CCK-26-33]; CCK-8 probe) bound to the type A CCK receptor.
5 imerization of that receptor with the type A CCK receptor.
6 agonist and antagonist peptides bound to the CCK receptor.
7 a full agonist and to specifically label the CCK receptor.
8 alent bond with an interacting domain of the CCK receptor.
9  only one (control) or both (target) MSH and CCK receptors.
10 s of our bifunctional peptides at opioid and CCK receptors.
11 eptors in this superfamily, the type A and B CCK receptors.
12 ced by co-expression of competing non-tagged CCK receptors.
13 ons at both sites is mediated through type A CCK receptors.
14  extracellular loops of the cholecystokinin (CCK) receptor.
15 l cells and human Caco-2 cells; both express CCK receptor 1 and 2 (CCK1R and CCK2R).
16 le in anxiogenesis through the activation of CCK receptor-2 (CCKR-2).
17 he mechanism by which the Gq protein-coupled CCK receptor activates Ras, however, is currently unknow
18 in the conformation of the helical bundle of CCK receptors affects both ligand binding at the extrace
19 ation of the structural features that govern CCK receptor affinity and the receptor subtype selectivi
20 ranes that were preincubated with CCK-8S and CCK receptor agonist and antagonist followed with 3H-DAM
21                    We found that the general CCK receptor agonist CCK8S (sulfated CCK octapeptide) st
22 odiazepines with peripheral cholecystokinin (CCK) receptor agonist activity.
23 ule ligand that is a type 1 cholecystokinin (CCK) receptor agonist and type 2 CCK receptor antagonist
24 an pancreatic acinar cells do not respond to CCK receptor agonists in terms of expected functional pa
25 olated from human pancreas were treated with CCK receptor agonists, CCK-8 and gastrin, and an agonist
26      Here, we study this probe at the type B CCK receptor and develop another probe with its fluoroph
27 ed and tested for binding to both opioid and CCK receptors and in functional assays.
28               In the brain, distributions of CCK receptors and opioid receptors have been demonstrate
29 rated spontaneous homodimerization of type A CCK receptors and the dissociation of those complexes by
30  the pancreatic acinar cell cholecystokinin (CCK) receptor and the establishment of two-dimensional p
31            We found that FSH cells express a CCK receptor, and our findings demonstrate that mutating
32 id-dose escalation in chronic pain states by CCK receptor antagonism represents a potentially importa
33                        Administration of the CCK receptor antagonist L364,718 did not affect pancreat
34 cystokinin (CCK) receptor agonist and type 2 CCK receptor antagonist, GI181771X.
35 hecal administration of the cholecystokinin (CCK) receptor antagonist L-365,260 (0.1 ng per rat), sug
36 ration of the non-selective cholecystokinin (CCK) receptor antagonist proglumide (10 micrograms) prio
37 t CCK-1 and CCK-2 receptors, but were potent CCK receptor antagonists in the GPI/LMMP assay (up to Ke
38                                    Moreover, CCK receptor antagonists may improve the reliability of
39                                        Also, CCK receptors are found in abundance in this brain regio
40                Type A and B cholecystokinin (CCK) receptors are highly homologous members of the clas
41 ed in 2175 non-agonist ligands of the type 1 CCK receptor (area under curve 78%).
42 ently bound to the specific sites within the CCK receptor as acceptor.
43 and mu opioid receptors as agonists and with CCK receptors as antagonists.
44 trate spontaneous homodimerization of type B CCK receptors, as well as heterodimerization of that rec
45 h pancreatic secretion and CCK release while CCK receptor blockade abolished the pancreatic response.
46 wever, although heterodimers of type A and B CCK receptors bound natural agonists normally, they exhi
47  peptide eliminated the disruptive effect on CCK receptor BRET, whereas the other mutant peptide beha
48 merization of that receptor had no effect on CCK receptor BRET.
49 logy with Orexin, NPFF, and cholecystokinin (CCK) receptors, but identification of the endogenous lig
50 ntracellular domains of the cholecystokinin (CCK) receptor by their over-expression in receptor-beari
51 evaluate whether the type A cholecystokinin (CCK) receptor can form oligomeric complexes in the plasm
52 isolated a cDNA encoding the X. laevis brain CCK receptor (CCK-XLR).
53 mark of the mammalian brain cholecystokinin (CCK) receptor, CCK-B/gastrin (CCK-BR), is its high affin
54  Cholecystokinin (CCK) stimulates the type 1 CCK receptor (CCK1R) to elicit satiety after a meal.
55                    As substrate, we used CHO-CCK receptor cells overexpressing functional recombinant
56 cholesterol enrichment may reflect change in CCK receptor conformation toward its inactive, uncoupled
57 luorescent ligand and use of a null-reactive CCK receptor construct.
58                             Pseudo-wild-type CCK receptor constructs having single reactive cysteine
59 d at each end of CCK as docked at the type B CCK receptor, contrasting this with analogous work using
60                                Unlike type A CCK receptor dimers, the homodimerization of type B CCK
61                    It covalently labeled the CCK receptor either within the amino terminus (between A
62                   Each was used to label the CCK receptor expressed on Chinese hamster ovary-CCKR cel
63  saporin, using either CCK-saporin to target CCK receptor expressing cells, or dermorphin-saporin to
64 g experiments suggested that the predominant CCK receptor from Xenopus laevis brain shares high affin
65 on of the G protein-coupled cholecystokinin (CCK) receptor has been demonstrated, but its molecular b
66 dence supporting the concept that opioid and CCK receptors have overlapping pharmacophores required f
67                  Both probes bound to type B CCK receptors in a saturable and specific manner and rep
68 nfluence of cholesterol and sphingolipids on CCK receptors in model Chinese hamster ovary cell system
69 e distributions of cholecystokinin (CCK) and CCK receptors in the central nervous system (CNS) overla
70 o distinct opioid receptors and antagonizing CCK receptors in the CNS.
71 change the number (Bmax) or affinity (Kd) of CCK receptors in the NTS.
72 ects of EB on the binding characteristics of CCK receptors in the nucleus tractus solitarius (NTS), a
73 of the carboxyl terminus of cholecystokinin (CCK) receptors in receptor internalization, the rat wild
74          Thus, lipid microenvironment of the CCK receptor is particularly important, with different l
75 ether, these results suggest that leptin and CCK receptors may both contribute to short-term satiety,
76                   These results suggest that CCK receptor mechanisms involved in the control of magno
77  that different affinity states of the vagal CCK receptors mediate different digestive functions.
78     The presence of an oligomeric complex of CCK receptor molecules was confirmed in co-immunoprecipi
79 amined cAMP responses in three sets of human CCK receptor mutants expressed in human embryonic kidney
80                                  Fluorescent CCK receptor mutants with residues 317, 321, and 325 rep
81                                      Neither CCK receptors nor alpha subunits of the sodium pump, bot
82                       Notably, disruption of CCK receptor oligomerization had no effect on agonist bi
83         This provides the first evidence for CCK receptor oligomerization in living cells, with insig
84                             These effects on CCK receptor oligomerization were concentration-dependen
85 fect on the basal level or agonist effect on CCK receptor oligomerization.
86         The presence and functional roles of CCK receptors on human acinar cells remain unclear.
87 ab11a (Rab-GTPase-11a), whereas knockdown of CCK receptors or inhibition of G protein betagamma dimer
88 e parent compounds of the 1,5-benzodiazepine CCK receptor photoaffinity ligands were originally prepa
89 ling by each probe, distinct from the type A CCK receptor regions labeled using the same probes (thir
90 th the two cyanogen bromide fragments of the CCK receptor representing the expected domains further s
91 w fluorescent probes of the cholecystokinin (CCK) receptor, representing structurally related peptide
92       Thus, the distal amino terminus of the CCK receptor resides above the docked ligand, compressin
93 nd its spatial approximation with the type A CCK receptor residue Arg(197) that has been predicted fr
94  study selectively photoaffinity-labeled the CCK receptor, resulting in the identification of a site
95  fully efficacious agonist that bound to the CCK receptor saturably and with high affinity (K(i) = 8.
96  triggered by activation of the low-affinity CCK receptor sites.
97               All of the probes bound to the CCK receptor specifically and with high affinity, and in
98  provide the link between Gq protein-coupled CCK receptor stimulation and Ras activation in these cel
99 variability is due to species differences in CCK receptor structure or to alterations in the cellular
100 65,260 demonstrated that EB failed to affect CCK receptor subtype number in the medial and lateral di
101 dues in the first intracellular loop of both CCK receptor subtypes are critical for Gs coupling.
102                These data indicate that both CCK receptor subtypes can mediate growth inhibitory resp
103 related radioiodinated ligands selective for CCK receptor subtypes that utilize the same allosteric l
104 and Panc-1 were transfected stably with both CCK receptor subtypes.
105 in (CCK) A, CCK-B, or a combination of these CCK receptor subtypes.
106  interactions between opioids and endogenous CCK receptor systems have suggested the need for a new p
107                           Oligomerization of CCK receptors tagged at the carboxyl terminus with Renil
108  the aqueous milieu when bound to the type B CCK receptor than to the type A CCK receptor.
109 , we explore domains of the cholecystokinin (CCK) receptor that are critical for ligand binding, usin
110  suggests that the lipid-exposed face of the CCK receptor TM VI most contributes to oligomerization a
111 Manipulation of the phosphorylation state of CCK receptor using protein kinase C activation with phor
112 ling the active site of the cholecystokinin (CCK) receptor, using a photolabile analogue of CCK havin
113 wild-type G protein-coupled cholecystokinin (CCK) receptor, using photoaffinity labeling with a CCK a
114  that the in vivo expression of both CCK and CCK receptors was mimicked in this in vitro model.
115 eptor dimers, the homodimerization of type B CCK receptors was not affected by ligand occupation.
116    As additional measures of EB's effects on CCK receptors, we also characterized EB's effects on CCK
117 ing each of the intracellular domains of the CCK receptor were coexpressed with wild-type receptor, a
118 ocking small molecule agonists to the type 1 CCK receptor were developed using a ligand-guided refine
119 representing TM I, II, V, VI, and VII of the CCK receptor were utilized as competitors.
120 inal polypeptide and the binding capacity of CCK receptors were not different between AGD and pigment
121                            All WT and mutant CCK receptors were stably expressed in NIH/3T3 cells.
122 ficacious with natural CCK, and bound to the CCK receptor with moderate affinity (IC50 = 450 +/- 126
123 n BRET signal was also observed for pairs of CCK receptors with a donor-acceptor pair situated in oth
124                                Occupation of CCK receptors with agonist ligands (CCK or gastrin-4) re
125          Ligation of the bile duct, blocking CCK receptors with proglumide or inhibition of Niemann-P

 
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