ライフサイエンスコーパス: CCK receptor

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 s of our bifunctional peptides at opioid and CCK receptors.

10 eptors in this superfamily, the type A and B CCK receptors.

11 ced by co-expression of competing non-tagged CCK receptors.

12 ons at both sites is mediated through type A CCK receptors.

13 only one (control) or both (target) MSH and 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 ation of the structural features that govern CCK receptor affinity and the receptor subtype selectivi

19 ranes that were preincubated with CCK-8S and CCK receptor agonist and antagonist followed with 3H-DAM

20 We found that the general CCK receptor agonist CCK8S (sulfated CCK octapeptide) st

21 odiazepines with peripheral cholecystokinin (CCK) receptor agonist activity.

22 ule ligand that is a type 1 cholecystokinin (CCK) receptor agonist and type 2 CCK receptor antagonist

23 an pancreatic acinar cells do not respond to CCK receptor agonists in terms of expected functional pa

24 olated from human pancreas were treated with CCK receptor agonists, CCK-8 and gastrin, and an agonist

25 Here, we study this probe at the type B CCK receptor and develop another probe with its fluoroph

26 ed and tested for binding to both opioid and CCK receptors and in functional assays.

27 In the brain, distributions of CCK receptors and opioid receptors have been demonstrate

28 rated spontaneous homodimerization of type A CCK receptors and the dissociation of those complexes by

29 the pancreatic acinar cell cholecystokinin (CCK) receptor and the establishment of two-dimensional p

30 id-dose escalation in chronic pain states by CCK receptor antagonism represents a potentially importa

31 Administration of the CCK receptor antagonist L364,718 did not affect pancreat

32 cystokinin (CCK) receptor agonist and type 2 CCK receptor antagonist, GI181771X.

33 hecal administration of the cholecystokinin (CCK) receptor antagonist L-365,260 (0.1 ng per rat), sug

34 ration of the non-selective cholecystokinin (CCK) receptor antagonist proglumide (10 micrograms) prio

35 t CCK-1 and CCK-2 receptors, but were potent CCK receptor antagonists in the GPI/LMMP assay (up to Ke

36 Moreover, CCK receptor antagonists may improve the reliability of

37 Also, CCK receptors are found in abundance in this brain regio

38 Type A and B cholecystokinin (CCK) receptors are highly homologous members of the clas

39 ed in 2175 non-agonist ligands of the type 1 CCK receptor (area under curve 78%).

40 ently bound to the specific sites within the CCK receptor as acceptor.

41 and mu opioid receptors as agonists and with CCK receptors as antagonists.

42 trate spontaneous homodimerization of type B CCK receptors, as well as heterodimerization of that rec

43 h pancreatic secretion and CCK release while CCK receptor blockade abolished the pancreatic response.

44 wever, although heterodimers of type A and B CCK receptors bound natural agonists normally, they exhi

45 peptide eliminated the disruptive effect on CCK receptor BRET, whereas the other mutant peptide beha

46 merization of that receptor had no effect on CCK receptor BRET.

47 logy with Orexin, NPFF, and cholecystokinin (CCK) receptors, but identification of the endogenous lig

48 ntracellular domains of the cholecystokinin (CCK) receptor by their over-expression in receptor-beari

49 evaluate whether the type A cholecystokinin (CCK) receptor can form oligomeric complexes in the plasm

50 isolated a cDNA encoding the X. laevis brain CCK receptor (CCK-XLR).

51 mark of the mammalian brain cholecystokinin (CCK) receptor, CCK-B/gastrin (CCK-BR), is its high affin

52 Cholecystokinin (CCK) stimulates the type 1 CCK receptor (CCK1R) to elicit satiety after a meal.

53 As substrate, we used CHO-CCK receptor cells overexpressing functional recombinant

54 cholesterol enrichment may reflect change in CCK receptor conformation toward its inactive, uncoupled

55 luorescent ligand and use of a null-reactive CCK receptor construct.

56 Pseudo-wild-type CCK receptor constructs having single reactive cysteine

57 d at each end of CCK as docked at the type B CCK receptor, contrasting this with analogous work using

58 Unlike type A CCK receptor dimers, the homodimerization of type B CCK

59 It covalently labeled the CCK receptor either within the amino terminus (between A

60 Each was used to label the CCK receptor expressed on Chinese hamster ovary-CCKR cel

61 saporin, using either CCK-saporin to target CCK receptor expressing cells, or dermorphin-saporin to

62 g experiments suggested that the predominant CCK receptor from Xenopus laevis brain shares high affin

63 on of the G protein-coupled cholecystokinin (CCK) receptor has been demonstrated, but its molecular b

64 dence supporting the concept that opioid and CCK receptors have overlapping pharmacophores required f

65 Both probes bound to type B CCK receptors in a saturable and specific manner and rep

66 nfluence of cholesterol and sphingolipids on CCK receptors in model Chinese hamster ovary cell system

67 e distributions of cholecystokinin (CCK) and CCK receptors in the central nervous system (CNS) overla

68 o distinct opioid receptors and antagonizing CCK receptors in the CNS.

69 change the number (Bmax) or affinity (Kd) of CCK receptors in the NTS.

70 ects of EB on the binding characteristics of CCK receptors in the nucleus tractus solitarius (NTS), a

71 of the carboxyl terminus of cholecystokinin (CCK) receptors in receptor internalization, the rat wild

72 Thus, lipid microenvironment of the CCK receptor is particularly important, with different l

73 These results suggest that CCK receptor mechanisms involved in the control of magno

74 that different affinity states of the vagal CCK receptors mediate different digestive functions.

75 The presence of an oligomeric complex of CCK receptor molecules was confirmed in co-immunoprecipi

76 amined cAMP responses in three sets of human CCK receptor mutants expressed in human embryonic kidney

77 Fluorescent CCK receptor mutants with residues 317, 321, and 325 rep

78 Neither CCK receptors nor alpha subunits of the sodium pump, bot

79 Notably, disruption of CCK receptor oligomerization had no effect on agonist bi

80 This provides the first evidence for CCK receptor oligomerization in living cells, with insig

81 These effects on CCK receptor oligomerization were concentration-dependen

82 fect on the basal level or agonist effect on CCK receptor oligomerization.

83 The presence and functional roles of CCK receptors on human acinar cells remain unclear.

84 ab11a (Rab-GTPase-11a), whereas knockdown of CCK receptors or inhibition of G protein betagamma dimer

85 e parent compounds of the 1,5-benzodiazepine CCK receptor photoaffinity ligands were originally prepa

86 ling by each probe, distinct from the type A CCK receptor regions labeled using the same probes (thir

87 th the two cyanogen bromide fragments of the CCK receptor representing the expected domains further s

88 w fluorescent probes of the cholecystokinin (CCK) receptor, representing structurally related peptide

89 Thus, the distal amino terminus of the CCK receptor resides above the docked ligand, compressin

90 nd its spatial approximation with the type A CCK receptor residue Arg(197) that has been predicted fr

91 study selectively photoaffinity-labeled the CCK receptor, resulting in the identification of a site

92 fully efficacious agonist that bound to the CCK receptor saturably and with high affinity (K(i) = 8.

93 triggered by activation of the low-affinity CCK receptor sites.

94 All of the probes bound to the CCK receptor specifically and with high affinity, and in

95 provide the link between Gq protein-coupled CCK receptor stimulation and Ras activation in these cel

96 variability is due to species differences in CCK receptor structure or to alterations in the cellular

97 65,260 demonstrated that EB failed to affect CCK receptor subtype number in the medial and lateral di

98 dues in the first intracellular loop of both CCK receptor subtypes are critical for Gs coupling.

99 These data indicate that both CCK receptor subtypes can mediate growth inhibitory resp

100 related radioiodinated ligands selective for CCK receptor subtypes that utilize the same allosteric l

101 and Panc-1 were transfected stably with both CCK receptor subtypes.

102 in (CCK) A, CCK-B, or a combination of these CCK receptor subtypes.

103 interactions between opioids and endogenous CCK receptor systems have suggested the need for a new p

104 Oligomerization of CCK receptors tagged at the carboxyl terminus with Renil

105 the aqueous milieu when bound to the type B CCK receptor than to the type A CCK receptor.

106 , we explore domains of the cholecystokinin (CCK) receptor that are critical for ligand binding, usin

107 suggests that the lipid-exposed face of the CCK receptor TM VI most contributes to oligomerization a

108 Manipulation of the phosphorylation state of CCK receptor using protein kinase C activation with phor

109 ling the active site of the cholecystokinin (CCK) receptor, using a photolabile analogue of CCK havin

110 wild-type G protein-coupled cholecystokinin (CCK) receptor, using photoaffinity labeling with a CCK a

111 that the in vivo expression of both CCK and CCK receptors was mimicked in this in vitro model.

112 eptor dimers, the homodimerization of type B CCK receptors was not affected by ligand occupation.

113 As additional measures of EB's effects on CCK receptors, we also characterized EB's effects on CCK

114 ing each of the intracellular domains of the CCK receptor were coexpressed with wild-type receptor, a

115 ocking small molecule agonists to the type 1 CCK receptor were developed using a ligand-guided refine

116 representing TM I, II, V, VI, and VII of the CCK receptor were utilized as competitors.

117 inal polypeptide and the binding capacity of CCK receptors were not different between AGD and pigment

118 All WT and mutant CCK receptors were stably expressed in NIH/3T3 cells.

119 ficacious with natural CCK, and bound to the CCK receptor with moderate affinity (IC50 = 450 +/- 126

120 n BRET signal was also observed for pairs of CCK receptors with a donor-acceptor pair situated in oth

121 Occupation of CCK receptors with agonist ligands (CCK or gastrin-4) re

122 Ligation of the bile duct, blocking CCK receptors with proglumide or inhibition of Niemann-P