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1 (via CCK-B receptors) and the periphery (via CCK-A receptors).
2 febrile response of rats to LPS requires the CCK-A receptor.
3 ly potent and selective full agonists at the CCK-A receptor.
4 y through a receptor other than the CCK-B or CCK-A receptor.
5 ific interactions with the N-terminus of the CCK(A) receptor.
6 molar affinity and 3500-fold selectivity for CCK-A receptors.
7  high affinity and 2100-fold selectivity for CCK-A receptors.
8 ng a compound with 6600-fold selectivity for CCK-A receptors.
9 on, an adenoviral construct encoding the rat CCK(A) receptor (AdCCK(A)R) was used to express the rat
10 hase 3 of Wistar rats can be attenuated by a CCK-A receptor agonist, sulphated CCK-8 (up to 0.17 micr
11 5-benzodiazepine peripheral cholecystokinin (CCK-A) receptor agonist 1 were prepared which explore su
12     Some neurones that express high-affinity CCK-A receptors also express 5-HT3 receptors.
13 nes that possessed high-affinity CCK type A (CCK-A) receptors also responded to luminal infusion of 5
14             Cholecystokinin (CCK) acting via CCK(A) receptors and gastrin acting via CCK(B) receptors
15 the N-terminal region (LDQPQPSKEWQSA) of rat CCK-A receptor and used it for localization studies with
16 ly suppression of food intake which involves CCK-A receptors and capsaicin-sensitive afferent fibers.
17 suggests that this inhibition is mediated by CCK-A receptors and involves PKC phosphorylation.
18 at these calcium elevations were mediated by CCK-A receptors and were dependent on intracellular calc
19 l deafferentation by perineural capsaicin or CCK A receptor antagonist (devazepide, 1 mg kg(-1), i.v.
20 sensory afferent fibers and by devazepide, a CCK-A receptor antagonist but not by the CCK-B receptor
21 se output can be completely inhibited by the CCK-A receptor antagonist L-364,718 and partially inhibi
22                                Devazepide (a CCK-A receptor antagonist, 1 mg/kg, i.p.) prevented the
23  low phase 3 of LE rats can be enhanced by a CCK-A-receptor antagonist, sodium lorglumide (4.3 microg
24 GS and SIIA cells; neither the CCK-B nor the CCK-A receptor antagonists blocked this effect.
25                                 In contrast, CCK-A receptor antagonists inhibited the stimulatory eff
26 5I-G-17 binding, whereas the CCK-preferring (CCK-A) receptor antagonists had no effect.
27                                    OX-R1 and CCK(A) receptors are expressed by human and rat vagal af
28 odel using only in vitro translation for the CCK-A receptor beginning with two signal anchor sequence
29 carbon resulted in acetamide 6, which showed CCK-A receptor binding selectivity and sub-micromolar ag
30 ivatives had improved affinity for the human CCK-A receptor but reduced agonist efficacy on the GPGB.
31         To determine the structural basis of CCK-A receptor (CCK-AR) functionally coupled to Gs, a se
32 ystokinin, CCK-8, with the N-terminus of the CCK(A)-receptor, CCK(A)-R(1-47), has been structurally c
33 ety, which is mediated by low-affinity vagal CCK-A receptors, CCK acts through high-affinity CCK-A re
34 lodaltons in Western blots of membranes from CCK-A receptor CHO-transfected cells; (2) cell surface s
35             Although most knowledge of vagal CCK-A receptors comes from research on rodents, physiolo
36 ed to express the rat receptor in acini from CCK(A) receptor-deficient mice (CCK(A)R -/-).
37 tween wild-type Long-Evans (LE) rats and the CCK-A-receptor-deficient Otsuka LE Tokushima Fatty (OLET
38                                 In contrast, CCK-A receptors exhibited a more selective pattern of ex
39 olecystokinin (CCK) inhibits food intake via CCK(A) receptors expressed on vagal afferent neurons.
40 sing receptor-specific riboprobes, localized CCK-A receptor expression to ductal cells, the presumed
41 iaphragmatic vagotomy reduced the density of CCK-A receptor fibers in the gastric mucosa by approxima
42 uthern blot analysis revealed no evidence of CCK-A receptor gene amplification or rearrangement in pa
43  that human pancreatic acini lack functional CCK-A receptors has been presented.
44                                              CCK-A receptor immunoreactivity was localized to myenter
45 ptor-transfected cells, (3) translocation of CCK-A receptor immunostaining in CCK-A receptor-transfec
46      The involvement of the cholecystokinin (CCK)-A receptor in fever was studied.
47  and tetrapeptides appear to interact at the CCK-A receptor in a similar manner.
48 lucidate the cellular sites of expression of CCK-A receptor in the rat stomach and small intestine.
49 (3)H) and Tac groups may not interact at the CCK-A receptor in the same location.
50 stokinin (CCK) to reduce food intake through CCK-A receptors in lean mice fasted for 24 h.
51                                              CCK-A receptor is expressed in functionally distinct neu
52                                              CCK-A receptor may mediate reflexes stimulated by CCK th
53     Because of its selective expression, the CCK-A receptor may serve as selective biomarker for panc
54                                         Many CCK-A receptor myenteric neurons contained the inhibitor
55 data suggest that species differences in the CCK(A) receptor of rats and mice account for the observe
56 ducts release endogenous CCK which activates CCK A receptors on vagal afferent nerve fibre terminals,
57 cells, and it is proposed that CCK activates CCK A receptors on vagal afferent nerve terminals.
58 e of high- and low-affinity cholecystokinin (CCK)-A receptors on rodent pancreatic acini is well esta
59  that may possess only high- or low-affinity CCK-A receptors or 5-HT3 receptors.
60 trait of this strain and not the lack of the CCK-A receptor per se.
61     Despite decreased affinity for the human CCK-A receptor, relative to CCK-8, some of these compoun
62 inities of 3.0 and 2900 nM for the CCK-B and CCK-A receptors, respectively.
63 within the tetrapeptide, resulted in loss of CCK-A receptor selectivity and development of a trend to
64 with the cDNA encoding the N terminus of the CCK-A receptor separated from the last 177 amino acids o
65 the H,K-ATPase beta subunit by cDNA encoding CCK-A receptor sequences of different lengths.
66 ith both the human CCK-BR and the peripheral CCK-A receptor subtypes.
67 6 produces potent anorectic activity via the CCK-A receptor system.
68 -A receptors, CCK acts through high-affinity CCK-A receptors to evoke pancreatic secretion, suggestin
69 location of CCK-A receptor immunostaining in CCK-A receptor-transfected cells after exposure to CCK;
70 nsfected cells; (2) cell surface staining of CCK-A receptor-transfected cells, (3) translocation of C
71 lly transferred rat and the endogenous mouse CCK(A) receptors was not different.
72  seven putative transmembrane domains of the CCK-A receptor were inserted individually into pGEM vect
73 RT-PCR indicated that the message levels for CCK-A receptors were approximately 30-fold lower than th
74                             Of significance, CCK-A receptors were expressed selectively in all pancre
75  expression in specific brain nuclei through CCK-A receptors while leptin alone had no effect.
76 ptor internalization, the rat wild type (WT) CCK-A receptor (WT CCKAR) and the rat WT CCK-B receptor

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