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1 [L-NNA] for NO synthesis, and VIP(10-28) for VIP receptor).
2 ember of the Gi family in signaling from the VIP receptor.
3  is probably due to the higher expression of VIP receptors.
4 can was positive for tumors known to express VIP receptors.
5  consistent with expression of high affinity VIP receptors.
6 sponses by activating two related receptors, VIP receptor 1 and 2 (VIPR1 and VIPR2).
7  m2, and m3 muscarinic receptor subtypes and VIP receptors 1 and 2 (VIPR1 and VIPR2).
8 l and GrB expression is mediated through the VIP receptors 1 and 2 and cAMP signaling through exchang
9 lls expressed vasoactive intestinal peptide (VIP) receptor 1 (VIPR1), and chemogenetic modulation of
10      Furthermore, differential expression of VIP receptor-1/VIP receptor-2 (VIPR1/VIPR2) was observed
11 ls engage in autocrine VIP signaling through VIP receptor 2 (VPAC2).
12  neuropeptide vasoactive intestinal peptide (VIP) receptor 2 (VPAC2), through which VIP modulates the
13 e, differential expression of VIP receptor-1/VIP receptor-2 (VIPR1/VIPR2) was observed between B6 and
14 onstructs containing various portions of the VIP receptor 5'-flanking sequences linked to the lucifer
15                      These results show that VIP receptor activation of lacrimal protein release is m
16  results, the authors conclude that Gs links VIP receptor activation to adenylyl cyclase and cyclic a
17 o the molecular basis of PACAP27 binding and VIP receptor activation.
18             Furthermore, T cells up-regulate VIP receptors after activation, identifying the VIP sign
19                                        Daily VIP receptor agonist treatment restored synchrony and rh
20 s upregulation was suppressed by a synthetic VIP receptor agonist.
21 ike and wave discharges, whereas blockade of VIP receptors almost completely abolished this form of e
22 ned to investigate whether human PDC express VIP receptors and whether VIP has immunological effects
23 ation, a downstream signaling pathway of the VIP receptor, and stimulated granzyme B and perforin exp
24 fect is mediated through the specific type 2 VIP receptor, and the cAMP/protein kinase A pathway.
25 eptor antagonist (exendin (9-39) amide) or a VIP receptor antagonist (hybrid of neurotensin 6-11 and
26                                          The VIP receptor antagonist reversed GLP1- and VIP-induced n
27                        NOS inhibitor L-NA or VIP receptor antagonist VIP(10-28), blocks the slow IJP
28 n in the presence of different levels of the VIP receptor antagonist, VIP(10-28), also delivered by m
29 ggest that the VIP hybrid is a breast cancer VIP receptor antagonist.
30 9 mol/L, 3 x 10(-)9 mol/L, respectively) and VIP-receptor antagonist (IC50, 3 x 10(-)7 mol/L, 5 x 10(
31                  Recent reports suggest that VIP receptors are expressed on a variety of malignant tu
32 retin and vasoactive intestinal polypeptide (VIP) receptors are responsible for the activation of ade
33 ibited reversibly by bath application of the VIP receptor-binding inhibitor L-8-K (5 microM) or the n
34  of VIP, acting through G(s)-protein-coupled VIP receptors, can induce LNCaP cell growth in the absen
35 dicted binding s of the VIP-R antagonists to VIP receptors correlated positively with their ability t
36  peptide (VIP) is overexpressed in PDAC, and VIP receptors expressed on T cells are a targetable path
37              These results indicate that the VIP receptor gene contains a negative glucocorticoid res
38                            The regulation of VIP receptor gene expression and the distribution of the
39  this study, the effect of glucocorticoid on VIP receptor gene expression was examined.
40 d glucocorticoid-mediated expressions of the VIP receptor gene in lung cells.
41 R-mediated transcriptional repression of the VIP receptor gene, but basal transcription is also reduc
42 he type 1 vasoactive intestinal polypeptide (VIP) receptor gene is highly expressed in the lung where
43 d was identified as Gi3 through capture of a VIP/receptor/ Gi3 ternary complex by covalent cross-link
44 pha i3 antiserum suppressed formation of the VIP/receptor/Gi3 ternary complex, demonstrating its func
45 transfection of GR expression vector and the VIP receptor GR binding site linked to the thymidine kin
46 P concentration of the E17 fetus and to have VIP receptors in the central nervous system.
47  significantly by VIP antagonist, a specific VIP receptor inhibitor.
48  Dexamethasone (100 n) suppresses endogenous VIP receptor mRNA expression in cultured lung cells.
49 ed glucocorticoid receptor (GR) binds to the VIP receptor promoter between -21 and -36 bp relative to
50 ng receptor autoradiography, PACAP and PACAP/VIP receptor (PVR) mRNAs by reverse transcription polyme
51  the uptake of 99mTc-TP3654 decreased in all VIP receptor-rich tissues except the kidneys.
52 active intestinal peptide (VIP) and a VPAC2 (VIP receptor subtype 2) receptor-specific agonist, Ro-25
53 erogeneity of these tumors, we also assessed VIP receptor subtype expression in seven well-characteri
54 mers was performed to characterize the PACAP/VIP receptor subtype(s).
55                Of the antibodies for the two VIP receptor subtypes (VIP1R and VIP2R), only VIP2R was
56 presence of the PACAP-specific but not PACAP/VIP receptor subtypes.
57 lly distinct G-protein-associated receptors, VIP receptor type 1 (VPAC1) and VIP receptor type 2 (VPA
58 to clusters of ILC3 that selectively express VIP receptor type 2 (VIPR2; also known as VPAC2).
59 d receptors, VIP receptor type 1 (VPAC1) and VIP receptor type 2 (VPAC2), mediate the biological effe
60 r gene shows that 126 base pairs (bp) of the VIP receptor upstream sequences are sufficient to mediat
61                  Blockade of delta-opioid or VIP receptors using naltrindole or VIP6-28, respectively
62  found in cutaneous nerves and mRNA, for the VIP receptor vasoactive intestinal peptide receptor type
63 uence variants to identify a higher-affinity VIP-receptor (VIP-R) antagonist, hypothesizing that spec
64                         Cloned are two novel VIP receptor (VIPR) mRNAs (VIPR1 and VIPR2) that also bi
65 oactive intestinal polypeptide (VIP) and the VIP receptor VPAC(2) (encoded by the gene Vipr2) may med
66 ound, but vasoactive intestinal polypeptide (VIP) receptor (VPAC) products were absent.
67 interact with vasoactive intestinal peptide (VIP) receptors (VPAC(1)-R and VPAC(2)-R) because of the
68  CE cells from human donor corneas expressed VIP receptor VPAC1 (not VPAC2).
69 ng activity is mediated through the specific VIP receptor VPAC1, and involves both cAMP-dependent and
70 and immunofluorescence, we demonstrated that VIP receptors VPAC1 and VPAC2 are expressed on PDC.
71 edicting increased binding affinity to human VIP receptors VPAC1 and VPAC2.
72                 Presence and localization of VIP receptors (VPAC1 and 2) were determined by RT-PCR, i
73 opsies were exposed to agents that block the VIP receptors (VPAC1 and VPAC2) or MCs.
74                                           CE VIP receptor was demonstrated (Western blot analysis).
75 VIP regulation of AR activation, mediated by VIP receptors, was protein kinase A (PKA)-dependent, and
76                                         Both VIP receptors were present in rat conjunctiva and cultur
77    Number of MCs and MCs that express VIP or VIP receptors were quantified by immunofluorescence.
78 Breast cancer vasoactive intestinal peptide (VIP) receptors were characterized.
79                            VPAC1, the type 1 VIP receptor, which is constitutively expressed in macro
80 es, and to a lesser degree VPAC2, the type 2 VIP receptor, which is induced upon macrophage activatio
81 iptional factors are mediated through type 2 VIP receptor with cAMP as secondary messenger.