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1 mulation of receptors with neurally released neurokinins.
2 ey were significantly less likely to express neurokinins.
3 d activation of the G alpha(q)-coupled human neurokinin 1 (hNK-1) receptor coexpressed with the WT-hN
5 ion between the G protein-coupled tachykinin neurokinin 1 (NK(1)) receptor, expressed in an inducible
7 key step for efficient synthesis of a potent neurokinin 1 (NK1 ) antagonist in 60 % overall yield.
9 nerve fibers and activation of its receptor neurokinin 1 (NK1) are important effectors in the transm
10 he neuropeptide substance P (SP) and cognate neurokinin 1 (NK1) nociceptor in PC activation and angio
11 substance P (SP) and its principal receptor neurokinin 1 (NK1) play a specific role in the behaviora
12 gic (Sendide) or non-peptidergic (L703, 606) neurokinin 1 (NK1) receptor antagonist in one masseter m
16 compared ERK1/2 activation by the wild-type neurokinin 1 (NK1) receptor with a chimeric NK1 receptor
17 m intracellular stores through its preferred neurokinin 1 (NK1) receptor, thus inducing NO production
19 ensin II type 1a (AT1a), vasopressin V2, and neurokinin 1 (NK1) receptors are seven-transmembrane rec
20 The effect is blocked by preincubation with neurokinin 1 (NK1; L-732138, 10 mum) and NK3 (SB222200,
21 use of the oral combination of netupitant (a neurokinin 1 [NK1] receptor antagonist) and palonosetron
23 E-1) in controlling substance P (SP) and the neurokinin 1 receptor (NK(1)R) in endosomes of myenteric
25 atory cytokines and of the substance P (SP), neurokinin 1 receptor (NK-1R) in the proximal mesenteric
26 e P (SP), a neuropeptide, interacts with the neurokinin 1 receptor (NK-1R) on immune cells to help co
30 stance P and microinjection of a substance P-neurokinin 1 receptor (NK1-R) antagonist into the NTS at
31 led an increase of the substance P-inducible neurokinin 1 receptor (NK1-R) in the retina of first, th
32 a interaction with its cognate receptor, the neurokinin 1 receptor (NK1-R), is produced by monocyte/m
34 h neurons in laminae III-IV that express the neurokinin 1 receptor (NK1r) and have dendrites that ent
35 ance P (SP) and hemokinin-1 (HK-1), bind the neurokinin 1 receptor (NK1R) and promote stimulatory imm
36 in the pre-Botzinger complex (pre-BotC), the neurokinin 1 receptor (NK1R) and somatostatin (Sst) pept
37 A subset of preBotzinger Complex (preBotC) neurokinin 1 receptor (NK1R) and somatostatin peptide (S
42 SP) induces endocytosis and recycling of the neurokinin 1 receptor (NK1R) in endothelial cells and sp
44 d by spinal opiates; however, when they used neurokinin 1 receptor (NK1R) internalization as an indic
46 stance P (SP) induces the association of the neurokinin 1 receptor (NK1R) with two classes of protein
49 ith those in laminae III-IV that express the neurokinin 1 receptor (NK1r), form a major route through
50 dulator substance P (SP) and its target, the neurokinin 1 receptor (NK1R), in the generation and regu
55 ypothesize substance P and its receptor, the neurokinin 1 receptor (NK1R; official name TACR1), play
56 s in the nucleus ambiguus also expressed the neurokinin 1 receptor and were labeled retrogradely from
57 VP release from HNS explants, but neither a neurokinin 1 receptor antagonist [L732,138 (N-acetyl-L-t
58 not evident when cells were treated with the neurokinin 1 receptor antagonist aprepitant before SP st
59 sphamide chemotherapy; and the addition of a neurokinin 1 receptor antagonist for adults who receive
61 enase inhibitors), pyrilamine, aprepitant (a neurokinin 1 receptor antagonist), or indomethacin with
62 led trials also support an expanded role for neurokinin 1 receptor antagonists in patients who are tr
63 III of the rat spinal cord that express the neurokinin 1 receptor are densely innervated by peptider
65 wn that blocking substance P (SP) binding to neurokinin 1 receptor with spantide I prevents Pseudomon
67 ibition caused endosomal retention of the SP neurokinin 1 receptor, beta-arrestins, and Src, resultin
68 kinins on platelets are mediated through the neurokinin 1 receptor, which may therefore offer a novel
69 n the monosynaptic C fiber input to lamina I neurokinin 1 receptor-expressing neurons (1-10 Hz stimul
73 xus (ICC-DMP) of the small intestine express neurokinin 1 receptors (NK1R) and internalize these rece
75 ble-stained with antibodies against MORs and neurokinin 1 receptors (NK1Rs) using immunofluorescence.
82 ity, brain-penetrant, hydroisoindoline-based neurokinin-1 (NK(1)) receptor antagonist with a long cen
83 as to determine the potential involvement of neurokinin-1 (NK(1)) receptors to active vasodilatation.
85 retreatment of LAD2 cells with two different neurokinin-1 (NK-1) receptor antagonists and siRNA inhib
86 We also assessed the role of the striatal neurokinin-1 (NK-1) receptor on pre- and post-synaptic M
87 xpression of high affinity receptors for SP (Neurokinin-1 (NK-1) receptors) on microglia and shown th
90 mission of pain and inflammation through the neurokinin-1 (NK1) receptor, a G protein-coupled recepto
91 with delta selectivity and as antagonist for neurokinin-1 (NK1) receptors were designed and synthesiz
92 possibly suggestive of an internalization of neurokinin-1 (NK1) receptors, which are highly specific
93 er ear; however, its high affinity receptor, neurokinin-1 (NK1), has not been identified and the phys
95 tifunctional ligands with opioid agonist and neurokinin-1 antagonist activities can be accomplished a
100 tic stimuli and clinical trials confirm that neurokinin-1 antagonists have significantly higher effic
101 developments involving antiemetics, such as neurokinin-1 antagonists, corticosteroids, dopamine anta
104 mmunoexpression of Substance P in week 8 and neurokinin-1 in weeks 8 and 12 in the superficial lamina
105 nalogue, but not significantly by tachykinin neurokinin-1 or neurokinin-2 receptor-selective agonists
106 uman colonic epithelial cells overexpressing neurokinin-1 receptor (NCM460 NK-1R) in response to SP s
107 alternative, nonapoptotic pcd induced by the neurokinin-1 receptor (NK(1)R) activated by its ligand S
109 mmation via binding to the G-protein-coupled neurokinin-1 receptor (NK-1R) and release of proinflamma
112 The substance P (SP)-preferring receptor neurokinin-1 receptor (NK-1R) has two forms: a full-leng
114 We have shown that substance P (SP) and its neurokinin-1 receptor (NK-1R) regulate intestinal angiog
116 the hypothesis that substance P (SP) and the neurokinin-1 receptor (NK-1R), both in vitro and in vivo
117 mmation that had been considered mediated by neurokinin-1 receptor (NK-1R), we sought to determine wh
124 euronal nitric oxide synthase (nNOS) and the neurokinin-1 receptor (NK1) have been proposed to be inv
126 (MOR/DOR) and antagonist bioactivity at the neurokinin-1 receptor (NK1R) have been designed and synt
128 e present study, we examined the role of the neurokinin-1 receptor (NK1R) in the modulation of respir
132 1) are neuropeptides that signal through the neurokinin-1 receptor (NK1R) to promote inflammation.
133 Substance P neuropeptide and its receptor, neurokinin-1 receptor (NK1R), are reported to present on
134 , protease-activated receptor-2 (PAR(2)) and neurokinin-1 receptor (NK1R), results in drastically dif
135 reBotzinger Complex (preBotC) that coexpress neurokinin-1 receptor (NK1R), SST, and sst2a are critica
140 in trigeminal subnucleus caudalis by NMDA or neurokinin-1 receptor activation, and whether inhibition
144 compound with delta/micro opioid agonist and neurokinin-1 receptor antagonist activities and with a h
145 can be reduced experimentally by intraductal neurokinin-1 receptor antagonist and clinically by use o
146 med a randomized trial of the ability of the neurokinin-1 receptor antagonist aprepitant to reduce sy
147 ogate for stroke volume) was improved in the neurokinin-1 receptor antagonist group during the first
148 Furthermore, in vivo treatment with the neurokinin-1 receptor antagonist in DED mice effectively
149 enal ulceration or oesophagitis, whereas the neurokinin-1 receptor antagonist maropitant citrate is l
150 E(2) synthesis in the presence of a specific neurokinin-1 receptor antagonist or in cells genetically
153 vival in cecal ligation and puncture sepsis (neurokinin-1 receptor antagonist survival = 79% vs vehic
156 vely, relative to controls and the selective neurokinin-1 receptor antagonist WIN-51,708 attenuated t
158 his paper will review the characteristics of neurokinin-1 receptor antagonists (NK1-RAs) and the new
163 ory to 5-HT3 serotonin receptor antagonists, neurokinin-1 receptor antagonists, and dexamethasone.
165 These data show that early activation of the neurokinin-1 receptor by substance P decreases sepsis su
166 eraction of substance P with the substance P neurokinin-1 receptor expressed by a variety of immune c
167 e present study, we assessed the role of the neurokinin-1 receptor in the production of striatal 3-ni
171 ent study examined whether inhibition of the neurokinin-1 receptor with a specific antagonist (CJ-12,
173 e formation of DVs by Sub P, implicating the neurokinin-1 receptor, a Gq type of G protein coupled re
175 prototypical G protein-coupled receptor, the neurokinin-1 receptor, during its different phases of ce
176 Substance P, the principal ligand for the neurokinin-1 receptor, is a potent proinflammatory media
177 impact of deficiency in SP or its receptor, neurokinin-1 receptor, on wound healing in mouse models.
179 e and formed numerous close appositions with neurokinin-1 receptor-ir pre-Botzinger complex neurons.
183 gh-affinity receptors for this neuropeptide (neurokinin-1 receptors [NK-1R]), and we have shown that
184 roduction of NO is modulated by the striatal neurokinin-1 receptors and that this receptor may partic
185 Attaching a single quantum dot to individual neurokinin-1 receptors enabled us to follow with high sp
186 investigating the participation of striatal neurokinin-1 receptors in the methamphetamine (METH)-ind
187 f calcitonin gene-related peptide (CGRP) and neurokinin-1 receptors with CGRP(8-37) and RP67580, resp
188 (SP), acting at 5-HT(2A/2C), 5-HT(4), and/or neurokinin-1 receptors, was required to maintain inspira
190 te, group I metabotropic glutamate receptor, neurokinin-1, and tyrosine receptor kinase receptors.
191 esent study, we investigated the role of the neurokinin-1, dopamine D1 and D2 receptors on the METH-i
192 ith spantide I, an antagonist of SP receptor Neurokinin-1, significantly reduced corneal neovasculari
194 gimen of ondansetron, dexamethasone, and the neurokinin-1-receptor antagonist casopitant mesylate was
196 but was not affected by spantide I. mRNA for neurokinin-1-receptor-1 (NK-1R) was detected in the norm
201 in-ir (immunoreactive) neurons expressed the neurokinin 3 receptor (NK3R) or nuclear estrogen recepto
204 trial assessed the effectiveness of an oral neurokinin 3 receptor antagonist (MLE4901) on menopausal
205 agents that have such properties-tachykinin neurokinin 3 receptor antagonists-is proposed as a way o
209 agonist LY306740 (0 and 50 nmol) but not the neurokinin-3 (NK3) antagonist SR142801 (0 and 50 nmol) l
210 y neurons by injecting a selective toxin for neurokinin-3 expressing neurons [NK(3)-saporin (SAP)] in
211 ant, two structurally diverse antagonists of neurokinin-3 receptor (NK3), displayed distinct modes of
213 ed that neurokinin B (NKB) and its receptor, neurokinin-3 receptor (NK3R), are essential elements for
214 achykinins or exogenous selective tachykinin neurokinin-3 receptor activation with senktide analogue
215 e were inhibited by the selective tachykinin neurokinin-3 receptor antagonists, SB 223412 or SB 23537
217 s mimicked by exogenously applied tachykinin neurokinin-3 receptor-selective agonist, senktide analog
218 These neurons are potentially modulated by neurokinin-3 receptors (NK3Rs) of the tachykinin family
219 onfocal microscopy, we identified tachykinin neurokinin-3 receptors on human bronchial parasympatheti
220 e provide the first evidence that tachykinin neurokinin-3 receptors regulate human bronchial parasymp
221 such as neuropeptides, substance P (SP), and neurokinin A (NK-A), which mediate hematopoietic stimula
222 f neuropeptides, including substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), that are enc
225 ceptors were able to bind to substance P and neurokinin A ligand with similar affinities; however, th
226 C1 (encoding the tachykinins substance P and neurokinin A) to be strongly activated by LP within the
227 ogues of SP, and the NK-2 endogenous ligand, neurokinin A, and is coupled to the phospholipase C path
228 of neuropeptides including substance P (SP), neurokinin A, and neurokinin B, which are recognized for
229 binding of the three peptides, substance P, neurokinin A, and propionyl[Met(O(2))(11)]SP(7-11), to t
230 , Lys-bradykinin, Lys-(des-Arg9)-bradykinin, neurokinin A, Met-Lys-bradykinin, histatin 8, and a myos
233 gents targeting other receptor sites include neurokinin and neurohormonal modulators, chloride channe
235 itors, opioids, cholecystokinin antagonists, neurokinin-antagonists, chloride channel activators, gua
238 Patients with loss-of-function mutation in neurokinin B (NKB) and its receptor show hypogonadotropi
239 Human genetic studies have revealed that neurokinin B (NKB) and its receptor, neurokinin-3 recept
240 determine whether preprodynorphin (Dyn) and neurokinin B (NKB) are coexpressed in Kiss1 neurons in t
244 derable evidence suggests that dynorphin and neurokinin B (NKB) neurons in the hypothalamic arcuate n
245 ction mutations in the genes encoding either neurokinin B (NKB) or its receptor, NK3 (NK3R), result i
246 procal plots of identical slope when [MePhe7]neurokinin B (NKB) was used as the other competition par
247 ng substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), that are encoded by the tac1 (SP and
248 conservation and physiological functions of neurokinin B (NKB), we identified tachykinin (tac) and t
249 in receptor (KISS1R, formerly called GPR54), neurokinin B (TAC3), and the neurokinin B receptor (TACR
251 te nucleus (ARC) that co-express kisspeptin, neurokinin B and dynorphin (KNDy cells) are essential fo
252 he Tac2 gene, which encodes the neuropeptide neurokinin B and its corresponding receptor neurokinin 3
253 called GPR54), neurokinin B (TAC3), and the neurokinin B receptor (TACR3) result in pubertal failure
258 ncluding substance P (SP), neurokinin A, and neurokinin B, which are recognized for their roles in th
260 arked alterations in hypothalamic kisspeptin/neurokinin B/dynorphin (KNDy) neurons, we hypothesized t
261 are also effects at the ARH to disrupt Kiss1/neurokinin B/dynorphin neuronal function through inhibit
264 ative feedback interactions mediated through neurokinin-B and dynorphin signaling respectively are co
265 second fish putative peptide, referred to as neurokinin F (NKF), is unique and found to be conserved
267 wide variety of human physiology through the neurokinin G protein-coupled receptor family, implicated
269 utamate transporters (VGlut2 and VGlut3) and neurokinin I receptors were found in distinct regions of
270 el pathways specifically activated by either neurokinin I, corticotropin-releasing factor receptor 1,
271 s tachykinin receptor 86C (also known as the neurokinin K receptor of D. melanogaster), now has been
272 tive sensory fibers and hemopoietic cells in neurokinin-mediated inflammation and suggest that such s
273 found a significant peripheral component in neurokinin NK-receptor mediated emesis, the authors unde
274 ce-based targets for antipsychotic agents: a neurokinin (NK(3)) antagonist (SR142801), a serotonin 2A
275 The current experiments examined whether neurokinin (NK) 1 and 2 receptors are involved in the ac
284 rved following intravenous pretreatment with neurokinin receptor antagonists (3+/-7% relaxations).
285 icular administration (20 nmol h(-1)) of the neurokinin receptor antagonists CP99994 or SB223412.
289 gonadotropin-releasing hormone antagonists, neurokinin receptor-1 antagonists), but available inform
290 n the efflux of cAMP from exocrine cells and neurokinin receptors are important in substance P-mediat
294 suggest that ICC-DMP are primary targets for neurokinins released from enteric motor neurones in the
296 ate an interaction between the nicotinic and neurokinin signaling systems that may form the basis for
299 R and DOPR similarly attenuates the DNIC and neurokinin type 1 receptor internalization induced eithe