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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
6 key step for efficient synthesis of a potent neurokinin 1 (NK1 ) antagonist in 60 % overall yield.
8 nerve fibers and activation of its receptor neurokinin 1 (NK1) are important effectors in the transm
9 he neuropeptide substance P (SP) and cognate neurokinin 1 (NK1) nociceptor in PC activation and angio
10 substance P (SP) and its principal receptor neurokinin 1 (NK1) play a specific role in the behaviora
11 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
21 The effect is blocked by preincubation with neurokinin 1 (NK1; L-732138, 10 mum) and NK3 (SB222200,
22 use of the oral combination of netupitant (a neurokinin 1 [NK1] receptor antagonist) and palonosetron
24 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
29 monocytic/macrophage THP-1 cells express the neurokinin 1 receptor (NK-1R), and that exposure of thes
30 oinflammatory molecule that interacts with a neurokinin 1 receptor (NK-1R), which is on T cells and h
32 stance P and microinjection of a substance P-neurokinin 1 receptor (NK1-R) antagonist into the NTS at
33 led an increase of the substance P-inducible neurokinin 1 receptor (NK1-R) in the retina of first, th
34 a interaction with its cognate receptor, the neurokinin 1 receptor (NK1-R), is produced by monocyte/m
36 h neurons in laminae III-IV that express the neurokinin 1 receptor (NK1r) and have dendrites that ent
37 ance P (SP) and hemokinin-1 (HK-1), bind the neurokinin 1 receptor (NK1R) and promote stimulatory imm
38 in the pre-Botzinger complex (pre-BotC), the neurokinin 1 receptor (NK1R) and somatostatin (Sst) pept
39 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 d the effects of selective activation of the neurokinin 1 receptor (NK1R) on signaling and traffickin
47 stance P (SP) induces the association of the neurokinin 1 receptor (NK1R) with two classes of protein
50 ith those in laminae III-IV that express the neurokinin 1 receptor (NK1r), form a major route through
51 dulator substance P (SP) and its target, the neurokinin 1 receptor (NK1R), in the generation and regu
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
64 in, nitric oxide synthase, somatostatin, and neurokinin 1 receptor but not with neuropeptide Y or cal
66 cetyltransferase, neuropeptide Y, serotonin, neurokinin 1 receptor protein, and somatostatin, was int
67 wn that blocking substance P (SP) binding to neurokinin 1 receptor with spantide I prevents Pseudomon
69 ibition caused endosomal retention of the SP neurokinin 1 receptor, beta-arrestins, and Src, resultin
70 kinins on platelets are mediated through the neurokinin 1 receptor, which may therefore offer a novel
71 n the monosynaptic C fiber input to lamina I neurokinin 1 receptor-expressing neurons (1-10 Hz stimul
75 xus (ICC-DMP) of the small intestine express neurokinin 1 receptors (NK1R) and internalize these rece
76 rnalization of mu-opioid receptors (MOR) and neurokinin 1 receptors (NK1R) was measured to assess opi
78 ble-stained with antibodies against MORs and neurokinin 1 receptors (NK1Rs) using immunofluorescence.
84 ity, brain-penetrant, hydroisoindoline-based neurokinin-1 (NK(1)) receptor antagonist with a long cen
85 as to determine the potential involvement of neurokinin-1 (NK(1)) receptors to active vasodilatation.
86 induced an upregulation of prodynorphin and neurokinin-1 (NK-1) in dorsal horn neurons, which was su
88 retreatment of LAD2 cells with two different neurokinin-1 (NK-1) receptor antagonists and siRNA inhib
89 onchoconstriction in young guinea pigs via a neurokinin-1 (NK-1) receptor mechanism at the first cent
90 We also assessed the role of the striatal neurokinin-1 (NK-1) receptor on pre- and post-synaptic M
91 creased during nociception, and SP activates neurokinin-1 (NK-1) receptors in the spinal cord and per
92 xpression of high affinity receptors for SP (Neurokinin-1 (NK-1) receptors) on microglia and shown th
95 nsistently and significantly attenuated by a neurokinin-1 (NK1) receptor antagonist (SR140333, 3 muM)
96 mission of pain and inflammation through the neurokinin-1 (NK1) receptor, a G protein-coupled recepto
97 with delta selectivity and as antagonist for neurokinin-1 (NK1) receptors were designed and synthesiz
98 possibly suggestive of an internalization of neurokinin-1 (NK1) receptors, which are highly specific
99 er ear; however, its high affinity receptor, neurokinin-1 (NK1), has not been identified and the phys
101 tifunctional ligands with opioid agonist and neurokinin-1 antagonist activities can be accomplished a
106 tic stimuli and clinical trials confirm that neurokinin-1 antagonists have significantly higher effic
107 developments involving antiemetics, such as neurokinin-1 antagonists, corticosteroids, dopamine anta
110 mmunoexpression of Substance P in week 8 and neurokinin-1 in weeks 8 and 12 in the superficial lamina
111 nalogue, but not significantly by tachykinin neurokinin-1 or neurokinin-2 receptor-selective agonists
112 uman colonic epithelial cells overexpressing neurokinin-1 receptor (NCM460 NK-1R) in response to SP s
113 alternative, nonapoptotic pcd induced by the neurokinin-1 receptor (NK(1)R) activated by its ligand S
115 mmation via binding to the G-protein-coupled neurokinin-1 receptor (NK-1R) and release of proinflamma
117 The substance P (SP)-preferring receptor neurokinin-1 receptor (NK-1R) has two forms: a full-leng
119 We have shown that substance P (SP) and its neurokinin-1 receptor (NK-1R) regulate intestinal angiog
121 the hypothesis that substance P (SP) and the neurokinin-1 receptor (NK-1R), both in vitro and in vivo
122 mmation that had been considered mediated by neurokinin-1 receptor (NK-1R), we sought to determine wh
128 euronal nitric oxide synthase (nNOS) and the neurokinin-1 receptor (NK1) have been proposed to be inv
130 (MOR/DOR) and antagonist bioactivity at the neurokinin-1 receptor (NK1R) have been designed and synt
132 e present study, we examined the role of the neurokinin-1 receptor (NK1R) in the modulation of respir
135 1) are neuropeptides that signal through the neurokinin-1 receptor (NK1R) to promote inflammation.
136 Substance P neuropeptide and its receptor, neurokinin-1 receptor (NK1R), are reported to present on
137 , protease-activated receptor-2 (PAR(2)) and neurokinin-1 receptor (NK1R), results in drastically dif
138 reBotzinger Complex (preBotC) that coexpress neurokinin-1 receptor (NK1R), SST, and sst2a are critica
142 in trigeminal subnucleus caudalis by NMDA or neurokinin-1 receptor activation, and whether inhibition
146 compound with delta/micro opioid agonist and neurokinin-1 receptor antagonist activities and with a h
147 can be reduced experimentally by intraductal neurokinin-1 receptor antagonist and clinically by use o
148 med a randomized trial of the ability of the neurokinin-1 receptor antagonist aprepitant to reduce sy
149 ogate for stroke volume) was improved in the neurokinin-1 receptor antagonist group during the first
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
172 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.
178 ubstance P peptide, a potent agonist for the neurokinin-1 receptor, with a nitroxide spin probe speci
180 e and formed numerous close appositions with neurokinin-1 receptor-ir pre-Botzinger complex neurons.
181 We sought to determine whether there are neurokinin-1 receptor-like-immunoreactive (NK-1R-LI) neu
184 gh-affinity receptors for this neuropeptide (neurokinin-1 receptors [NK-1R]), and we have shown that
185 roduction of NO is modulated by the striatal neurokinin-1 receptors and that this receptor may partic
186 Attaching a single quantum dot to individual neurokinin-1 receptors enabled us to follow with high sp
187 investigating the participation of striatal neurokinin-1 receptors in the methamphetamine (METH)-ind
188 f calcitonin gene-related peptide (CGRP) and neurokinin-1 receptors with CGRP(8-37) and RP67580, resp
189 (SP), acting at 5-HT(2A/2C), 5-HT(4), and/or neurokinin-1 receptors, was required to maintain inspira
192 te, group I metabotropic glutamate receptor, neurokinin-1, and tyrosine receptor kinase receptors.
193 esent study, we investigated the role of the neurokinin-1, dopamine D1 and D2 receptors on the METH-i
196 gimen of ondansetron, dexamethasone, and the neurokinin-1-receptor antagonist casopitant mesylate was
198 but was not affected by spantide I. mRNA for neurokinin-1-receptor-1 (NK-1R) was detected in the norm
203 in-ir (immunoreactive) neurons expressed the neurokinin 3 receptor (NK3R) or nuclear estrogen recepto
206 trial assessed the effectiveness of an oral neurokinin 3 receptor antagonist (MLE4901) on menopausal
207 agents that have such properties-tachykinin neurokinin 3 receptor antagonists-is proposed as a way o
211 agonist LY306740 (0 and 50 nmol) but not the neurokinin-3 (NK3) antagonist SR142801 (0 and 50 nmol) l
212 y neurons by injecting a selective toxin for neurokinin-3 expressing neurons [NK(3)-saporin (SAP)] in
213 ant, two structurally diverse antagonists of neurokinin-3 receptor (NK3), displayed distinct modes of
215 ed that neurokinin B (NKB) and its receptor, neurokinin-3 receptor (NK3R), are essential elements for
216 achykinins or exogenous selective tachykinin neurokinin-3 receptor activation with senktide analogue
217 e were inhibited by the selective tachykinin neurokinin-3 receptor antagonists, SB 223412 or SB 23537
219 s mimicked by exogenously applied tachykinin neurokinin-3 receptor-selective agonist, senktide analog
220 These neurons are potentially modulated by neurokinin-3 receptors (NK3Rs) of the tachykinin family
221 onfocal microscopy, we identified tachykinin neurokinin-3 receptors on human bronchial parasympatheti
222 e provide the first evidence that tachykinin neurokinin-3 receptors regulate human bronchial parasymp
223 er of labeled neurons containing Substance P/Neurokinin A (approximately 20% of total labeled neurons
224 f neuropeptides, including substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), that are enc
226 ceptors were able to bind to substance P and neurokinin A ligand with similar affinities; however, th
227 C1 (encoding the tachykinins substance P and neurokinin A) to be strongly activated by LP within the
228 ogues of SP, and the NK-2 endogenous ligand, neurokinin A, and is coupled to the phospholipase C path
229 of neuropeptides including substance P (SP), neurokinin A, and neurokinin B, which are recognized for
230 binding of the three peptides, substance P, neurokinin A, and propionyl[Met(O(2))(11)]SP(7-11), to t
231 , Lys-bradykinin, Lys-(des-Arg9)-bradykinin, neurokinin A, Met-Lys-bradykinin, histatin 8, and a myos
234 gents targeting other receptor sites include neurokinin and neurohormonal modulators, chloride channe
236 eceiving highly emetogenic chemotherapy, the neurokinin antagonist aprepitant significantly enhanced
237 itors, opioids, cholecystokinin antagonists, neurokinin-antagonists, chloride channel activators, gua
240 Patients with loss-of-function mutation in neurokinin B (NKB) and its receptor show hypogonadotropi
241 Human genetic studies have revealed that neurokinin B (NKB) and its receptor, neurokinin-3 recept
242 determine whether preprodynorphin (Dyn) and neurokinin B (NKB) are coexpressed in Kiss1 neurons in t
246 derable evidence suggests that dynorphin and neurokinin B (NKB) neurons in the hypothalamic arcuate n
247 ction mutations in the genes encoding either neurokinin B (NKB) or its receptor, NK3 (NK3R), result i
248 procal plots of identical slope when [MePhe7]neurokinin B (NKB) was used as the other competition par
249 ng substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), that are encoded by the tac1 (SP and
250 conservation and physiological functions of neurokinin B (NKB), we identified tachykinin (tac) and t
251 in receptor (KISS1R, formerly called GPR54), neurokinin B (TAC3), and the neurokinin B receptor (TACR
253 he Tac2 gene, which encodes the neuropeptide neurokinin B and its corresponding receptor neurokinin 3
254 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
259 arked alterations in hypothalamic kisspeptin/neurokinin B/dynorphin (KNDy) neurons, we hypothesized t
260 are also effects at the ARH to disrupt Kiss1/neurokinin B/dynorphin neuronal function through inhibit
263 idromic release of substance P, and of other neurokinins encoded by the preprotachykinin A (PPT-A) ge
264 second fish putative peptide, referred to as neurokinin F (NKF), is unique and found to be conserved
267 utamate transporters (VGlut2 and VGlut3) and neurokinin I receptors were found in distinct regions of
268 el pathways specifically activated by either neurokinin I, corticotropin-releasing factor receptor 1,
269 s tachykinin receptor 86C (also known as the neurokinin K receptor of D. melanogaster), now has been
270 tive sensory fibers and hemopoietic cells in neurokinin-mediated inflammation and suggest that such s
271 found a significant peripheral component in neurokinin NK-receptor mediated emesis, the authors unde
272 ce-based targets for antipsychotic agents: a neurokinin (NK(3)) antagonist (SR142801), a serotonin 2A
273 The current experiments examined whether neurokinin (NK) 1 and 2 receptors are involved in the ac
275 was designed to test the hypotheses that (1) neurokinin (NK) receptor activity modulates hyperventila
277 e response mediated by the G-protein-coupled neurokinin NK1 receptor and the tyrosine kinase-linked p
283 in rat superficial dorsal horn that express neurokinin receptor 1 (NK1), a receptor for substance P,
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.
287 gonadotropin-releasing hormone antagonists, neurokinin receptor-1 antagonists), but available inform
288 n the efflux of cAMP from exocrine cells and neurokinin receptors are important in substance P-mediat
293 suggest that ICC-DMP are primary targets for neurokinins released from enteric motor neurones in the
295 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
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