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1 r loop, and transmembrane VII regions of the neurotensin receptor.
2 a nonpeptide antagonist of the high-affinity neurotensin receptor (0.25 or 2.5 microgram, i.c.v., or
3 groups were inherently detrimental to human neurotensin receptor 1 (hNTR1) binding affinity or recep
4 peutic efficacy of oAd/DCN/LRP-PEG-NT toward neurotensin receptor 1 (NTR)-overexpressing pancreatic c
5 cally induced hypothermia (PIH) by the novel neurotensin receptor 1 (NTR1) agonist ABS-201 in a focal
6 mbinations that preferentially interact with neurotensin receptor 1 (NTR1) and our stabilized mutants
9 In this study, we define the high-affinity neurotensin receptor 1 (NTR1) as a tractable new molecul
14 quired for this network disturbance, we used neurotensin receptor 1 (Ntsr1) cre-driver mice to ablate
15 STR1, SSTR2), kisspeptin recepotor (KissR1), neurotensin receptor 1 (NTSR1), neuropeptide S receptor
18 receptors (angiotensin II type 1A receptor, neurotensin receptor 1, vasopressin V2 receptor, thyrotr
20 of the GHS-R is most closely related to the neurotensin receptor-1 (NT-R1) (35% overall protein iden
25 te as to whether a peripherally administered neurotensin receptor agonist represents a sound strategy
26 ta further support a role for NT69L or other neurotensin receptor agonists to treat nicotine addictio
27 tained high affinity and agonist potency for neurotensin receptors and exhibited dramatically improve
28 ural elements for species specificity of the neurotensin receptors, and may expedite developing nonpe
29 ither the protein phosphatase calcineurin or neurotensin receptors, and persists surprisingly long af
30 otensin analogs, biological functions of the neurotensin receptors, and structural elements for speci
31 eadministration of a mu opioid receptor or a neurotensin receptor antagonist into the ventral PAG.
33 r to be the high-affinity receptor since the neurotensin receptor antagonist SR48692, when given i.c.
35 administered peripherally, serum levels and neurotensin receptor binding potency of 1 peaked within
36 e a basis for rationalizing mutations of the neurotensin receptor gene but also offer insights into u
37 e constructed a series of chimeric rat/human neurotensin receptor genes and expressed them by transie
40 he C-terminal region of NT1-13 recognized by neurotensin receptors, modulate distension-induced relea
41 roscopic immunolabeling of the high-affinity neurotensin receptor (NTR) and neurotensin in these subd
42 the present study, we have cloned the human neurotensin receptor (NTR) gene, determined its structur
46 e promoter region of the mouse high affinity neurotensin receptor (Ntr-1) gene was characterized, and
48 l and hydrodynamic experiments that purified neurotensin receptor NTS1, a class A GPCR, dimerizes in
51 We previously determined the structure of neurotensin receptor NTSR1 in an active-like conformatio
52 and a hormone through the activation of the neurotensin receptor NTSR1, a G-protein-coupled receptor
53 re of a constitutively active, agonist-bound neurotensin receptor (NTSR1) and molecular dynamics simu
54 opeptide growth factor, and its two specific neurotensin receptors, NTSR1 and NTSR2, were shown to be
55 (AS-MOR MM), antisense PNAs targeted to the neurotensin receptor subtype 1 (AS-NTR1), or saline and
56 ur results led us to propose a region of the neurotensin receptor that may be involved in determining
57 ding only to microspots corresponding to the neurotensin receptor; this specificity was further demon
58 pitates with G(alpha)q/11 upon activation of neurotensin receptors; this association is inhibited by
59 c pocket on the extracellular surface of the neurotensin receptor to accommodate its ligands apparent
62 cosylated Thr10 contulakin-G for a number of neurotensin receptor types including the human neurotens
64 the observed Kd values at the rat and human neurotensin receptors were 0.046 and 5.8 nM, respectivel
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