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1 ceptor, angiotensin II type 1A receptor, and substance P receptor.
2 we constructed chimeras between PAR1 and the substance P receptor.
3 tail sequestered and recycled like wild-type substance P receptor.
4 th high (nM) affinity and specificity to the substance P receptor.
5 amina I spinal cord neurons that express the substance P receptor.
6  were equally effective at desensitizing the substance P receptor, a classic reversibly activated GPC
7 study, the effects of microinjections of the substance P receptor agonist, [Sar9.Met(O2)11]-substance
8 h a cell maintains responsiveness to PAR1 or substance P receptor agonists over time.
9                                              Substance P receptor and the P/S chimera showed little d
10 dicative of pain, the internalization of the substance P receptor, and c-Fos expression in lamina I n
11 ify NALCN as the cation channel activated by substance P receptor, and suggest that UNC-80 and Src fa
12 5-HT3 label was only present in small GABA-, substance P receptor-, and calbindin-containing neurons
13 cribes an asymmetric synthesis of the potent substance P receptor antagonist (+)-CP-99,994 from 4-phe
14                          Administration of a substance P receptor antagonist in mice.
15                                          The substance P receptor antagonist, CP-96,345, not only blo
16                              The nonpeptide, substance P receptor antagonist, CP96-345, significantly
17                 Administration of a specific substance P-receptor antagonist (CP-96,345) reduced toxi
18 e P release and pretreatment with a specific substance P-receptor antagonist blocked LTB4-induced sub
19                     The effect of a specific substance P-receptor antagonist was also studied.
20 oduced by NMDA were significantly reduced by substance P-receptor antagonists or by elimination of su
21            By contrast, wild-type PAR1 and a substance P receptor bearing the cytoplasmic tail of PAR
22 5'ET4 cells, nor was DAB389 GRP cytotoxic to substance P receptor-bearing cells.
23 n cells stably transfected with the bullfrog substance P receptor (bfSPR).
24                        In the present study, substance P receptor binding was localized in the dorsal
25  thyrotropin-releasing hormone receptor, and substance P receptor) bound both betaarrestin isoforms w
26 the radiolabeled peptides in the presence of substance P receptor caused covalent attachment of the p
27 mitations in the Ag-specific CTL response in substance P receptor-deficient mice could result from lo
28                                 Furthermore, substance P receptor-deficient mice showed a reduced CTL
29 , wild-type animals were markedly reduced in substance P receptor-deficient mice.
30 rmeable AMPA receptors are expressed by some substance P receptor-expressing (NK1R+) neurons in lamin
31                                We focused on substance P receptor-expressing (NK1R+) projection neuro
32 ing protein saporin that specifically target Substance P receptor-expressing cells.
33                            The importance of substance P receptor expression in vivo was further sugg
34  fact by investigating the contribution that substance P receptor expression makes toward immunity ag
35          The ability of Salmonella to induce substance P receptor expression on cultured macrophages
36 stration that mice, genetically deficient in substance P receptor expression, showed an increased vir
37 ntibody constant region (Fc) receptor or the substance P receptor fail to produce a model inflammator
38  ability of macrophages to express authentic substance P receptors (i.e., NK-1 receptors) has been in
39 la (BLA) are reported to specifically lesion substance P receptor immunoreactive (SPR-IR) interneuron
40 dies demonstrate that genetic elimination of substance P receptors in mice results in an increased ga
41 stimulation of the medial amygdala activates substance P receptors in the medial hypothalamus, thus t
42 gical methods to determine the role of NK(1)-Substance P receptors in the midbrain periaqueductal gra
43  results demonstrate a major requirement for substance P receptors in the pathogenesis of acute infla
44 rated the presence of: (1) high densities of substance P receptors in the ventromedial hypothalamus,
45                                    Wild-type substance P receptor internalized and recycled after act
46 ut also a large-scale internalization of the substance P receptor into dorsal horn neurons, as well a
47 estioned the contribution that expression of substance P receptors makes to the protective response f
48                          The distribution of substance P receptors may reconcile apparent mismatches
49 ella induced rapid and dramatic increases in substance P receptor mRNA expression within Peyer's patc
50 o acid identity to the tachykinin receptors (substance P receptor, neurokinin A receptor, and neuroki
51                      Both fluoxetine and the substance P receptor (NK(1)R) antagonist (SPA) L-0007607
52              Gene-targeted disruption of the substance P receptor (NK-1R) protected the lung from imm
53 y altering the trafficking fates of PAR1 and substance P receptor, one can dictate the efficiency wit
54 on; PAR1 bearing the cytoplasmic tail of the substance P receptor (P/S) behaved similarly.
55 rneurons, identified with immunostaining for substance P-receptor, parvalbumin, and mGluR1a-receptor,
56 amina I spinal cord neurons that express the substance P receptor play a pivotal role in the transmis
57 ssion rather than basket cell death, because substance P receptor-positive interneurons, some of whic
58 phosphorylate purified and reconstituted rat substance P receptor (rSPR).
59                  A chimeric PAR1 bearing the substance P receptor's cytoplasmic carboxyl tail sequest
60 ggest that the cytoplasmic tails of PAR1 and substance P receptor specify their distinct intracellula
61 that loss of spinal neurons that possess the substance P receptor (SPR) attenuated pain and hyperalge
62                                          The substance P receptor (SPR) gene is expressed at high lev
63 on and ligand-induced internalization of the substance P receptor (SPR) in the spinal cord in acute,
64                                          The substance P receptor (SPR) is a G protein-coupled recept
65 ndogenous substance P (SP) activation of the substance P receptor (SPR) on enteric neurons in the rat
66             The striatal distribution of the substance P receptor (SPR) protein was examined in relat
67 soactive intestinal peptide receptor (VIPR), substance P receptor (SPR), and gastrin-releasing peptid
68                                              Substance P receptor (SPR), which plays a key role in pa
69                                              Substance P receptor (SPR)-expressing spinal neurons wer
70                      The recent finding that Substance P receptors (SPRs) are expressed exclusively i
71    Unexpectedly, however, antagonists to the substance P receptor (the NK1 receptor) could achieve th
72 anisms responsible for this improvement, the substance P receptor was blocked in mice after traumatic
73 xin, DAB389 SP, directed to cells expressing substance P receptors, was not cytotoxic to 5'ET4 cells,
74 s individually expressing neuropeptide Y and substance P receptors were mixed in the same well.
75                                Activation of substance P receptors, which are coupled to Galpha(q), i
76  belong to peptide receptor subfamily (e.g., substance P receptor), with more distant relationship to

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