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1 ce deficient in the gustducin alpha-subunit (alpha-gustducin).
2 hereas sucralose internalized T1R2, T1R3 and alpha-gustducin.
3 t receptor antagonist lactisole or siRNA for alpha-gustducin.
4 to lingual taste cells and strongly express alpha-gustducin.
5 ce, but not in knockout mice lacking T1R3 or alpha-gustducin.
6 Mouse intestinal L cells also express alpha-gustducin.
7 y pertussis toxin and by genetic deletion of alpha-gustducin.
8 t not all, bitter-responsive cells expressed alpha-gustducin.
9 5 kDa (SNAP-25), and to a lesser extent with alpha-gustducin.
10 li was reduced by 70% in mutant mice lacking alpha-gustducin.
11 ets using the molecular markers Vimentin and alpha-Gustducin.
12 group antigen, whether or not they expressed alpha-gustducin.
13 ceptors and the tastant-associated G protein alpha-gustducin.
14 for immunoreactivity to an antibody against alpha-gustducin.
15 lls express T2R "bitter-taste" receptors and alpha-gustducin, a G protein involved in chemosensory tr
16 fy the subset of type II cells that contains alpha-gustducin, a G-protein involved in bitter transduc
17 distributions of these antigens with that of alpha-gustducin, a G-protein subunit implicated in respo
23 ys, we generated a dominant-negative form of alpha-gustducin and expressed it as a transgene from the
24 differentiated light cells that also express alpha-gustducin and may be involved in intercellular int
25 which were incubated with antibodies against alpha-gustducin and the human blood group A antigen.
27 te receptors are coupled through G-proteins, alpha-gustducin and transducin, to activate phospholipas
28 ordings of single and double KO mice lacking alpha-gustducin and/or alpha(t-rod) confirmed the involv
29 e Cbeta2 (PLCbeta2) or the G-protein subunit alpha-gustducin, and serotonin (5HT) as markers of type
31 chemical and genetic studies have implicated alpha-gustducin as a key component in the transduction o
32 control experiments, expression of wild-type alpha-gustducin as a transgene in alpha-gustducin-null m
35 2P, introduced into the C-terminal region of alpha-gustducin critical for receptor interaction render
36 he normal vallate papilla had a mean of 8.37 alpha-gustducin-expressing cells and 5.22 A-expressing c
38 (8.4)) from the upstream region of the mouse alpha-gustducin gene acts as a fully functional promoter
39 ly proving that the targeted deletion of the alpha-gustducin gene caused the taste deficits of the nu
40 lthough "knock-out" animals deficient in the alpha-gustducin gene clearly demonstrate that gustducin
41 essed with taste-signaling molecules such as alpha-gustducin, Ggamma13, phospholipase C-beta2 (PLC-be
44 or alpha(t-rod) confirmed the involvement of alpha-gustducin in bitter (quinine and denatonium) and s
45 ter and sweet compounds, the precise role of alpha-gustducin in bitter and sweet taste is presently u
46 direct involvement of the G-protein subunit alpha-gustducin in bitter taste transduction in taste ce
49 eared on taste-bud cells that also expressed alpha-gustducin in the order: foliate and vallate papill
50 7) taste and demonstrated the involvement of alpha-gustducin in umami [monosodium glutamate (MSG), mo
55 behavioral sensitivity to bitter stimuli in alpha-gustducin knock-out mice thus appears to be the co
58 binding regulatory proteins expressed in the alpha-gustducin lineage of taste cells mediate these res
60 olated small bowel and intestinal villi from alpha-gustducin null mice showed markedly defective GLP-
62 wild-type alpha-gustducin as a transgene in alpha-gustducin-null mice fully restored responsiveness
63 bitter and sweet taste responsiveness of the alpha-gustducin-null mice suggests that other guanine nu
65 here was a normal number of cells expressing alpha-gustducin or the A antigen in regenerated taste bu
68 which transgene expression was driven by an alpha-gustducin promoter coupling BDNF expression to the
69 cin and expressed it as a transgene from the alpha-gustducin promoter in both wild-type and alpha-gus
72 d, the mutant transgene inhibited endogenous alpha-gustducin's interactions with taste receptors, i.e
73 responses to bitter and sweet compounds via alpha-gustducin's regulation of phosphodiesterase (PDE)
74 markers neuronal cell adhesion molecule and alpha-gustducin, suggesting that both the taste receptor
75 ated Ca2+ channels, K(+)ATP channels and the alpha-gustducin taste pathway do not appear to be involv
76 The human L cell line NCI-H716 expresses alpha-gustducin, taste receptors, and several other tast
77 et and bitter taste, apparently unrelated to alpha-gustducin, that increase cyclic AMP or inositol 1,
78 al sweeteners, which act through T1R2 + T1R3/alpha-gustducin to activate PLC beta2 and PKC betaII.
79 1Rs are colocalized with each other and with alpha-gustducin, transducin or phospholipase C beta2 to
80 with reciprocal regulation of T1R2, T1R3 and alpha-gustducin versus T1R1, transducin and phospholipas
81 labeled with antibodies against Vimentin and alpha-Gustducin were easily identified and counted under
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