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1 icient in the gustducin alpha-subunit (alpha-gustducin).
2 mmunoreactivity to an antibody against alpha-gustducin.
3 a bitter-responsive receptor that activates gustducin.
4 s and the tastant-associated G protein alpha-gustducin.
5 sucralose internalized T1R2, T1R3 and alpha-gustducin.
6 ptor antagonist lactisole or siRNA for alpha-gustducin.
7 ussis toxin and by genetic deletion of alpha-gustducin.
8 ngual taste cells and strongly express alpha-gustducin.
9 t not in knockout mice lacking T1R3 or alpha-gustducin.
10 Mouse intestinal L cells also express alpha-gustducin.
11 all, bitter-responsive cells expressed alpha-gustducin.
12 ing the molecular markers Vimentin and alpha-Gustducin.
13 (SNAP-25), and to a lesser extent with alpha-gustducin.
14 reduced by 70% in mutant mice lacking alpha-gustducin.
15 antigen, whether or not they expressed alpha-gustducin.
16 ate specific tastant-dependent activation of gustducin, a G protein implicated in bitter signaling.
17 press T2R "bitter-taste" receptors and alpha-gustducin, a G protein involved in chemosensory transduc
18 subset of type II cells that contains alpha-gustducin, a G-protein involved in bitter transduction,
19 butions of these antigens with that of alpha-gustducin, a G-protein subunit implicated in responses t
24 eins derived from visual transducin or taste gustducin alpha subunits, but no other Galpha HD protein
26 weet and amino acid taste receptors, and the gustducin alpha-subunit GNAT3 leads to male-specific ste
33 generated a dominant-negative form of alpha-gustducin and expressed it as a transgene from the alpha
35 entiated light cells that also express alpha-gustducin and may be involved in intercellular interacti
37 nds on an interaction with the C terminus of gustducin and requires G-protein betagamma subunits to p
43 pressed in bovine taste tissue and that both gustducin and transducin, in the presence of bovine tast
44 eptors are coupled through G-proteins, alpha-gustducin and transducin, to activate phospholipase C be
45 taste transduction cascade involving Galpha-gustducin and transient receptor potential melastatin 5.
46 s of single and double KO mice lacking alpha-gustducin and/or alpha(t-rod) confirmed the involvement
47 a2 (PLCbeta2) or the G-protein subunit alpha-gustducin, and serotonin (5HT) as markers of type I, II,
48 s sweet taste receptors, the taste G protein gustducin, and several other taste transduction elements
49 s sweet taste receptors, the taste G protein gustducin, and several other taste transduction elements
51 nd their associated heterotrimeric G protein gustducin are involved in sugar and amino acid sensing i
52 al and genetic studies have implicated alpha-gustducin as a key component in the transduction of both
53 l experiments, expression of wild-type alpha-gustducin as a transgene in alpha-gustducin-null mice fu
54 All Lewis(b)-positive cells expressed alpha-gustducin, but only a fraction of alpha-gustducin-positi
55 the activation in response to denatonium of gustducin by presumptive bitter-responsive receptors pre
56 tivity should be reflected in the numbers of gustducin-containing cells in different taste bud popula
58 troduced into the C-terminal region of alpha-gustducin critical for receptor interaction rendered the
59 eceptor subunit T1R3 and the taste G protein gustducin, expressed in enteroendocrine cells, underlie
60 ssion was found exclusively in the G-protein gustducin-expressing bitter receptor cells, while TNF wa
61 fungiform taste buds contained twice as many gustducin-expressing cells (6.8/taste bud) as those of t
62 mal vallate papilla had a mean of 8.37 alpha-gustducin-expressing cells and 5.22 A-expressing cells p
64 t family considered to be a component of the gustducin G-protein heterotrimer involved in bitter and
65 cin Galpha (Galphat) and the closely related gustducin (Galphag), but not Galphai1, Galphas, or Galph
67 from the upstream region of the mouse alpha-gustducin gene acts as a fully functional promoter to ta
68 ving that the targeted deletion of the alpha-gustducin gene caused the taste deficits of the null mic
69 h "knock-out" animals deficient in the alpha-gustducin gene clearly demonstrate that gustducin is an
70 hancer from the distal portion of the murine gustducin gene that, in combination with the minimal pro
71 with taste-signaling molecules such as alpha-gustducin, Ggamma13, phospholipase C-beta2 (PLC-beta2) a
78 lls that contain the G protein alpha subunit gustducin, implying that they function as gustducin-link
79 ha(t-rod) confirmed the involvement of alpha-gustducin in bitter (quinine and denatonium) and sweet (
80 d sweet compounds, the precise role of alpha-gustducin in bitter and sweet taste is presently unclear
81 t involvement of the G-protein subunit alpha-gustducin in bitter taste transduction in taste cells ha
83 mmunoreactivity to antisera directed against gustducin in taste buds of rat circumvallate papilla.
86 on taste-bud cells that also expressed alpha-gustducin in the order: foliate and vallate papillae > n
87 te and demonstrated the involvement of alpha-gustducin in umami [monosodium glutamate (MSG), monopota
88 ng paper, we demonstrate that T2Rs couple to gustducin in vitro, and respond to bitter tastants in a
89 t compounds, and to elicit the nature of the gustducin-independent pathways, we generated a dominant-
96 lpha-gustducin gene clearly demonstrate that gustducin is an essential molecule for tasting certain b
99 These data support the hypothesis that alpha-gustducin is involved in the transduction of both sweet-
102 ioral sensitivity to bitter stimuli in alpha-gustducin knock-out mice thus appears to be the conseque
105 g regulatory proteins expressed in the alpha-gustducin lineage of taste cells mediate these responses
107 cted results with knockout mice suggest that gustducin may be directly involved in both bitter and sw
110 patterns of GAD with the TRC protein markers gustducin, neural cell adhesion molecule, protein gene p
112 ed small intestine and intestinal villi from gustducin null mice displayed markedly defective glucago
114 small bowel and intestinal villi from alpha-gustducin null mice showed markedly defective GLP-1 secr
115 t alpha-gustducin restored responsiveness of gustducin null mice to both bitter and sweet compounds,
117 type alpha-gustducin as a transgene in alpha-gustducin-null mice fully restored responsiveness to bit
118 and sweet taste responsiveness of the alpha-gustducin-null mice suggests that other guanine nucleoti
120 ivity for the taste cell-specific G protein, gustducin, occurs in a subset ofrENaC positive taste cel
121 as a normal number of cells expressing alpha-gustducin or the A antigen in regenerated taste buds; in
125 a common second-messenger cascade involving gustducin, phospholipase C beta2, and the transient rece
126 bitter taste signaling cascade (i.e., TAS2R-gustducin-phospholipase Cbeta [PLCbeta]- inositol 1,4,5-
127 ste buds of the fungiform papillae had fewer gustducin-positive cells (3.1/taste bud) than those of o
130 r to target lacZ transgene expression to the gustducin-positive subset of taste receptor cells (TRCs)
131 transgene expression was driven by an alpha-gustducin promoter coupling BDNF expression to the postn
132 d expressed it as a transgene from the alpha-gustducin promoter in both wild-type and alpha-gustducin
135 Nevertheless, some taste cells lacking alpha-gustducin responded to bitter stimuli, suggesting that o
137 mutant transgene inhibited endogenous alpha-gustducin's interactions with taste receptors, i.e., it
138 nses to bitter and sweet compounds via alpha-gustducin's regulation of phosphodiesterase (PDE) and Gb
140 rs neuronal cell adhesion molecule and alpha-gustducin, suggesting that both the taste receptor cells
141 a2+ channels, K(+)ATP channels and the alpha-gustducin taste pathway do not appear to be involved.
142 e human L cell line NCI-H716 expresses alpha-gustducin, taste receptors, and several other taste sign
143 bitter taste, apparently unrelated to alpha-gustducin, that increase cyclic AMP or inositol 1,4,5 tr
145 e colocalized with each other and with alpha-gustducin, transducin or phospholipase C beta2 to differ
147 eciprocal regulation of T1R2, T1R3 and alpha-gustducin versus T1R1, transducin and phospholipase C be
148 from the GUS(8.4) promoter and of endogenous gustducin was coordinately lost after nerve section and
149 d with antibodies against Vimentin and alpha-Gustducin were easily identified and counted under a lig
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