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1                                              G beta 1 gamma 2 interacted preferentially with tubulin-
2                                              G beta 5 bound to the G protein gamma subunit-like domai
3                                              G beta gamma appears to be the major effector of the 1-M
4                                              G beta gamma has little effect of its own but potentiate
5                                              G beta gamma sequestration of tubulin reduced the inhibi
6                                              G beta may then recruit Cdc42-bound MAPKKKK Ste20 to MAP
7                                              G beta subunits are thought to lock G alpha in the GDP-b
8                                              G beta subunits were barely detectable in purified Golgi
9                                              G beta/tubulin colocalization increased after pretreatme
10                           Full-length RGS9-1.G beta(5) bound to R9AP-containing vesicles with high af
11 se-accelerating protein (GAP) complex RGS9-1.G beta(5) plays an important role in the kinetics of lig
12 n of the association between R9AP and RGS9-1.G beta(5) represents a potential mechanism for the regul
13 in rod cells different pools exist of RGS9-1.G beta(5) that are either associated with R9AP or not, r
14 G beta subunits, only G beta(1)/G gamma(13), G beta(3)/G gamma(13), and G beta(4)/G gamma(13) pairing
15 pha(GDP) subunits can bind to the PLC-beta 2.G beta gamma complex to allow for rapid deactivation wit
16       The off rate shows that the PLC-beta 2.G beta gamma complexes are long-lived ( approximately 12
17 embrane binding similar to PLC delta 1 and a G beta gamma interaction energy close to that of PLC del
18 l activity of PLC beta 2, PLC delta 1, and a G beta gamma-activable PH beta 2-PLC delta 1 chimera.
19 sis toxin but insensitive to inhibition by a G beta gamma-sequestering peptide (beta ARK1ct).
20 ase activity of G alpha h are inhibited in a G beta h concentration dependent manner.
21 resence of DEP and GGL domains, the latter a G beta 5-interacting domain.
22 tion by pheromone or the pheromone-activated G beta gamma complex, because the CRIB point mutations a
23                                 In addition, G beta h copurifies with an alpha 1-agonist, adrenocepto
24                           Antibodies against G beta had no effects.
25 reas intracellularly loaded antibody against G beta subunit blocked OT-evoked bursts.
26 a(1)/G gamma(13), G beta(3)/G gamma(13), and G beta(4)/G gamma(13) pairings were found to form stable
27 een the laterally associating PLC-beta 2 and G beta gamma on membrane surfaces by fluorescence resona
28 ied by a parallel reduction in G beta 35 and G beta 36 subunits and by a 30-50% increase in alpha i3.
29 encode sites involved in GTPase activity and G beta-binding, NorpA (phospholipase C)-binding, and rho
30      Activation of PLC beta 3 by G alpha and G beta gamma subunits has been fairly well characterized
31  investigate the distribution of G alpha and G beta gamma subunits in the rat exocrine pancreas which
32 in-coupled receptors might evoke G alpha and G beta gamma to orchestrate regulation of phospholipase
33                                  G alpha and G beta subunits were not found on membranes of zymogen g
34 ng multiple assays of G beta association and G beta gamma effector modulation.
35 es of these species for adenylyl cyclase and G beta gamma to vary in a reciprocal fashion.
36                   The loop between the F and G beta strands (FG loop) of the bacteriophage MS2 coat p
37 ncipally at the FG-loop connecting the F and G beta-strands in each subunit, yielding an asymmetric s
38 resence of alpha subunits of Gs, Gi3, G0 and G beta.
39 P gamma S was dependent on agonist (GRP) and G beta gamma subunits.
40 ther trimeric (G alpha q/11, G alpha i3, and G beta) or monomeric (p21rhoA and p21ras) G-protein or p
41 1rhoA, p21ras, G alpha q/11, G alpha i3, and G beta) or protein kinase C (types alpha, beta 1, beta 2
42 activation is independent of PI 3-kinase and G beta gamma, our results are consistent with a role for
43 ly, suckling caused dissociation of OTRs and G beta subunits from G alpha(q/11) subunits shown by coi
44 he peptide was able to inhibit PI(4,5)P2 and G beta gamma activation of the PH-PLC delta 1 PH-PLC bet
45  that were transfected with D1A receptor and G beta 1 and G gamma 2 cDNAs.
46        We show that Gi-coupled receptor- and G beta gamma-stimulated MAP kinase activation is attenua
47 ssociate into GTP-bound G alpha subunits and G beta gamma dimers, either of which can modulate many d
48 een min post-carbachol addition, tubulin and G beta colocalized in vesicle-like structures in the cyt
49 abditis elegans suggests that the A-beta and G-beta genes arose by duplication early in the evolution
50          The sequences for mature A-beta and G-beta in mouse and human were completed and verified by
51 ever, pairwise comparisons of the A-beta and G-beta sequences revealed <53% identity.
52 - and GTP-specific beta-subunits (A-beta and G-beta, respectively) in pigeon are 54% identical.
53 beta 2, respectively) for lipid bilayers and G-beta gamma subunits.
54                                      An anti-G beta gamma or anti-Gi alpha antibody was without effec
55 and beta subunits (anti-G alpha common, anti-G beta, anti-G alpha i1/2/3, and anti-G alpha o) were us
56 x of G beta does not inhibit folding because G beta does not fold even when this region is removed.
57 ains the consensus motif (QXXER) for binding G beta gamma, reduced the fast (pertussis toxin (PTX)-se
58 imilar mechanism involving Far1, which binds G beta in addition to Cdc24 and Bem1.
59  to picomolar concentrations of biotinylated G beta gamma.
60             The apparent Kd for bovine brain G beta gamma in this assay was 60 nM, and the Km for squ
61  123 s) and that activation of PLC-beta 2 by G beta gamma would be sustained without a deactivating f
62  GYG-to-SYG mutation (i) is not activated by G beta gamma subunits, but instead shows constitutive ac
63               PLC beta 2 can be activated by G beta gamma subunits, whereas PLC delta 1 can be activa
64 ults in reversal of PLC-beta 2 activation by G beta gamma during the time of the assay (30 s).
65 at are involved in binding and activation by G beta gamma, a series of fragments of PLC-beta 3 as glu
66 xcised patch abrogates channel activation by G beta gamma.
67 tic parameters are only slightly affected by G beta gamma [Km = 3.6 +/- 1.0 nM and Vmax = 2.2 +/- 0.2
68  1 B) channels by their beta subunits and by G beta gamma dimers, heterologously expressed in COS-7 c
69 kappa receptor agonist, were also blocked by G beta and PLC-beta 3 antibodies.
70 plasma membranes were selectively blocked by G beta antibody and PLC-beta 3 antibody; contractions st
71   Polymerization of microtubules elicited by G beta gamma overrode tubulin translocation to the membr
72 , the receptor, and Gh, is also inhibited by G beta h.
73 y PI(4,5)P2 through the PH domain but not by G beta gamma.
74 of phosphoinositide 3-kinase is regulated by G beta gamma subunits and is particularly abundant in ph
75 ent or significantly delayed and weakened by G beta(2) knockdown.
76                                      Group C/G beta-hemolytic streptococcus was detected in 9.0% of p
77                             In resting cells G beta gamma localized predominantly at the cell membran
78 way, and they suggest that in J774A.1 cells, G beta(2)-derived G beta gamma is the most effective med
79                  The components that connect G beta gamma to MPF and MAP kinase activation in oocytes
80                              Newly cytosolic G beta gamma/tubulin complexes might promote microtubule
81 est that in J774A.1 cells, G beta(2)-derived G beta gamma is the most effective mediator of chemotaxi
82  co-expression of G gamma(13) with different G beta subunits, only G beta(1)/G gamma(13), G beta(3)/G
83 ducin (Pdc) is a G protein beta gamma dimer (G beta gamma) binding protein, highly expressed in retin
84 e-dependent inhibition results from a direct G beta gamma-Ca2+ channel interaction.
85 eins appear to comprise a preformed effector-G beta subunit assembly and function at the endosome rat
86                           Deletion of either G beta subunit or BDM-1 produces identical phenotypes.
87 ism in which protein phosphorylation enables G beta gamma gating of the channel complex.
88 s that the yeast STE4 and STE18 genes encode G beta and G gamma subunits, respectively, that the G be
89             Our findings identify endogenous G beta gamma as the mediator of the voltage-dependent, P
90 uppress or enhance the release of endogenous G beta gamma.
91 e by itself, but overexpression of exogenous G beta subunits is sufficient to cause channel modulatio
92 (13) was observed to associate with all five G beta subunits (G beta(1-5)) upon co-translation in vit
93  in vitro, as well as function with all five G beta subunits in the modulation of Kir3.1/3.4 (GIRK1/4
94 implying that they have a lower affinity for G beta gamma.
95 finity and specifically reduced the EC50 for G beta gamma-dependent activation of the mutant enzyme 3
96 hese findings provide the first evidence for G beta 5-independent functions of the GGL domain and for
97 sin-resistant structures because, except for G beta gamma, their functions are not known or cannot be
98 at the VDCC beta subunit must be present for G beta gamma to induce voltage-dependent modulation of N
99  of the gamma 2 polypeptide was required for G beta gamma/tubulin interaction.
100 entified protein(s) which can substitute for G beta gamma subunits.
101                               Affinities for G-beta gamma were in the following order: PH-beta 2 >/=
102 nd show here that it interacts with the free G beta gamma complex.
103 tion of G-proteins and elevation of the free G beta gamma dimer concentration.
104 ates G proteins by dissociating G alpha from G beta gamma subunits, and GTP hydrolysis by G alpha sub
105 clase, promotes dissociation of alpha s from G beta gamma, accelerates removal of covalently attached
106 a indicate that G gamma(13) forms functional G beta gamma dimers with a range of G beta subunits.
107 we show by fluorescence that G alpha i1(GDP).G beta gamma.PLC-beta 2 can form.
108 e reversed by overexpression of either human G beta(2) or mouse G beta(1).
109                                 Importantly, G beta gamma binding to Pdc was enhanced by Ca(2+) chela
110  of phosphatidylinositol 3-kinase (PI-3K) in G beta gamma-mediated MAP kinase activation.
111 i2 is accompanied by a parallel reduction in G beta 35 and G beta 36 subunits and by a 30-50% increas
112 mma, and G alpha plays an inhibitory role in G beta gamma-mediated signal transduction.) AKR1 could s
113 ll-length protein and may play a key role in G-beta gamma recognition.
114 ing that phosphorylation of BDM-1 influences G beta stability.
115      This PLC-beta 3 fragment also inhibited G beta gamma-stimulated PLC-beta activity in a reconstit
116 se (beta ARKct), which specifically inhibits G beta gamma signaling, but was not affected by the prot
117 pendent protein kinase specifically inhibits G beta gamma-activated PLC-beta 2 activity but not that
118  We describe a signaling mechanism involving G beta gamma, PAK-associated guanine nucleotide exchange
119     (The active subunit of this G protein is G beta gamma, and G alpha plays an inhibitory role in G
120 involves the alpha 1-adrenoceptor and 50 KDa G beta h, reveal that the 50 kDa protein is indeed a G a
121 teins, including G alpha2 and the only known G beta subunit, and the second of which requires ERK2.
122  coupled G alpha2 subunit and the only known G beta subunit.
123  immunofluorescence and immunogold labeling, G beta subunits were detected on PM but not on Golgi mem
124 G beta(2) but is unaffected in cells lacking G beta(1), G alpha i(2), or G alpha i(3).
125 on in both wild-type cells and cells lacking G beta(1).
126 tors C5a and C3a is ablated in cells lacking G beta(2) but is unaffected in cells lacking G beta(1),
127               The phenotype of cells lacking G beta(2) can be reversed by overexpression of either hu
128                                Cells lacking G beta(2) retain the rapid response but cannot sustain p
129 eta subunit, we found a significantly larger G beta gamma-dependent inhibition of alpha 1 B channel a
130 ein, beta Trcp, formed large aggregates like G beta, suggesting that it may also require a partner pr
131 linositol 3-kinase, PI-3 kinase-gamma, links G beta gamma to the MAP kinase activation pathway.
132 xpression of either human G beta(2) or mouse G beta(1).
133                                     Multiple G beta/G gamma(13) pairings were also functional in cell
134  951 amino acids and a protein with multiple G-beta WD40 repeats.
135 is inserted in the central cavity of the NiV-G beta-propeller.
136 econstituted by activated Galphai/o, but not G beta gamma, subunits.
137                      Supporting this notion, G beta h accelerated GTP gamma S release from G alpha h
138 phorylation is strong even in the absence of G beta gamma.
139 G beta 5 and subcellular localization and of G beta 5 on RGS6 protein localization was examined in CO
140 ith G beta subunits using multiple assays of G beta association and G beta gamma effector modulation.
141 es a > or = 2.7-fold higher concentration of G beta h than the G alpha h alone, indicating that the r
142                  Based on the coordinates of G beta, we have constructed a model for the structure of
143  was correlated with a parallel depletion of G beta and protein phosphatase 1 from the oligomeric GIR
144 ead affects the kinase cascade downstream of G beta gamma, so that the kinase Ste20p and components d
145 ing that PI-3 kinase functions downstream of G beta gamma.
146 pathway upstream of Ste20p but downstream of G beta gamma.
147   The lack of a strong stimulatory effect of G beta gamma on GRK2-catalyzed phosphorylation of hSPR i
148 nd gamma 2 subunits prevented the effects of G beta gamma dimers on basal Ca2+ channel behaviour in a
149  The mutation Y92P, which is near the end of G beta-strand, produced sawtooth patterns with all-or-no
150 nucleolar localization, and co-expression of G beta 5 promoted nuclear localization of RGS6 proteins.
151        Similarly, injection or expression of G beta gamma subunits in sympathetic ganglion neurons in
152 oexpression restored all of the hallmarks of G beta gamma modulation.
153  non-WD-repeat amino terminal alpha helix of G beta does not inhibit folding because G beta does not
154 ssociate with Golgi membranes independent of G beta subunits and have distinctive distributions withi
155 tor of the 1-MA receptor, since injection of G beta gamma, but not activated G alpha i, leads to the
156                               Involvement of G beta gamma endogenously present in membranes is ruled
157                            Overexpression of G beta 1 gamma 2, which mimicked the voltage-dependent i
158 udies revealed the spatiotemporal pattern of G beta gamma/tubulin interaction during carbachol stimul
159 ghtly (1.3-fold increase) in the presence of G beta gamma.
160 nctional G beta gamma dimers with a range of G beta subunits.
161  in intracellular calcium and the release of G beta gamma subunits from heterotrimeric G proteins, pl
162 unctions of the GGL domain and for a role of G beta 5 in RGS protein localization.
163 a manner consistent with the sequestering of G beta gamma.
164 s predicted on the basis of the structure of G beta.
165 tachment of GFP mutants to the N-terminus of G beta 1 or G gamma 2 does not qualitatively impair thei
166                              Transfection of G beta gamma into cells expressing P/Q-type Ca2+ channel
167                           Removal by urea of G beta(5L) from endogenous or recombinant RGS9-1 bound t
168 ,5-bisphosphate [PI(4,5)P2] and inclusion of G-beta gamma subunits had little affect on their membran
169 chestnut blight, contains three G alpha, one G beta, one G gamma subunits and phosducin-like protein
170 mma(13) with different G beta subunits, only G beta(1)/G gamma(13), G beta(3)/G gamma(13), and G beta
171 , but it is not known whether the G alpha or G beta gamma subunits are responsible for modulation of
172  proteins are activated either by G alpha or G beta gamma subunits of heterotrimeric G proteins.
173  effects, whereas inhibitors of G alpha i or G beta gamma were without effect.
174 irectly bound and activated by the G protein G beta gamma subunit.
175 nd specific interactions between the protein G beta 2 domain and goat IgG that had been covalently im
176  crystal structure of one WD-repeat protein (G beta) has now been solved and reveals that the seven r
177 only studied example of a WD-repeat protein, G beta, synthesized in vitro in a rabbit reticulocyte ly
178 h RGS9-1 and the other GAP complex proteins (G beta 5, R9AP) accelerates the conversion of T alpha GT
179                                     Purified G beta gamma, alone or with phosphatidylinositol 4,5-bis
180 e knockdown of seven proteins (C5a receptor; G-beta-2; G-alpha,i-2,3; regulator of G-protein signalin
181 and 161Lys to Glu within this region reduced G beta gamma binding affinity and specifically reduced t
182      An important functional feature of RGS9-G beta 5 is its ability to activate transducin GTPase mu
183  Here we show that different domains of RGS9-G beta 5 make opposite contributions toward this selecti
184 ctor-kappa B (NF-kappa B) by a PTX-sensitive G beta gamma subunit-mediated pathway.
185  or a cell-permeable peptide that sequesters G beta gamma-subunits.
186  G-protein composed of FadA (G alpha), SfaD (G beta), and a presumed G gamma.
187  phosphorylation of hSPR is surprising since G beta gamma potently stimulates GRK2-catalyzed phosphor
188  multiple G alpha subunits but only a single G beta and G gamma subunit suggesting that the specific
189 f RGS9-1 with or without the partner subunit G beta(5L) were constructed with or without the C-termin
190 soform of the type 5 G-protein beta subunit (G beta 5) and the RGS9 anchor protein (R9AP).
191  of RGS9 with type 5 G protein beta subunit (G beta 5) is abundant in photoreceptors, where it stimul
192         The trimeric G-protein beta subunit (G beta) appears to be the most closely related beta-prop
193  to associate with all five G beta subunits (G beta(1-5)) upon co-translation in vitro, as well as fu
194 way requiring G-protein beta gamma subunits (G beta gamma) and many of the same intermediates involve
195  the data provide evidence for an N-terminal G beta gamma binding region of PLC-beta 3 that is involv
196                               The N-terminal G beta gamma binding region was delineated further to th
197                     Here we demonstrate that G beta gamma interaction with tubulin down-regulates thi
198                          Here we report that G beta gamma subunits can modulate Ca2+ channels.
199                     Our results suggest that G beta gamma binds PAK1 and, via PAK-associated PIX alph
200                   Our data also suggest that G beta h does not directly interact with alpha 1-adrenoc
201                         It is suggested that G beta gamma/tubulin interaction mediates internalizatio
202                           This suggests that G beta-gamma levels may be regulated passively through d
203                                          The G beta gamma complex of the pheromone receptor-coupled G
204                                          The G beta subunit of heterotrimeric guanine nucleotide bind
205 partially reduced by pertussis toxin and the G beta gamma scavenger transducin, and enhanced by co-ex
206 h its binding partners, p115(RhoGEF) and the G beta subunit.
207 omone response pathway at a step between the G beta subunit and Ste5p, the scaffolding protein that b
208 or overexpression of STE4, which encodes the G beta subunit of this G protein, suggesting that pherom
209 trate that PI-3K activity is required in the G beta gamma-mediated MAP kinase signaling pathway at a
210        In contrast, mutating residues in the G beta-strand gave results that were dependent on amino
211 tes the opening conformational change of the G beta gamma-bound channel.
212 ants resulted in reduced accumulation of the G beta subunit, suggesting that phosphorylation of BDM-1
213       The mutation I88P in the middle of the G beta-strand resulted in native like unfolding sawtooth
214 ng the second pathway, the detachment of the G beta-strands is involved in the first unfolding event.
215 hat this negative effect does not act on the G beta gamma complex but instead affects the kinase casc
216 bsence of coexpressed VDCC beta subunit, the G beta gamma dimers, either expressed tonically or eleva
217             Additionally, we report that the G beta subunit is not detectable in absence of BDM-1.
218 ediate synaptic transmission seem to use the G beta gamma, and not the G alpha, subunits of the trime
219 o search for proteins that interact with the G beta gamma complex and that might be involved in cell
220 h contains six WD repeat motifs found in the G-beta transducin family of proteins and other proteins,
221 uences show >89% identity to each other; the G-beta sequences are similarly related.
222                                         This G beta gamma-PAK1/PIX alpha/Cdc42 pathway is essential f
223 hile the GRK3 fusion protein binds all three G beta isoforms.
224 s toxin-sensitive manner, presumably through G beta gamma released from the Gi proteins.
225    If WD proteins form structures similar to G beta, their hydrodynamic properties should be those of
226 kely to form propeller structures similar to G beta.
227 e required for proper recruitment of Ste5 to G beta.
228 man and mouse that were highly homologous to G-beta and A-beta, respectively.
229                          We show that unlike G beta, several proteins with WD-repeats are able to fol
230 ed by co-injecting either tagged or untagged G beta 1 and G gamma 2 with excess G alpha(oA) cDNA.
231 ve G alpha(oA) and either tagged or untagged G beta 1 gamma 2 subunits.
232 e pheromone-responsive kinase cascade, until G beta gamma is activated by pheromone.
233 -1 is critical for membrane binding, whereas G beta(5L) does not play an important role in membrane a
234 o a non-plasma membrane compartment, whereas G beta gamma localization was unaltered.
235                       The mechanism by which G beta gamma mediates tyrosine phosphorylation of Shc, h
236 unctional range of G gamma(13) assembly with G beta subunits using multiple assays of G beta associat
237  to the plasma membrane and colocalized with G beta.
238 a mutation in vivo and formed a complex with G beta gamma that was able to undergo nucleotide exchang
239  the cell's axis in a signaling complex with G beta gamma, PAK1, and PIX alpha; while Rho, activated
240 GGL) domains which dimerize exclusively with G beta(5) subunits.
241 ts with complete GGL domains interacted with G beta 5, irrespective of the type of N-terminal domain,
242 S6 splice variants in their interaction with G beta 5 and subcellular localization and of G beta 5 on
243 ay not directly mediate the interaction with G beta gamma, the data provide evidence for an N-termina
244 ether these domains laterally associate with G-beta gamma subunits bound to membrane surfaces using f
245 , docking of the PH domain of PLC-beta2 with G-beta gamma is comparable to that of the full-length pr
246 , the PH domain of PLC-beta 1 interacts with G-beta gamma in isolation, but not in the context of the

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