コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 nide group and binding to a specific site on Gbeta.
2 nknown putative interfaces on the surface of Gbeta.
3 ed the evolution of the molecular surface of Gbeta.
4 g of the Gbetagamma dimer, via contacts with Gbeta.
5 a with Gbeta is necessary for this action of Gbeta.
6 affecting the surface expression of GIRK or Gbeta.
7 synchronized following acute inactivation of Gbeta.
8 e nucleotide-binding protein subunit beta-1, Gbeta.
9 iary complex with CCT preloaded with nascent Gbeta.
10 ich allowed us to uncover divergent roles of Gbeta(1) and Gbeta(2) in the regulation of neutrophil fu
15 onal yeast two-hybrid assays showed that the Gbeta(1) subunit also interacts with the N-terminal segm
16 the active Gbeta(2) subunit and the inactive Gbeta(1) subunit, we identified a cluster of amino acids
17 s in TRPM3 and their interacting partners in Gbeta(1) that are individually necessary for TRPM3 inhib
19 otide exchange at Galphaq in the presence of Gbeta(1)gamma(1) and NT was crucially affected by the li
22 tion by light, the dissociated G(t)alpha and Gbeta(1)gamma(1) subunits of transducin translocate from
23 nt, and the apparent affinity of Galphaq and Gbeta(1)gamma(1) to activated NTS1 increased with increa
24 a 1) forms a heterotrimeric complex with rod Gbeta(1)gamma(1), 2) substitutes equally for rTalpha in
29 erent phenotypes that result from removal of Gbeta 13F from each region demonstrate a striking divisi
31 vation was dependent on the presence of free Gbeta 1gamma 2 since its sequestration in the presence o
35 he PH domain of PLC-eta2 is not required for Gbeta 1gamma 2-mediated regulation since a purified frag
43 In addition, knockdown of Gbeta(1) but not Gbeta(2) inhibited the ability of neutrophils to kill in
45 augmented Gbeta(2) levels in the nucleus and Gbeta(2) interacted with specific nucleosome core histon
47 in II type 1 receptor specifically augmented Gbeta(2) levels in the nucleus and Gbeta(2) interacted w
49 By exchanging residues between the active Gbeta(2) subunit and the inactive Gbeta(1) subunit, we i
50 tagamma through demonstrating interaction of Gbeta(2) with integral components of chromatin and effec
52 -mediated chemotaxis requires Galpha(i2) and Gbeta(2), but not Ca(2+) signaling, and membrane protrus
55 whose genome-wide binding accounted for the Gbeta(2)-dependent regulation of approximately 2% genes.
56 nt Gbetagamma subunits to establish that the Gbeta(2)gamma(2) dimer can selectively reconstitute the
57 nhibition of unitary currents by recombinant Gbeta(2)gamma(2) dimers but does not disrupt dimer bindi
58 se A (PKA) as a molecular switch that allows Gbeta(2)gammax dimers to effect voltage-independent inhi
65 ctivated auto alpha(2a)ARs, whereas we found Gbeta(4) and Ggamma(12) preferentially interacted with a
66 namic intramolecular interaction between the Gbeta(5) and DEP domains, which suggested that the Gbeta
67 assays reveal that R9AP co-localizes RGS11 x Gbeta(5) and Galpha(o) on the membrane and allostericall
69 e identified point mutations that weaken DEP-Gbeta(5) binding, presumably stabilizing the open state,
71 with Gbeta(5)-RGS7 causes the DEP domain and Gbeta(5) to dissociate from each other and bind to the C
72 of mGluR6-Galpha(o) signaling by the RGS11 x Gbeta(5) x R9AP complex and establish R9AP as a general
73 which is permanently bound to Gbeta subunit Gbeta(5), and the RGS domain responsible for the interac
75 ng in Xenopus oocytes indicates that RGS11 x Gbeta(5)-mediated GTPase acceleration in this system req
76 f the M3R C-tail could not bind to wild-type Gbeta(5)-RGS7 but could associate with its open mutant a
77 following model: interaction of the M3R with Gbeta(5)-RGS7 causes the DEP domain and Gbeta(5) to diss
78 5) and DEP domains, which suggested that the Gbeta(5)-RGS7 dimer could alternate between the "open" a
79 idea that the M3R can effectively induce the Gbeta(5)-RGS7 dimer to open; such a mechanism would requ
81 that these mutations facilitated binding of Gbeta(5)-RGS7 to the recombinant third intracellular loo
82 e Gbeta(5)-RGS7; however, the open mutant of Gbeta(5)-RGS7 was able to inhibit signaling by the trunc
84 the regulator of G protein signaling (RGS), Gbeta(5)-RGS7, can inhibit signal transduction via the M
86 e M3R insensitive to inhibition by wild-type Gbeta(5)-RGS7; however, the open mutant of Gbeta(5)-RGS7
90 en translated Ggamma was added to translated Gbeta, a new band of low apparent molecular mass (approx
93 rabidopsis thaliana contains one Galpha, one Gbeta (AGB1), and at least three Ggamma subunits, allowi
94 ll wall integrity as mutants impaired in the Gbeta- (agb1-2) or Ggamma-subunits have an altered wall
96 ne canonical and three extra-large Galpha, 1 Gbeta and 3 Ggamma proteins represent the heterotrimeric
97 only possible following acute inhibition of Gbeta and are masked by slow compensation in genetic kno
98 ctivate the heterotrimeric G protein subunit Gbeta and find that this acute perturbation triggers per
100 ein components, which includes two copies of Gbeta and Ggamma genes, but no canonical Galpha Instead,
103 pecific peptides corresponding to regions on Gbeta and Ggamma shown to be important for the interacti
104 terotrimeric G-proteins comprised of Galpha, Gbeta and Ggamma subunits are important signal transduce
105 of exogenous G-proteins depends on both the Gbeta and Ggamma subunits being overexpressed in the cel
106 , we investigated the in vivo specificity of Gbeta and Ggamma subunits to auto-alpha(2a)ARs and heter
107 ntitative MRM proteomic analysis of neuronal Gbeta and Ggamma subunits, and co-immunoprecipitation of
108 ections of the dopamine receptor subtype and Gbeta and Ggamma subunits, each labeled with a different
109 pts the folding of Gbeta and the assembly of Gbeta and Ggamma subunits, events normally assisted by P
110 ein complex, consisting of canonical Galpha, Gbeta and Ggamma subunits, is involved in transducing si
113 insights into the multiplicity of genes for Gbeta and Ggamma, and the mechanisms underlying GPCR sig
115 uorescence resonance energy transfer between Gbeta and Ggamma1 in the absence of Galpha overexpressio
117 that one such novel interface occurs between Gbeta and phospholipase C beta2 (PLC-beta2), a mammalian
118 revealed that PhLPs disrupts the folding of Gbeta and the assembly of Gbeta and Ggamma subunits, eve
120 t of Ggamma required the presence of ambient Gbeta and was enhanced by low doses of coexpressed Gbeta
121 of antibodies against the G protein subunit Gbeta and was mimicked by the myristoylated betagamma-bi
122 protein, each of which consists of a Galpha, Gbeta, and Ggamma subunit, making it difficult to deline
123 meric G-protein complexes comprising Galpha, Gbeta, and Ggamma subunits and their regulatory RGS (Reg
124 n Arabidopsis thaliana involving the Galpha, Gbeta, and Ggamma subunits of heterotrimeric G-protein c
125 Heterotrimeric G proteins comprising Galpha, Gbeta, and Ggamma subunits regulate many fundamental gro
126 or the entire G-protein complex, the Galpha, Gbeta, and Ggamma subunits, and the REGULATOR OF G-PROTE
127 rotrimeric G proteins, consisting of Galpha, Gbeta, and Ggamma subunits, are a conserved signal trans
128 rotrimeric G proteins, consisting of Galpha, Gbeta, and Ggamma subunits, play important roles in plan
129 eterotrimeric G-proteins, comprising Galpha, Gbeta, and Ggamma subunits, regulate key signaling proce
130 terotrimeric G-proteins comprised of Galpha, Gbeta, and Ggamma subunits, which influence many aspects
133 ha and Gbeta mutants, the ER localization of Gbeta, and the differential stabilities of Galpha and Gb
134 tinct signaling mechanism by two Galpha, one Gbeta, and two Ggamma proteins for pheromone responses,
137 However, although effectors of Galpha and Gbeta are known in mammals, no Gbeta effectors were prev
138 he C-terminal tail in GPCR signaling, and of Gbeta as scaffold for recruiting Galpha subunits and G p
139 directs the redistribution of the G protein Gbeta as well as adherens junction proteins and Rho guan
140 ere, we report that G protein beta subunits (Gbeta) bind to DDB1 and that Gbeta2 targets GRK2 for ubi
141 majority of these 13 mutations affect known Gbeta binding sites, which suggests that a likely diseas
144 addition of Ggamma to previously synthesized Gbeta caused its release from the CCT/TRiC complex.
145 ates in the Gbetagamma assembly process, the Gbeta-CCT and the PhLP1-Gbeta-CCT complexes, were isolat
146 ssembly process, the Gbeta-CCT and the PhLP1-Gbeta-CCT complexes, were isolated and analyzed by a hyb
149 nits from HEK293 or Neuro-2a cells with FLAG-Gbeta constructs identified multiple Ggamma subunits by
153 amma1 localizes to protoplast membranes, but Gbeta exhibits membrane localization only when the Ggamm
158 tathione S-transferase (GST)-RP2 pulled down Gbeta from retinal lysates and the interaction was speci
160 was stable throughout the 1-2000 bars range, Gbeta gamma binding was stable only at high membrane con
161 terminal region of phospholipase C-beta1) or Gbeta gamma subunits (transducin and the carboxyl-termin
163 ng mechanisms: a fast inhibition mediated by Gbeta gamma, a slow inhibition mediated by Galpha(q/11),
164 nt of inhibition was attenuated by buffering Gbeta gamma, whereas a slow component of inhibition was
165 s gives rise to a flexible sub-population of Gbeta/gamma heterodimers that are not necessarily restri
166 n plants homozygous for a null allele of the Gbeta gene, Galpha is associated with smaller complexes
169 lacking specific combinations of Galpha and Gbeta genes, performed extensive phenotypic analysis, an
171 all Ggamma subunit isoforms, generally with Gbeta/Ggamma stoichiometries between 0.2:1 and 0.5:1.
172 RP2 did not appear to interact with the Gbeta:Ggamma heterodimer, in contrast Ggamma1 competed w
174 fungus Cryptococcus neoformans, noncanonical Gbeta Gib2 promotes cAMP signaling in cells lacking norm
176 nce complementation studies suggest that the Gbeta-GPSM3 complex is formed at, and transits through,
177 etagamma dimer, including association of the Gbeta-GPSM3 complex with phosducin-like protein PhLP and
179 B1/amino-terminal yellow fluorescent protein-Gbeta heterodimer were localized in the plasma membrane,
187 direct contact interactions at the Galphai1-Gbeta interface; remarkably, the presence of R1 at the s
188 sphorylation permits the release of a PhLP x Gbeta intermediate from CCT, allowing Ggamma to associat
190 he naive endothelium Gbeta1, the predominant Gbeta isoform is sequestered by receptor for activated C
199 wo-hybrid screen, we have identified a novel Gbeta-like/RACK1 protein homolog, Gib2, from the human p
200 -cystamine) modification of a single site on Gbeta, likely GbetaCys204, and inhibits Gbetagamma more
203 Gpa2 forms a protein complex with the kelch Gbeta mimic subunits Gpb1/2, and previous studies demons
204 ites what, if any, additional regions of the Gbeta molecular surface comprise interaction interfaces
206 to control the width of the appendage while Gbeta mutant leading roof cells fail to direct the elong
209 The different Tm sensitivities of Galpha and Gbeta mutants, the ER localization of Gbeta, and the dif
213 to complement well-established phenotypes of Gbeta-null mutants revealed AGB1 residues critical for s
215 s, the phenotypes of plants lacking the sole Gbeta or all Ggamma genes are similar, as expected.
216 coexpressed Gbeta, whereas excess of either Gbeta or Ggamma imparted suboptimal activation, possibly
219 rphine treatment; it negated the increase in Gbeta phosphorylation and PKCgamma translocation while r
220 ne treatment of these cells increased AC and Gbeta phosphorylation, membrane protein kinase Cgamma (P
222 ssembly in which PhLP stabilizes the nascent Gbeta polypeptide until Ggamma can associate, resulting
223 sults reveal a non-canonical function of the Gbeta protein as a ubiquitin ligase component and a mech
224 he late peak is normal in plants lacking the Gbeta protein but missing in plants lacking the Galpha p
228 together, these observations imply that the Gbeta protein, which forms a stable heterodimer with the
231 larization of the mating-specific Galpha and Gbeta proteins and that the changes in G protein localiz
232 expressing pPLAIIIdelta, suggesting that the Gbeta proteins are negative regulators of pPLAIIIdelta.
234 d the differential stabilities of Galpha and Gbeta proteins during the UPR suggest that the Gbetagamm
235 rogated expression of most of the Galpha and Gbeta proteins expressed in these cells, singly and some
236 demonstrate that recurrent mutations in the Gbeta proteins GNB1 and GNB2 confer cytokine-independent
237 However, the presence of single Galpha and Gbeta proteins in both these species has significantly u
238 a), an oil seed crop, we uncovered a role of Gbeta proteins in controlling anisotropic cell expansion
239 s employed to silence the natively expressed Gbeta proteins in rat SG tissue and to examine the coupl
241 entially caused by the direct interaction of Gbeta proteins with a specific patatin-like phospholipas
246 comprise interaction interfaces essential to Gbeta's role as a nexus in numerous signaling cascades.
247 We provide evidence that GPSM3 increases Gbeta stability until formation of the Gbetagamma dimer,
248 at one of the three XLG genes, XLG3, and the Gbeta subunit (AGB1) of the Arabidopsis G-protein hetero
249 idopsis thaliana) Galpha subunit (GPA1), the Gbeta subunit (AGB1), and the candidate G-protein-couple
250 ctions as a novel scaffold that binds to the Gbeta subunit as well as to all three tiers of the MAPK
252 (GGL) domain, which is permanently bound to Gbeta subunit Gbeta(5), and the RGS domain responsible f
253 amily of RGS proteins bound to the divergent Gbeta subunit Gbeta5 is a crucial regulator of G protein
256 ls the receptor C-terminal tail bound to the Gbeta subunit of the G protein, providing a structural f
258 phenotype is independently modulated by the Gbeta subunit of the heterotrimeric G-protein complex.
260 subunits functioning in fungi, only a single Gbeta subunit per species has been identified, suggestin
261 is mediated by Gbetagamma, but the specific Gbeta subunit that modulates the channels is not known.
262 ort that the sole Arabidopsis heterotrimeric Gbeta subunit, AGB1, is required for four guard cell Ca(
263 complex is formed between PhLP, the nascent Gbeta subunit, and CCT that does not include Ggamma.
264 ependent posttranslational modification of a Gbeta subunit, establish Ste4 as a new substrate of the
265 and form obligatory dimers with the atypical Gbeta subunit, Gbeta5 They also interact with other prot
266 findings reveal the existence of an unusual Gbeta subunit, one having multiple functions within the
270 mutant lacking the heterotrimeric G protein Gbeta-subunit exhibited a remarkably higher [Ca(2+)](cyt
272 f crystal structures of complexes containing Gbeta subunits and complementary biochemical data highli
273 aperonin CCT/TRiC complex binds to and folds Gbeta subunits and that CCT/TRiC mediates Gbetagamma dim
275 tematically silencing each of the Galpha and Gbeta subunits by using small interfering RNA while quan
276 ime-lapse microscopy to elucidate Galpha and Gbeta subunits contributing to complement C5a receptor-m
280 we report that GPSM3 also interacts with the Gbeta subunits Gbeta1 to Gbeta4, independent of Ggamma o
282 ble the binding of Galpha subunits to either Gbeta subunits or effectors, but it instead represents a
283 determined by the combination of Gialpha and Gbeta subunits rather than by the identity of an individ
284 correlated with the ability of the different Gbeta subunits to efficiently form dimers with Ggamma.
285 contrast, in vitro translated, (35)S-labeled Gbeta subunits traveled at a high apparent molecular mas
290 determining the concentrations of Galpha and Gbeta subunits; 2) examining receptor-dependent activiti
297 and was enhanced by low doses of coexpressed Gbeta, whereas excess of either Gbeta or Ggamma imparted