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1 known as regulators of G protein signaling (RGS proteins).
2 t reversible small-molecule inhibitors of an RGS protein.
3 ied the first small-molecule inhibitor of an RGS protein.
4 Pases in the intracellular trafficking of an RGS protein.
5 one Galpha, one Gbeta, three Ggamma, and one RGS protein.
6 ctivity, to mimic in cis the GAP function of RGS proteins.
7 ise from the consensus GoLoco motif found in RGS proteins.
8 face between Gbeta5 and the N terminus of R7 RGS proteins.
9 d pathway under strong inhibitory control by RGS proteins.
10 the extent of inhibition by the R4 family of RGS proteins.
11 subfamilies consisting of over 20 different RGS proteins.
12 f Galpha12, a behavior consistent with other RGS proteins.
13 ates RGS18 and RGS14 without modifying other RGS proteins.
14 may generally extend to other receptors and RGS proteins.
15 rotein cycle is regulated by the activity of RGS proteins.
16 urface expression and through recruitment of RGS proteins.
17 the Galpha subunit, a reaction catalyzed by RGS proteins.
18 Rs (MOR and D2R) on the G protein bias of R7 RGS proteins.
19 g G protein and GPCR selectivity of striatal RGS proteins.
20 ervous system, is mediated exclusively by R7 RGS proteins.
21 maintaining proteolytic stability of the R7 RGS proteins.
22 s, and the REGULATOR OF G-PROTEIN SIGNALING (RGS) protein.
23 ivity of "regulator of G-protein signaling" (RGS) proteins.
24 rolled by regulator of G protein signalling (RGS) proteins.
25 led by the regulator of G protein signaling (RGS) proteins.
26 led by the regulator of G-protein signaling (RGS) proteins.
27 ction with regulator of G-protein signaling (RGS) proteins.
28 r of the "regulator of G protein signaling" (RGS) proteins.
29 ression of regulator of G protein signaling (RGS) proteins.
30 amily of "regulator of G protein signaling" (RGS) proteins.
31 eract with regulator of G protein signaling (RGS) proteins.
36 including nucleotide binding, intrinsic and RGS protein-accelerated GTP hydrolysis, and interactions
39 enuated by regulator of G protein signaling (RGS) proteins acting as GTPase-activating proteins for G
41 Galphaq, Galphaq-G188S, that is resistant to RGS protein action were sensitized to the development of
43 s there are concomitant, independent LSEs of RGS proteins along with an extraordinary diversification
45 rotein is readily inactivated by its cognate RGS protein and forms a stable, GDP-bound, heterotrimeri
46 protein-coupled receptors, Galpha subunits, RGS proteins and downstream effectors in mammalian syste
49 endrites by varying the concentration of key RGS proteins and measuring the impact on transmission of
51 at the spatiotemporal-specific expression of RGS proteins and their target components, as well as the
52 th Loco, a regulator of G-protein signaling (RGS) protein and a known effector of glia specification.
53 lso binds regulators of G protein signaling (RGS) proteins and the third intracellular loop (3iL) of
54 o still bind the N-terminal DEP domain of R7 RGS proteins, and mutant Gbeta5-R7 RGS complexes initial
55 nteract with all members of the R7 family of RGS proteins, and palmitoylation of R7BP can target R7 R
57 protein inactivation, which is modulated by RGS proteins, and the rate of G protein activation, whic
58 including Regulator of G protein Signaling (RGS) proteins, and has been implicated in membrane targe
59 ypothesize Regulator of G-Protein Signaling (RGS) proteins, and specifically RGS5, are endogenous rep
63 regulator of Hh-mediated signaling and that RGS proteins are potential targets for novel therapeutic
65 influence of RGS proteins on these pathways, RGS proteins are regulators of cardiovascular physiology
78 Regulators of G protein signaling (RGSs, or RGS proteins) are responsible for the subsecond turn off
80 indings reveal a hitherto overlooked role of RGS proteins as noise suppressors and demonstrate an abi
81 nd also reveal a potential novel function of RGS proteins as positive regulators of opioid spinal ant
82 entify RGS6, a member of the R7 subfamily of RGS proteins, as a key regulator of GABA(B)R signaling i
83 f these small-molecule inhibitors against 12 RGS proteins, as well as against the cysteine-null mutan
86 cytes with a Galphai2 mutation that disables RGS protein binding accumulated in the perivascular chan
91 uss a rationale for therapeutic targeting of RGS proteins by regulation of expression or allosteric m
97 spectroscopic probe to measure intrinsic and RGS protein-catalyzed nucleotide hydrolysis by Galphao.
102 annel assembly with allosterically regulated RGS protein complexes, which provide a target for modula
104 family of regulators of G protein signaling (RGS) proteins, comprising RGS6, RGS7, RGS9, and RGS11, r
105 For example, members of the R7 family of RGS proteins contain a DEP, GGL, and novel DHEX domain a
107 which is responsible for GAP activity, most RGS proteins contain other distinct structural motifs.
109 attendant regulators of G-protein signaling (RGS) proteins control both intercellular signaling and a
110 y a role in pathophysiological processes and RGS proteins could represent novel cardiovascular therap
117 at loss of RSBP-1 phenocopies loss of the R7 RGS protein EAT-16, but does not disrupt function of the
121 CCG-4986, lack of inhibition indicates that RGS proteins exhibit fundamental differences in their re
123 se and heart rate regulation, and changes in RGS protein expression and/or function are believed to p
126 etics, the regulator of G-protein signaling (RGS) protein family modulates the timing of GIRK activit
127 of the R7 regulators of G protein signaling (RGS) protein family of neuronal RGS, is a critical regul
128 ber of the Regulator of G protein Signaling (RGS) protein family, as a nuclear factor that suppresses
129 ber of the regulator of G-protein signaling (RGS) protein family, possesses an N-terminal RGS domain,
131 r Galpha(i)G203A), as well as GRK2NT-GFP (an RGS protein for G(q/11)) but neither p115RhoGEFRGS-GFP (
132 ich has the largest complement of Galpha and RGS proteins for any eukaryote, provides new insights in
133 of the regulators of G-protein signaling (R7 RGS) proteins form multi-subunit complexes that play cru
134 Most studies searching for modulators of RGS protein function have been focused on inhibiting the
137 Recent findings have established that R7 RGS proteins function as macromolecular complexes with t
138 t is unclear which of the more than 20 known RGS proteins function to negatively regulate and thereby
140 ai2 (G184S/G184S) mutation that disables all RGS protein/Galphai2 interactions exhibit an unexpectedl
146 , while G-proteins are widespread in plants, RGS proteins have been reported to be missing from the e
151 ctions between activated Galpha subunits and RGS proteins have yielded a substantial number of inhibi
152 Endogenous regulator of G-protein signaling (RGS) proteins have been implicated as key inhibitors of
153 ears ago, regulators of G protein-signaling (RGS) proteins have received considerable attention as po
154 thway-selective manner, and (3) suggest that RGS proteins help to prevent unwarranted platelet activa
157 ering promotes downregulation by placing the RGS protein in proximity to its substrate (receptor-acti
158 o downregulate signaling, loss of a specific RGS protein in sensory neurons can lead to defective res
159 These findings highlight the central role of RGS proteins in [Ca(2+)](i) oscillations and reveal a pr
161 ese findings establish an essential role for RGS proteins in B cell chemoattractant signaling and for
166 cate that the level and functional status of RGS proteins in DCs significantly impact their response
168 evidence has revealed key roles for specific RGS proteins in multiple signaling pathways at neuronal
170 ervations (1) demonstrate an active role for RGS proteins in regulating platelet responsiveness, (2)
171 enes (rgsA, rgsB and rgsC) encoding putative RGS proteins in the genome of Aspergillus nidulans.
173 he role of regulator of G protein signaling (RGS) proteins in the modulation of these pathways in hum
179 or screening for modulators of the G protein-RGS protein interaction by assaying the amount of produc
183 identified that the binding site for R7BP in RGS proteins is formed by pairing of the DEP (Disheveled
185 ly of the regulators of G protein signaling (RGS) proteins is represented by four members broadly exp
186 , the first biochemical function ascribed to RGS proteins, is sufficient to explain the activation ki
190 After injury, the complex gradually releases RGS proteins, limiting platelet activation and providing
191 These data provide the first evidence that RGS proteins may be important modulators of cancer risk
192 ent evidence has raised the possibility that RGS proteins may interact directly with G-protein-couple
193 uggest that drug discovery efforts targeting RGS proteins may represent a novel mechanism to manipula
196 on that Galpha(i) subunits remain GTP bound, RGS proteins modulate chemoattractant receptor signaling
200 In the striatum, members of the R7 family of RGS proteins modulate signaling via D2 dopamine and mu-o
203 fects caused by deletion of flbA encoding an RGS protein negatively controlling FadA-mediated vegetat
208 aling pathways and the profound influence of RGS proteins on these pathways, RGS proteins are regulat
209 truncated regulator of G protein signaling (RGS) protein or a Gbetagamma-sequestering domain to a se
210 t for the adaptive coevolution of the Galpha:RGS protein pair based on single amino acid substitution
214 al mushrooms show LSEs of Galphas but not of RGS proteins pointing to the probable differentiation of
217 20-residue RGS homology domain or "RGS box." RGS proteins regulate signaling via G protein-coupled re
221 in vitro, but the physiological function of RGS proteins remains poorly defined in part because of f
222 neficial effects of serotonin, inhibition of RGS proteins represents a therapeutic approach for the t
223 encodes a regulator of G protein signaling (RGS) protein, restores chemosensation in Ce-grk-2 mutant
228 highlight the current knowledge of specific RGS proteins (RGS2, RGS4, RGS7, RGS9-2, and RGS14) that
230 ecrease in RGS2 (but not other major cardiac RGS proteins (RGS3-RGS5)) that occurs prior to hypertrop
233 R7 family regulators of G protein signaling (RGS) proteins (RGS6, RGS7, RGS9, and RGS11) instead of G
234 ntains two Regulator of G-protein Signaling (RGS) proteins RGS7 and RGS11 that directly act on Go and
236 ruits the regulators of G-protein signaling (RGS) proteins, RGS7 and RGS11, to the dendritic tips of
237 conditions two equally abundant striatal R7 RGS proteins, RGS9-2 and RGS7, are unequally coupled to
238 loops of GPCRs selectively recruit specific RGS protein(s) via their N termini to regulate the linke
239 live cells, members of the B/R4 subfamily of RGS proteins selectively modulate G protein signaling de
240 ence that regulators of G-protein signaling (RGS) proteins serve this role in platelets, using mice w
247 the yeast regulator of G protein signaling (RGS) protein Sst2 and demonstrate that the DEP domains i
249 of the R7 regulator of G-protein signaling (RGS) protein subfamily are versatile regulators of G-pro
253 RK2 and p63RhoGEF respond similarly to these RGS proteins supports the hypothesis that GRK2 is a bona
254 NRB bind all members of the R4 subfamily of RGS proteins tested (RGS1, RGS2, RGS4, RGS16) and GAIP.
256 , a palmitoylated allosteric modulator of R7 RGS proteins that accelerate deactivation of Gi/o class
258 understanding of the molecular diversity of RGS proteins that control MOR signaling, their circuit s
260 GS7 and RGS9-2 belong to the R7 subfamily of RGS proteins that form macromolecular complexes with R7-
261 as well as regulator of G protein signaling (RGS) proteins that contain a Ggamma-like subdomain.
262 rolled by regulators of G protein signaling (RGS) proteins that shape the duration and extent of the
265 EP domain in mediating the interaction of an RGS protein to the C-terminal tail of a GPCR, thus placi
266 yses and homology modeling of the Galpha and RGS proteins to address their expansion and its potentia
267 ing that RGS2 arose from the R4-subfamily of RGS proteins to have specialized activity as a potent an
269 we examine whether GPCRs selectively recruit RGS proteins to modulate linked G protein signaling.
270 ings point to a critical role for endogenous RGS proteins to suppress the antidepressant-like effects
271 s to evaluate the contribution of endogenous RGS proteins to the antinociceptive effects of morphine
273 ns, and palmitoylation of R7BP can target R7 RGS proteins to the plasma membrane in cultured cells.
275 ain GTP bound, and the loss of an individual RGS protein typically enhances chemokine receptor signal
276 n of gene transcription, can be regulated by RGS proteins via both allosteric and GAP mechanisms.
279 ion-based adaptive coevolution of the Galpha:RGS proteins was proposed to enable the loss of RGS in m
280 of these regulators of G protein signaling (RGS) proteins was perturbed either by hypoxia or in cell
283 (GAPs), both phospholipase C (PLC)-betas and RGS proteins, when assayed in solution under single turn
284 heterotrimeric G-protein-coupled receptors, RGS proteins, which act as GTPase-activating proteins fo
285 ne nucleotide exchange factors (GEFs) and by RGS proteins, which act as guanosine triphosphatase (GTP
286 ) is a member of a family of proteins called RGS proteins, which function as GTPase-activating protei
287 ve NFR1 receptors phosphorylate and activate RGS proteins, which help maintain the Galpha proteins in
288 ns and the regulator of G-protein signaling (RGS) proteins, which accelerate the inherent GTPase acti
289 ) bound by regulator of G-protein signaling (RGS) proteins, which function as GTPase-activating prote
291 ped by the regulator of G protein signaling (RGS) proteins, which promote G protein deactivation.
292 Rgs6(-/-) mice is attributable to another R7 RGS protein whose influence on M2R-IKACh signaling is ma
294 The soybean genome encodes two chimeric RGS proteins with an N-terminal seven transmembrane doma
295 g 9-1 (RGS9-1) and RGS9-2 are highly related RGS proteins with distinctive C termini arising from alt
297 se findings argue that the association of R7 RGS proteins with the membrane environment provides a ma
298 mplexes of regulator of G-protein signaling (RGS) proteins with G-protein beta5 (Gbeta5) subunits are
299 regulation, and functional role of canonical RGS proteins, with a special focus on the healthy heart
300 At neuronal synapses, GPCRs, G proteins, and RGS proteins work in coordination to regulate key aspect
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