ライフサイエンスコーパス: GDI

1 GDI vehicle PN EFs were found to increase by up to 240%

2 guanine nucleotide dissociation inhibitor-1 (GDI).

3 The fleet included 15 GDI vehicles, including 8 GDIs certified to the most-str

4 , we compare emissions of a flex-fuel Euro-5 GDI vehicle operated with gasoline (E0) and two ethanol/

5 fleet included 15 GDI vehicles, including 8 GDIs certified to the most-stringent emissions standard,

6 strate that eIF2B has a second activity as a GDI displacement factor (GDF) that can recruit eIF2 from

7 ing cells; Rac isoforms partially exist as a GDI-free pool at the membrane of resting cells, whereas

8 This study investigates the presence of a GDI for transducin in photoreceptor cells.

9 Expression of a GDI-1 mutant form (C-GDI) containing the C terminus (aa

10 b from the cytosol, possibly by regulating a GDI-Rab receptor.

11 ich led us to propose that there might be a 'GDI-displacement factor' to catalyse dissociation of Rab

12 promotes GTP hydrolysis by Ypt7p, and added GDI captures Ypt7p in its GDP-bound state during nucleot

13 ha and Rho-GDIgamma, thereby eliminating all GDI activity in the brain, would produce an observable p

14 re emitted mostly during cold-start from all GDI and PFI vehicles.

15 motifs strongly potentiate their binding and GDI activity toward G alpha i1 even though the amino aci

16 GDP/GTP status is regulated by eIF5 (GAP and GDI functions) and eIF2B (GEF and GDF activities), while

17 onella pneumophila could act as both GEF and GDI-displacement factor (GDF) for Rab1.

18 ked complexes contain Rab escort protein and GDI-1.

19 78D)CLLL, which remains deficient in REP and GDI association is, nonetheless, delivered to the Golgi

20 of Rab1B (i.e. Y78D) that abolishes REP and GDI interaction without disrupting nucleotide binding or

21 Although REP and GDI share common Rab-binding properties, GDI cannot assi

22 e able to partially function as both REP and GDI.

23 organic compounds emissions between PFI and GDIs, including benzene, toluene, ethylbenzene, and xyle

24 s-phase pollutant emissions between PFIs and GDIs.

25 ose that the conserved Yip proteins serve as GDI-displacement factors for the targeting of Rab GTPase

26 cal to the ability of GPR-proteins to act as GDIs.

27 Selective beta8 stimulation enhanced beta8-GDI interaction as well as Rac1 (but not RhoA) activatio

28 ediated cycling and help distinguish between GDI-dependent and -independent mechanisms, including ves

29 ree investigation of the interaction between GDI and Rab GTPases in a membrane environment.

30 The late endosomal, prenyl Rab9 binds GDI with very high affinity, which led us to propose tha

31 lization and to counteract the extraction by GDI.

32 ction of Rab GTPases from model membranes by GDI.

33 ation of the GTPase cycle of Rab proteins by GDI proteins.

34 Expression of a GDI-1 mutant form (C-GDI) containing the C terminus (aa 69 to 204) also preve

35 cial users from lab.rockefeller.edu/casanova/GDI.

36 cytosis via the interaction between the Cav1 GDI region and Cdc42.

37 data suggest that Cav-1 functions as a Cdc42 GDI in beta-cells, maintaining Cdc42 in an inactive stat

38 suggested a novel role for Cav-1 as a Cdc42 GDI in beta-cells.

39 SULEV certified GDIs have a factor of 2 lower PM mass emissions than GDI

40 stability and sensitivity of the GC/CNT-CHIT-GDI-GDH biosensor allowed for the interference-free dete

41 sitivity (42 mA M(-1) cm(-2)) of the Pt/CHIT-GDI-AY9-GOx biosensor toward glucose.

42 e of platinum electrodes to form robust CHIT-GDI-AY9-GOx films for glucose biosensing.

43 ucose oxidase (GOx), was mixed with the CHIT-GDI-AY9 solution and cast on the surface of platinum ele

44 We compared GDI with the leading gene-level approaches, genic intole

45 ed its affinity for G alpha i1 and conferred GDI activity similar to that of AGS3-C itself.

46 Mutation of the conserved GDI motif creates a dominant-negative form of Sestrin th

47 chia coli (E. coli) crude extract containing GDI, suggest that this analogue will be an effective and

48 D4-GDI could prove to be a potential new target for therape

49 D4-GDI is a Rho GDP dissociation inhibitor that is widely e

50 anchorage-independent culture conditions, D4-GDI-depleted cells undergo rapid apoptosis (anoikis), wh

51 The Rho GDP dissociation inhibitor D4-GDI is overexpressed in some human breast cancer cell li

52 The cells lacking D4-GDI grown on Matrigel revert to a normal breast epitheli

53 Here, we show that silencing of D4-GDI by RNA interference abrogates tumor growth and lung

54 Knockdown of D4-GDI expression in MDA-MB-231 cells by RNA interference b

55 Reintroduction of D4-GDI fully restored both beta1-integrin expression and ce

56 Knockdown of D4-GDI in BT549 cells results in a similar effect.

57 activities and the spontaneous anoikis of D4-GDI knockdown cells.

58 Silencing of D4-GDI results in constitutive Rac1 activation and transloc

59 Silencing D4-GDI expression inhibits beta1-integrin expression and ce

60 We also found that D4-GDI associates with Rac1 and Rac3 in breast cancer cells

61 Here, we found that D4-GDI is expressed in a panel of breast cancer cell lines,

62 These results show that D4-GDI modulates breast cancer cell invasive activities.

63 These results suggest that D4-GDI regulates cell function by interacting primarily wit

64 ysis by mechanisms distinct from its defined GDI activity.

65 is the first example of a calcium-dependent GDI for heterotrimeric G proteins.

66 l Yellow 9 (AY9), using glutaric dialdehyde (GDI) as a molecular tether.

67 ing the system with the glutaric dialdehyde (GDI)-modified CHIT.

68 he CNT-CHIT films using glutaric dialdehyde (GDI).

69 , and cross-linked with glutaric dialdehyde (GDI).

70 pecialized proteins are required to displace GDI from Rab GTPases before Rab activation by guanosine

71 Therefore, the effective GDI displacement that is observed is caused by inhibitio

72 lacing PFI vehicles with more fuel efficient GDI vehicles remain uncertain.

73 etics of eIF2 release from the eIF2*GDP/eIF5 GDI complex and determine the effect of eIF2B on this re

74 that can recruit eIF2 from the eIF2*GDP/eIF5 GDI complex prior to GEF action.

75 s provide support for the importance of eIF5 GDI activity in vivo and demonstrate that eIF2beta acts

76 ssor mutation in eIF2beta that prevents eIF5 GDI and alters cellular responses to reduced eIF2B activ

77 how that the eIF2beta mutation prevents eIF5 GDI stabilizing nucleotide binding to eIF2, thereby alte

78 distinct from its RGS domain and established GDI activity.

79 RGS14 exerts GDI activity on Galphai1, but not Galphao.

80 eing prerequisites to constitute a bona fide GDI displacement factor.

81 s of Rabs can also modulate the affinity for GDI and thus cause effective displacement of GDI from Ra

82 containing only the residues responsible for GDI activity), with Ric-8A:Galpha(il) and that of Ric-8A

83 complexes or rat brain cytosol as source for GDI.Rab3A.

84 /3 glucosamine units of chitosan and 25 free GDI tethers/1 molecule of GOx.

85 In this study, BC emissions from GDI and PFI vehicles were compiled and BC emissions scen

86 t for a small set, how the PM emissions from GDI vehicles change over their lifetime.

87 omplexes and to enable transfer of Rabs from GDI onto membranes.

88 infection to effectively displace Rabs from GDI.

89 Rab1 released from GDI was inserted into liposomal membranes and was used a

90 easured 14.5% decrease in CO2 emissions from GDIs was much greater than the potential climate forcing

91 notoxic emissions on this specific flex-fuel GDI vehicle; however, other GDI vehicle types should be

92 ctron conductive films of such CHIT-NAD+-GDH-GDI-CHIT macrocomplexes (MC) were prepared on glassy car

93 Because the Rab:GDP:GDI complex is of high affinity, the question arises of

94 ifications may compensate for altered GTPase-GDI balance in disease scenarios.

95 rsinia depends strongly upon mimicry of host GDI proteins by YpkA.

96 of high affinity, the question arises of how GDI can be displaced efficiently from Rab protein in ord

97 The structural data demonstrate how GDIs serve as negative regulators of small GTP-binding p

98 However, GDIs had, on average, a factor of 2 higher particulate m

99 terminal GoLoco region exhibiting G alpha(i) GDI activity.

100 /=18 mmHg in whom glaucoma drainage implant (GDI) surgery was planned were randomized to implantation

101 th ratios for patients experiencing improved GDI QoL scores was 1.31 versus 1.56 for those without Qo

102 ded to understand BC formation mechanisms in GDI engines to ensure that the climate impacts of this e

103 Corticosterone also triggers an increased GDI phosphorylation at Ser-213 by the serum- and glucoco

104 ing a potential climate impact for increased GDI vehicle production.

105 this end, we derived the gene damage index (GDI): a genome-wide, gene-level metric of the mutational

106 sessment Scale (MSAS)-Global Distress Index (GDI) and Functional Assessment of Cancer Therapy-Breast

107 letion of PKC prevented the thrombin-induced GDI phosphorylation and Rho activation, thereby indicati

108 rine chloride abrogated the thrombin-induced GDI phosphorylation and Rho activation.

109 Inhibiting GDI-1 phosphorylation at S96 is a potential therapeutic

110 Finally, eIF5 GDP dissociation inhibition (GDI) activity can antagonize eIF2 reactivation by compet

111 e guanine nucleotide dissociation inhibitor (GDI) activity of a GoLoco motif near their carboxy-termi

112 t guanine nucleotide dissociation inhibitor (GDI) activity, inhibiting the rate of exchange of GDP fo

113 t guanine nucleotide dissociation inhibitor (GDI) by contacting key residues in the regulatory switch

114 cytoplasm by the GDP dissociation inhibitor (GDI) chaperone.

115 on1-Ccz1), a Rab-GDP dissociation inhibitor (GDI) complex (prenylated Ypt7-GDI), and a Rab effector c

116 P guanine nucleotide dissociation inhibitor (GDI) complexes with the GDP-bound form of Rho and inhibi

117 at acts as a guanine dissociation inhibitor (GDI) for G(i/o)(alpha) subunits.

118 t guanine nucleotide dissociation inhibitor (GDI) for Galpha(i1).

119 a guanine nucleotide dissociation inhibitor (GDI) for Galphas using the same motif that allows it to

120 a guanine nucleotide dissociation inhibitor (GDI) for Gialpha.

121 rotein (GAP) and GDP dissociation inhibitor (GDI) functions, and eIF2B is the guanine nucleotide exch

122 eracted with Rho GDP dissociation inhibitor (GDI) in vivo, but Flag-TrkBT1DeltaC did not.

123 egulation by guanine dissociation inhibitor (GDI) proteins like LGN, a mammalian homolog of Drosophil

124 e guanine nucleotide dissociation inhibitor (GDI) Rdi1 recycles Cdc42 through the cytoplasm.

125 The GDP dissociation inhibitor (GDI) solubilizes prenylated Rab GTPases from and shuttle

126 with the protein GDP dissociation inhibitor (GDI) that binds to prenylated inactive (GDP-bound) Rab p

127 a guanine nucleotide dissociation inhibitor (GDI) that contains four G protein regulatory (GPR) or Go

128 a guanine nucleotide dissociation inhibitor (GDI) through its GoLoco motif.

129 a guanine nucleotide dissociation inhibitor (GDI), binds and stabilizes Galpha subunits in their GDP-

130 behaves as a guanine dissociation inhibitor (GDI), inhibiting the rate of exchange of GDP for GTP by

131 a guanine nucleotide dissociation inhibitor (GDI), mediates a fast recycling pathway, while actin pat

132 bs interact with GDP dissociation inhibitor (GDI), resulting in the dissociation of a Rab.GDI complex

133 a guanine nucleotide dissociation inhibitor (GDI), which inhibits Cdc42 activation.

134 Guanosine nucleotide dissociation inhibitor (GDI), which regulates the cycle of Rab proteins between

135 e guanine-nucleotide dissociation inhibitor (GDI)-like domain of YopO cooperate for maximal anti-phag

136 r guanine nucleotide dissociation inhibitor (GDI)-like domains, and demonstrate that the presence of

137 h Guanine nucleotide Dissociation Inhibitor (GDI)-mediated membrane extraction and vesicle traffickin

138 n that acts as a GDP dissociation inhibitor (GDI).

139 ol by binding to GDP-dissociation inhibitor (GDI).

140 a guanine nucleotide dissociation inhibitor (GDI).

141 o-guanine nucleotide dissociation inhibitor (GDI)alpha.

142 d guanine-nucleotide-dissociation-inhibitor (GDI).

143 ase cycle-Gdi1p (GDP-dissociation inhibitor [GDI]) or Gyp1p/Gyp7p (GTPase-activating protein)-this ki

144 both sensitive to the Rab-GTPase inhibitor, GDI, and to mutations in the vacuolar tether complex, HO

145 ncoding Rho guanine-dissociation inhibitors (GDI), known regulators of RhoGTPases/cytoskeleton.

146 Guanine nucleotide dissociation inhibitors (GDIs) bind and sequester GTPases in the cytosol, restric

147 guanine nucleotide dissociation inhibitors (GDIs) for G(alpha) subunits from the Gi family.

148 guanine nucleotide dissociation inhibitors (GDIs) for RAGA/B, and interact with GATOR2 with unknown

149 guanine nucleotide dissociation inhibitors (GDIs) for RagA/B.

150 uanidine nucleotide dissociation inhibitors (GDIs) of the Rho GTPases.

151 guanine nucleotide dissociation inhibitors (GDIs), form a complex with the GDP-bound form of the Rho

152 guanine nucleotide dissociation inhibitors (GDIs), GTPase-activating proteins (GAPs), or the chapero

153 e diphosphate (GDP) dissociation inhibitors (GDIs), such as activators of G protein signaling (AGS)-1

154 guanine nucleotide dissociation inhibitors (GDIs), which suggested a novel role for Cav-1 as a Cdc42

155 guanine nucleotide dissociation inhibitors (GDIs).

156 guanine-nucleotide dissociation inhibitors (GDIs).

157 s including Rab GDP dissociation inhibitors (GDIs).

158 ) engine exhaust, gasoline direct injection (GDI) engine exhaust has higher emissions of black carbon

159 Gasoline direct injection (GDI) is a new engine technology intended to improve fuel

160 enger vehicle and gasoline direct injection (GDI) vehicle were tested on a constant velocity driving

161 s from light-duty gasoline direct injection (GDI) vehicles (2013 Ford Focus) in an urban near-road en

162 from two pairs of gasoline direct injection (GDI) vehicles and port fuel injection (PFI) vehicles ove

163 oline and also in gasoline direct injection (GDI) vehicles, which are quickly replacing traditional p

164 vehicle, and six gasoline direct injection (GDI) vehicles.

165 les equipped with gasoline direct-injection (GDI) engines.

166 from a light-duty gasoline-direct-injection (GDI) vehicle, over the FTP-75 and US06 transient drive c

167 r (GPR) domains that are responsible for its GDI function.

168 ndothelial cells transduced with full-length GDI-1.

169 tor 2 (RhoGDI2; also known as ARHGDIB and Ly-GDI) is associated with metastatic disease in patients w

170 The selected peptides also maintain GDI activity for G(i)(alpha)(1), inhibiting both the exc

171 ed between the Baerveldt 250 mm2 and 350 mm2 GDIs, respectively.

172 icant improvement in QoL as assessed by MSAS-GDI (P =.004) and FACT-B (P =.028).

173 Phosphodefective mutant GDI-1 also suppressed myosin light chain phosphorylation

174 protein AnkX, interferes with the ability of GDI to extract Rab35 from the membrane.

175 stitution rescued the inhibitory activity of GDI-1 toward RhoA but did not alter the thrombin-induced

176 ased engine power are reported advantages of GDI vehicles.

177 reveals that the lower apparent affinity of GDI for RacGTP compared to RacGDP can be fully explained

178 us of GDI-1 at Ser96 reduced the affinity of GDI-1 for RhoA and thereby enabled RhoA activation.

179 the GTPase and hence can inhibit binding of GDI to Rab:GDP complexes.

180 This analysis can reveal details of GDI-mediated cycling and help distinguish between GDI-de

181 GDI and thus cause effective displacement of GDI from Rab:GDI complexes.

182 f GDI at Ser-213, increases the formation of GDI-Rab4 complex, facilitating the functional cycle of R

183 developed to evaluate the climate impact of GDI vehicles using global warming potential (GWP) and gl

184 The kinetics of GDI activity, however, are different for the selected pe

185 We also show that the mechanism of GDI activity of sNUCB1 is unique and does not arise from

186 13-acetate induced rapid phosphorylation of GDI and the activation of Rho-A in human umbilical venul

187 t corticosterone, via SGK phosphorylation of GDI at Ser-213, increases the formation of GDI-Rab4 comp

188 KC-epsilon induced marked phosphorylation of GDI in vitro.

189 e-associated Rab may regulate recruitment of GDI-Rab from the cytosol, possibly by regulating a GDI-R

190 of Rab3A results in the immediate release of GDI from the membrane.

191 of the phosphorylation of the C terminus of GDI-1 at S96 in selectively activating RhoA.

192 ediated phosphorylation of the C terminus of GDI-1 at Ser96 reduced the affinity of GDI-1 for RhoA an

193 ant mechanism by which the Sestrin family of GDIs regulates the nutrient-sensing Rag GTPases to contr

194 ty of GPR-proteins is different from that of GDIs for monomeric GTPases and from the GDI-like activit

195 costerone are altered by mutating Ser-213 on GDI.

196 differences in the effects of cold-start on GDIs and PFIs.

197 finities between GTPases and membrane and/or GDI on the amount of membrane bound GTPase.

198 f nucleotide dissociation inhibitors (NDI or GDI) for regulatory GTPases.

199 ecific flex-fuel GDI vehicle; however, other GDI vehicle types should be analyzed.

200 To the best of our knowledge, no other GDI has been described for heterotrimeric G proteins.

201 n regulatory(GPR) sequence, a 28-mer peptide GDI derived from the GoLoco (Galpha(i/0)-Loco interactio

202 this is the first example for a prokaryotic GDI, targeting a bacterial G protein-coupled membrane pr

203 and GDI share common Rab-binding properties, GDI cannot assist in Rab prenylation and REP cannot retr

204 We show that GEFs, but none of the proposed GDI displacement factors, are essential for the correct

205 a) subunits and the mechanism of GPR-protein GDI activity.

206 These results, obtained using purified GDI as well as Escherichia coli (E. coli) crude extract

207 ment factor' to catalyse dissociation of Rab-GDI complexes and to enable transfer of Rabs from GDI on

208 Prenyl Rab-GDI complexes contain all of the information necessary t

209 Yip1p function requires Rab-GDI and Rab proteins, and several mutations that abrogat

210 GDI), resulting in the dissociation of a Rab.GDI complex, which in turn serves as a precursor for the

211 cause effective displacement of GDI from Rab:GDI complexes.

212 occur after spontaneous dissociation of Rab:GDI complexes within their natural equilibrium.

213 s caused by inhibition of reformation of Rab:GDI complexes.

214 ate that PKC-alpha is critical in regulating GDI phosphorylation, Rho activation, and in signaling Rh

215 Rendering GDI-1 phosphodefective with a Ser96 --> Ala substitution

216 nal and evolutionary organization of the REP/GDI superfamily.

217 The striking selectivity observed for RGS14 GDI activity in vitro points to Galphai1 and Galphai3 as

218 Galphai2 be rendered sensitive to RGS14 GDI activity by replacement of residues within the alpha

219 her all three isoforms were subject to RGS14 GDI activity.

220 The overexpression of bovine Rho GDI alpha disrupted membrane translocation of Rho, Rac a

221 e regulation of receptor coactivators by Rho GDI.

222 , which binds CBP/p300, is necessary for Rho GDI to modulate GRIP1 activity.

223 Indeed, Rho GDI cooperates with GRIP1 to increase ER ligand-independ

224 d bovine Rho GDP dissociation inhibitor (Rho GDI alpha), which serves as a negative regulator of Rho,

225 anine nucleotide dissociation inhibitor (Rho GDI), as a positive regulator of ER transactivation.

226 ivation, thus phenocopying the effect of Rho GDI expression on ER transactivation.

227 hibitor alpha (RhoGDIalpha), a member of Rho GDI family that is involved in cytoskeletal reorganizati

228 CBP activity, we find that the effect of Rho GDI on ER transactivation is CBP/p300-dependent.

229 We now demonstrate that Rho GDI-dependent increase in ER transactivation is dependen

230 At E14.5, the size of the Rho GDI alpha Tg lenses was larger compared to wild type (WT

231 the ability of CBP/p300 to transduce the Rho GDI signal to ER occurs through both GRIP1-dependent and

232 ed the expression of the gene encoding a Rho-GDI homolog in the human fungal pathogen Cryptococcus ne

233 isrupts the interaction between RhoA and Rho-GDI (guanine nucleotide dissociation inhibitor) and prom

234 iation inhibitor (Rho-GDI) from an ezrin/Rho-GDI complex.

235 ation of Rho GDP dissociation inhibitor (Rho-GDI) from an ezrin/Rho-GDI complex.

236 ssion of Rho GDP dissociation inhibitor (Rho-GDI), inhibited the strain-induced activation of NF-kapp

237 Rho-GDP dissociation inhibitors (Rho-GDI) are repressors of Rho-type monomeric GTPases that c

238 In addition, reduction of Rho-GDI by small interfering RNA in pRb-transfected cells pr

239 The release of Rho-GDI results in increased interaction with Rac1 GTPase an

240 dation resistant mutant IkappaBalpha) or Rho-GDI blocked the strain-induced proliferation of C2C12 ce

241 3 and another known ERM binding protein, Rho-GDI.

242 elies on SPIKE1 Rho-GEF, SUPERCENTIPEDE1 Rho-GDI, and ACTIN7 (ACT7) function and to a lesser extent o

243 ted flat cell formation, suggesting that Rho-GDI plays an important role in contributing to cellular

244 ed mechanism of RhoA activation from the Rho-GDI-1 complex and its role in mediating increased endoth

245 Two Rho-GDI isoforms are expressed in the brain, Rho-GDIgamma an

246 Rho-GDIs are a family of Rho GDP-dissociation inhibitors tha

247 Photolysis experiments with 2 and RhoGDI (GDI), a protein which interacts with prenylated Rho prot

248 f GIV-Galphas complexes, and activates GIV's GDI function.

249 expressing the phospho-mimicking mutant S96D-GDI-1 protein induced RhoA activity and increased endoth

250 ted impact on BC emissions from the selected GDI and PFI vehicles during hot-starts.

251 (GPF) reduced BC emissions from the selected GDI vehicle by 73-88% at various ambient temperatures ov

252 complex that functions as a RhoA-selective, GDI dissociation factor.

253 gnaling mechanism by which TrkBT1 sequesters GDI and activates RhoA signaling.

254 The stock-GDI vehicle emits graphitized fractal-like aggregates ov

255 e-matter emission, the results for the stock-GDI vehicle, that is, the vehicle in its original config

256 t 20% larger than those emitted by the stock-GDI vehicle.

257 e a factor of 2 lower PM mass emissions than GDIs certified as ultralow-emission vehicles (3.0 +/- 1.

258 e, and de novo excess, and demonstrated that GDI performed best for the detection of false positives

259 -based analysis, it was also determined that GDI vehicles are climate beneficial within <1-20 years;

260 uated total reflection experiments show that GDI genuinely accelerates the intrinsic Rab membrane dis

261 The GDI BC emissions spanned 2 orders of magnitude and varie

262 The GDI server, data, and software are freely available to n

263 cell culture experiments, the kinase and the GDI domains of YpkA act synergistically to promote cytos

264 Other than for NOx and CO, the GDI engine had elevated emissions compared to the Toront

265 reas a cell-permeable peptide containing the GDI motif inhibits mTORC1 signaling.

266 cking phosphorylation on Thr494 enhanced the GDI activity of RGS14 toward Galpha(i) nearly 3-fold, wi

267 BC concentrations were higher for the GDI vehicles than the PFI and hybrid vehicles, suggestin

268 10 was found to reduce BC emissions from the GDI vehicle by 15% at standard temperature and by 75% at

269 , the GPF reduced BC mass emissions from the GDI vehicle by 59-80% at various temperatures.

270 ity can coordinate Rab1 recruitment from the GDI-bound pool.

271 t of GDIs for monomeric GTPases and from the GDI-like activity of G(betagamma) subunits.

272 e of myristoylated ciliary proteins from the GDI-like solubilizing factor UNC119a/b.

273 We identified the GDI-1-regulated mechanism of RhoA activation from the Rh

274 Our data suggest that a mechanism of the GDI activity of GPR-proteins is different from that of G

275 st, the amino-terminal regulatory arm of the GDI binds to the switch I and II domains of Cdc42 leadin

276 RhoGDI2 is a member of the GDI family that acts as a metastasis suppressor in a var

277 The size of the GDI may not be associated with surgical outcomes.

278 over the level accomplished by action of the GDI-like domain alone.

279 ssible effects of PKA phosphorylation on the GDI activity of RGS14.

280 s were observed on the PFI vehicles than the GDI vehicles.

281 th prenylated Rho proteins, suggest that the GDI is in direct contact with the isoprenoid moiety.

282 We found that the GDI was correlated with selective evolutionary pressure,

283 ssion of Cav2, or a Cav1 mutant in which the GDI region was altered to the corresponding sequence in

284 uggest that GAP activity cooperates with the GDI to counteract the dissipative effect of a previously

285 The GDIs are made up of two domains: a flexible N-terminal d

286 Thereby, GDI is revealed to actively extract monogeranylgeranylat

287 This GDI activity is isolated to a region of the protein dist

288 ated Rabs also occur in the cytosol bound to GDI (guanine nucleotide dissociation inhibitor), which b

289 sociate complexes of endosomal Rabs bound to GDI, and to deliver them onto membranes.

290 Thus, switching from PFI to GDI vehicles will likely lead to a reduction in net glob

291 ts particle mass and number emissions of two GDI vehicles as a function of mileage up to 150K miles.

292 ve cycle, the BC mass emissions from the two GDI vehicles at 0 degrees F (-18 degrees C) varied from

293 Moreover, 5MP1 is not a GEF but a weak GDI for yeast eIF2.

294 y improvements ranging from 0.14 to 14% with GDI vehicles are required to offset BC-induced warming.

295 -like nanoparticles are also associated with GDI technology with yet unknown health impacts.

296 The cross-linking of such films with GDI further increased their permselectivity as well as t

297 in part regulated by their interactions with GDI proteins.

298 ge the K(D) for the interaction of Rac1 with GDI, and similar to that previously observed for Cdc42,

299 a Y. pseudotuberculosis mutant lacking YpkA GDI activity shows attenuated virulence in a mouse infec

300 ion inhibitor (GDI) complex (prenylated Ypt7-GDI), and a Rab effector complex (HOPS).