ライフサイエンスコーパス: GAP

1 GAP activity toward Rap2 is not altered by phosphorylati

2 GAP exhibited a unique combination of features: dual-exc

3 GAP-43 (+) nerve fiber density increased gradually from

4 GAP-43 is a neuronal protein that regulates actin dynami

5 GAP-43 protein was primarily located in excitatory neuro

6 Together our data suggest that CYK-4 GAP activity opposes Rac (and perhaps Cdc42) during cyto

7 r myosin-II at the division plane when CYK-4 GAP activity was reduced, suggesting that CYK-4 is not u

8 owed increased growth associated protein 43 (GAP-43) expression in brain samples resected from patien

9 5 (PGP9.5) and growth-associated protein 43 (GAP-43), a marker of regenerating nerve axons, was perfo

10 A GAP domain in ArhGAP44 triggers local Rac-GTP hydrolysis

11 ROCK and histone deacetylase 6 but not by a GAP-mutant form of ARHGAP18.

12 the Cdc42 GTPase activating protein CdGAP, a GAP for Rac1 and Cdc42, at cell-cell contacts.

13 ifies a previously unknown requirement for a GAP in DLP function.

14 ARHGEF6 is constitutively linked to GIT1, a GAP of Arf family small G proteins, and that ARHGEF6 pho

15 usion, thus suggesting extended control of a GAP cascade beyond Rab interactions.

16 findings illustrate how retromer recruits a GAP, which is likely to be involved in the timing of Rab

17 trate modulation of Cdc42 activity through a GAP during mating.

18 rating spinal cord axons contain beta-actin, GAP-43, Neuritin, Reg3a, Hamp, and Importin beta1 mRNAs.

19 rea victoria proteins, GFP and apo-aequorin (GAP).

20 products, as revealed by (1)H NMR analysis; GAP washing consistently increases the diastereopurity o

21 dependent H-Ras activation (GTP binding) and GAP-catalyzed H-Ras deactivation (GTP hydrolysis) at nan

22 We show that both C2 and GAP domains are required for the membrane targeting of C

23 the TIM-catalyzed deprotonation of DHAP and GAP by both wild-type TIM and its I170A, L230A, and I170

24 ed defects in both GEF-mediated exchange and GAP-mediated GTP hydrolysis, consistent with NMR-detecte

25 RhoA/B/C FRET sensors show localized GEF and GAP activity and reveal spatial activation differences b

26 Despite the partial defect in both GEF and GAP regulation, KRAS K104Q did not alter steady-state GT

27 ded for optimal RanGAP1-NPC localization and GAP exchange activity.

28 y for GAP-43 was observed at 5d post-PH, and GAP-43 (+) PTs percentage increased thereafter with a pe

29 LY 294002 prevented Akt phosphorylation and GAP-43 protein expression rise in NCX1.4 overexpressing

30 duced an increase in Akt phosphorylation and GAP-43 protein expression.

31 and inactivation of Rab GTPases by GEFs and GAPs promotes or terminates vesicle tethering to organel

32 ns; however, the identity of an antagonistic GAP remains elusive.

33 ted by ARAP2 knockdown and depended on ARAP2 GAP activity.

34 s determined, in part, by the associated Arf GAP.

35 We report that the conserved Arf GAP Asap is required for cleavage furrow ingression in t

36 in-like (GLD), pleckstrin homology (PH), Arf GAP, and ankyrin repeat domains.

37 E6, focal adhesion kinase, and the GIT1 ARF-GAP protein for binding to paxillin are required but not

38 of opposing action defined by distinct Arf6 GAPs.

39 We tested this idea by comparing the Arf6 GAPs ARAP2 and ACAP1.

40 The specificities of ELMOD1-3 as GAPs for six different members of the ARF family were de

41 GAP activities of the three human ELMODs as GAPs we developed new preparations of each after overexp

42 Baseline GAP-43 expression was higher in CD animals compared to c

43 This immune-boosting GAP highlights an important role of opsonized parasite-m

44 These additive effects indicate that both GAPs collaborate in the spatial regulation of active Cdc

45 RhoA activation dynamics indicates that both GAPs regulate different spatiotemporal Rho GTPase pools,

46 at uses the ancestry coordinates inferred by GAP to accurately account for ancestry-induced correlati

47 Accuracies of the predictions made by GAP are significantly improved compared with other metho

48 extension; these phenotypes were rescued by GAP-43 knockdown.

49 C-GAP spatially restricts RhoA pathway activity to a centr

50 RhoGEF2 pulses precede myosin, and C-GAP is required for pulsation, suggesting that contracti

51 ation of RhoA, mediated by its antagonist, C-GAP, is essential for effective contractility to occur.

52 Finally, C-GAP expression level influences the transition from reve

53 tical role for a RhoA GAP, Cumberland GAP (C-GAP), which coordinates with a RhoA GEF, RhoGEF2, to org

54 ing and modulating the ratio of RhoGEF2 to C-GAP are required for tissue folding.

55 Spatial distribution of a Cdc42 GAP in coordination with G1 progression may thus be crit

56 ere that Rga6 is another fission yeast Cdc42 GAP which shares some functions with Rga4.

57 se of the well known marker of growth cones, GAP-43; and an enhancement of endoplasmic reticulum (ER)

58 ses Gap-43 mRNA translation and consequently GAP-43 function.

59 In contrast, GAP-43 remained up-regulated in CD rats, and over 50% de

60 We created GAP mice by crossing Tg2576 mice that over-express the S

61 The CT- GAP gender, age, and physiology model (a modification of

62 P gender, age, and physiology model (the CT- GAP gender, age, and physiology model) with comparable p

63 y a critical role for a RhoA GAP, Cumberland GAP (C-GAP), which coordinates with a RhoA GEF, RhoGEF2,

64 complex in vivo with DGAP1, a Dictyostelium GAP protein.

65 eIF2 GDP/GTP status is regulated by eIF5 (GAP and GDI functions) and eIF2B (GEF and GDF activities

66 telets from thrombocytopenic mice expressing GAP-deficient Rasa3 (H794L) show increased spreading on

67 We identified seven atypical FG-GAP domains in the extracellular domain, which potential

68 ty, which reveals a novel mode of action for GAP proteins.

69 At 6 m post-PH, immunoreactivity for GAP-43 was not detectable.

70 In contrast, immunoreactivity for GAP-43 was observed at 5d post-PH, and GAP-43 (+) PTs pe

71 Further, GAP-induced apoptosis is partially mediated by JNK1/2, b

72 interacting molecules: upstream enzymes (GEF/GAP) regulate Ras's ability to recruit multiple competin

73 ange factors/GTPase-activating proteins (GEF/GAP).

74 tated by a complex mechanism involving GEFs, GAPs, effectors, and C-terminal interaction with membran

75 P/GDP) catalytic domain, the K-Ras4B(WT)-GTP-GAP complex, and the mutants (K-Ras4B(G12C/G12D/G12V)-GT

76 mes and identified 34 out of 186 Rab GTPase, GAP and GEF family members as potential autophagy regula

77 We show that Drosophila PlexA has GAP activity for the Rap1 GTPase, which is known to regu

78 ctility, with little investigation as to how GAPs may be important.

79 However, GAP-43 expression decreased by day 15 post-seizure in co

80 ion of r-synGAP by CaMKII increases its HRas GAP activity by 25% and its Rap1 GAP activity by 76%.

81 horylation by CDK5 increases r-synGAP's HRas GAP activity by 98% and its Rap1 GAP activity by 20%.

82 Even though all impair GAP-assisted GTP --> GDP hydrolysis, the mutation freque

83 silico homology modeling predicted impaired GAP function in the corresponding mutant.

84 disturb the R789/Q61 organization, impairing GAP-mediated GTP hydrolysis.

85 Importantly, GAP not only donates its R789 arginine finger, but stabi

86 ites, Ser-773 and Ser-802, is an increase in GAP activity.

87 e) either in the sclerotic skin in NSF or in GAP.

88 Kif2A increased GAP activity of AGAP1, and a protein composed of the GLD

89 An acute seizure increased GAP-43 expression in both CD and control rats.

90 0% developed chronic epilepsy with increased GAP-43 levels in their serum.

91 vates initiation at UUG codons by increasing GAP function.

92 the Ras activator GEF and the Ras inhibitor GAP.

93 nable Rac1 activators (GEFs) and inhibitors (GAPs) to act in concert to regulate Rac1 signaling.

94 ermine the interactomes of three interacting GAP/GEF proteins at the PSD, including the RasGAP Syngap

95 in division after ring closure, although its GAP activity is only required until just prior to closur

96 ed that the inhibitory effect depends on its GAP activity.

97 Through its GAP activity, it modulates the actin cytoskeleton networ

98 Besides the known GAPs in the malaria parasite, the complex included GAP40

99 Values of (k(cat)/K(m))GAP for triosephosphate isomerase-catalyzed reactions of

100 d-glyceraldehyde 3-phosphate [(k(cat)/K(m))(GAP) and (k(cat)/K(m))DHAP] and of the substrate pieces

101 f carbon monoxide test results in a modified GAP gender, age, and physiology model (the CT- GAP gende

102 f these RhoGAPs, ArhGAP11A (also known as MP-GAP) and RacGAP1 (also known as MgcRacGAP), in promoting

103 Alternative exon 23a falls within the Nf1 GAP domain coding sequence and is tightly regulated in f

104 stabilization of LThDP, whereas addition of GAP converts DXPS to the open conformation that coincide

105 NPRL3 is a component of GAP Activity Towards Rags 1, a negative regulator of the

106 (S1R) was identified as a novel effector of GAP activity of ELMOD1-3 proteins as its direct binding

107 We also utilize Agap2 as an example of GAP/GEFs localized within multiple neuronal compartments

108 Inhibition of GAP-43 expression by shRNA significantly reduced seizure

109 /- 0.16] between k(cat) for isomerization of GAP and K(d)() for phosphite dianion binding to the tran

110 either ELMOD1 or ELMOD2 resulted in loss of GAP activity.

111 rat model of CD to examine the regulation of GAP-43 in the brain and serum over the course of epilept

112 regulate adherens junctions is dependent on GAP activity and signaling via the RhoA pathway.

113 1 silencing prevented NGF-induced effects on GAP-43 expression, Akt phosphorylation, and neurite outg

114 Rga4 is the only GAP described as negative regulator of fission yeast Cdc

115 The performance of the original GAP gender, age, and physiology model did not change sig

116 iology model (a modification of the original GAP gender, age, and physiology model that replaces diff

117 accuracy comparable to that of the original GAP gender, age, and physiology model, with a C index of

118 ation with genetically attenuated parasites (GAP) would be an attractive alternative approach.

119 Plasmodium genetically attenuated parasites (GAPs) have been generated in rodent models that cause se

120 s triggered by d-glyceraldehyde 3-phosphate (GAP).

121 sphate (DHAP) to d-glyceraldehyde phosphate (GAP), via general base catalysis by E165.

122 CX1 silencing prevented Akt phosphorylation, GAP-43 and MAP2 overexpression, and neurite elongation.

123 ew condition, gadolinium-associated plaques (GAP), is reported in 2 patients.

124 eal datasets from diverse human populations, GAP exhibits substantially lower error in reconstructing

125 r algorithm Geographic Ancestry Positioning (GAP) relates local genetic distances between samples to

126 highly dependent on the balance of positive (GAP) and negative (GEF) regulators in the system.

127 eated with gingival augmentation procedures (GAPs) and untreated homologous contralateral sites.

128 The Geographic Atrophy Progression (GAP) study was designed to assess the rate of geographic

129 l, called Generalized Aggregation Proneness (GAP), could successfully distinguish between amyloid fib

130 Consistent with the proposed GAP role for ELMOD1, the ARF6 GTP/GDP ratio was signific

131 tore levels of the growth-associated protein GAP-43 in the hippocampus, though not in the cerebral co

132 augments their GTPase-accelerating protein (GAP) activity, ultimately accelerating deactivation of G

133 Arf6 and the Arf6 GTPase-activating protein (GAP) ACAP1 are established regulators of integrin traffi

134 d GATOR1 displays GTPase activating protein (GAP) activity for RAGA and RAGB (RAGA/B) and GATOR2 has

135 usions, where its GTPase-activating protein (GAP) activity is required for directional migration.

136 rminal domain has GTPase-activating protein (GAP) activity.

137 the engagement of GTPase-activating protein (GAP) and GTP hydrolysis.

138 as a Ras-specific GTPase activating protein (GAP) and Spred1 acting on hitherto undefined components

139 he Cdc42-directed GTPase-activating protein (GAP) Bem2 in Cdc42 polarization.

140 ss belongs to the GTPase Activating Protein (GAP) complex that catalyzes Go inactivation upon light-i

141 failure when the GTPase-activating protein (GAP) CYK-4 is disrupted, Rac activity was proposed to be

142 ses an N-terminal GTPase-activating protein (GAP) domain and a C-terminal ADP-ribosyltransferase (ADP

143 aling through its GTPase-activating protein (GAP) domain and Cdc42.

144 e factor (GEF) or GTPase-activating protein (GAP) enzymes, and is exclusive to membrane-localized Rab

145 ucleoside triphosphatase activating protein (GAP) for ARF6, as the most highly enriched ARF regulator

146 2) functions as a GTPase-activating protein (GAP) for ARL3 (Arf-like protein 3), a small GTPase.

147 1p functions as a GTPase activating protein (GAP) for Dnm1p in vitro.

148 te that TBC1d5, a GTPase-activating protein (GAP) for Rab7, is a high-affinity ligand of the retromer

149 with GATOR1, the GTPase activating protein (GAP) for RagA/B.

150 GATOR1 is a GTPase activating protein (GAP) for RagB whereas GATOR2 functions as an inhibitor o

151 icted to encode a GTPase activating protein (GAP) for Ras.

152 BCK is a putative GTPase-activating protein (GAP) for small GTPases of the Rab family and has been sh

153 dentified Rga2, a GTPase-activating protein (GAP) for the Cdc42 Rho-type GTPase, as a calcineurin sub

154 eIF5 is the GTPase activating protein (GAP) for the eIF2 . GTP . Met-tRNAi (Met) ternary comple

155 cific Ras and Rap GTPase-activating protein (GAP) found in high concentrations in the postsynaptic de

156 mmalian Tsc1-Tsc2 GTPase activating protein (GAP) heterodimer is a critical negative regulator of Rhe

157 es cerevisiae Arf GTPase-activating protein (GAP) homolog Gcs1p uses a related WxxF motif at its extr

158 actor (GEF) and a GTPase activating protein (GAP) is an efficient method for Ras inhibitor high-throu

159 also recruits the GTPase-activating protein (GAP) Msb3.

160 The Ras GTPase-activating protein (GAP) p120RasGAP inhibits Ras activity and mediates neuri

161 nd its regulatory GTPase activating protein (GAP) Retinitis Pigmentosa 2 (RP2).

162 type I (Nf1) is a GTPase-activating protein (GAP) that inactivates the oncoprotein Ras and plays impo

163 nGAP is a Ras/Rap GTPase-activating protein (GAP) that is a major constituent of postsynaptic densiti

164 1 (DLC1) is a RHO GTPase-activating protein (GAP) that negatively regulates RHO.

165 cluding GATOR1, a GTPase activating protein (GAP), and GATOR2, a positive regulator of unknown molecu

166 ich encodes for a GTPase-activating protein (GAP), is a key regulatory hub connecting the familial PD

167 f its guanine nucleotide-activating protein (GAP), Sec23-Sec24, and blocked upon addition of guanosin

168 ntrinsic and TSC2 GTPase-activating protein (GAP)-mediated GTP hydrolysis by displacing the hydrolyti

169 ors, and that the GTPase-activating protein (GAP)-related domain (GRD) is sufficient to suppress the

170 ct as GTPase-activity accelerating proteins (GAPs) for the Galpha protein to attenuate its activity.

171 GTPase-activating proteins (GAPs) and guanine exchange factors (GEFs) play essential

172 l roles for Arf1 GTPase-activating proteins (GAPs) are less clear.

173 ELMOD family as GTPase-activating proteins (GAPs) for ARL2 that displayed crossover activity for ARF

174 his by acting as GTPase activating proteins (GAPs) for Galpha subunits and accelerating the turnoff o

175 anosine triphosphatases-activating proteins (GAPs) have been implicated in this process: AS160 for in

176 Fs) activate and GTPase-activating proteins (GAPs) inhibit RhoA activity.

177 nge factors, and GTPase-activating proteins (GAPs) is differentially dysregulated in response to OGD/

178 ct RhoA-specific GTPase-activating proteins (GAPs) leads to opposite neurite outgrowth phenotypes.

179 factors (GEFs), GTPase-activating proteins (GAPs), and also post-translational modification.

180 hibitors (GDIs), GTPase-activating proteins (GAPs), or the chaperone/GEF Ric-8A], while favoring high

181 regulated by the GTPase-activating proteins (GAPs), which are important for the spatial specificity o

182 re stimulated by GTPase-activating proteins (GAPs), which contain a RhoGAP domain equipped with a cha

183 ctors (GEFs) and GTPase-activating proteins (GAPs), which partner with one Rab to regulate the subseq

184 er resistance to GTPase-activating proteins (GAPs).

185 ctors (GEFs) and GTPase-activating proteins (GAPs).

186 and several glideosome-associated proteins (GAPs).

187 Group-assisted purification (GAP) has been utilized to give the pure amides without u

188 d the other involves CDC-42 and its putative GAP CHIN-1.

189 revealing that a catalytically inactive Rab GAP promotes rather than terminates vesicle tethering at

190 licated Arg511 as a required residue for Rab-GAP function, and in silico homology modeling predicted

191 These results suggest that loss of Rab-GAP activity is the underlying mechanism of disease.

192 chondrial Rab GTPase-activating protein (Rab-GAP), governs autophagosome biogenesis and morphology do

193 RUND-1 also interacts with the Rab2 GAP protein TBC-8 and the BAR domain protein RIC-19, a R

194 type III secretion effectors, SopD2, a Rab32 GAP, and GtgE, a specific Rab32 protease.

195 plex composed of a Rac-GEF (Tiam1) and a Rac-GAP (Bcr) that cooperate to control excitatory synapse d

196 CHN1, which encodes alpha2-chimaerin, a Rac-GAP GTPase that affects cytoskeletal dynamics.

197 the cortical actin cytoskeleton via the Rac-GAP-containing protein RICH2 (ARHGAP44), and a naturally

198 Here we show that the Rac1 GAP breakpoint cluster region (BCR) associates with NMDA

199 nsity of both types of synapses via its Rac1-GAP activity.

200 n, through binding and antagonizing the RAC1-GAP protein ARHGAP24.

201 nGAP's HRas GAP activity by 98% and its Rap1 GAP activity by 20%.

202 es its HRas GAP activity by 25% and its Rap1 GAP activity by 76%.

203 In contrast to Ras . GAP catalysis, the bond breakage of the beta-gamma-phosp

204 We report here that neurofibromin, a Ras-GAP encoded by Nf1, has an overlapping expression patter

205 complements the Saccharomyces cerevisiae Ras-GAP ira1 mutant and the encoded MadC protein interacts w

206 These findings demonstrate a role for Ras-GAP activity in suppressing the hemogenic potential of t

207 RASAL2 acted independently of its RAS-GAP catalytic activity in TNBC; however, RASAL2 promoted

208 xamined the potent SG-nucleating protein Ras-GAP SH3-binding protein 1 (G3BP1), and found that G3BP1

209 exhibits Ras GTPase activating protein (Ras-GAP) activity that is thought to mediate cellular functi

210 on of the Ras-GTPase activating protein (Ras-GAP) neurofibromin, a 5-HT6 receptor partner.

211 association of the SG effector protein, Ras-GAP SH3-binding protein 1 (G3BP1), with the MRV nonstruc

212 lts suggest that exon 23a suppresses the Ras-GAP activity of Nf1.

213 mice showed a prominent decrease in the Ras-GAP calcium-sensing protein RASAL1.

214 n engineered into the active site of the Ras-GAP domain is sufficient to reproduce ectopic blood isla

215 rs that up-regulate (GEF) and down-regulate (GAP) RAS activity.

216 vides an additional mechanism for regulating GAP-43 expression and function and may be critical for n

217 synGAP activity; CaMKII shifts the relative GAP activity toward inactivation of Rap1, and CDK5 shift

218 ced robust fusion by a process that required GAP-dependent actin remodeling and BAR domain-dependent

219 functionally substitute to the bona fide Rho GAP, GRAF1 (GTPase Regulator Associated with Focal Adhes

220 Rho GAPs are important regulators of Rho GTPases, which are

221 ncluding a Rho family GTPase-activating (Rho-GAP) domain, and a Bin-Amphiphysin-Rvs (BAR) domain.

222 HvELMOD_C interacts with the central RHO-GAP domain of HvMAGAP1.

223 its localization to focal adhesions, its Rho-GAP activity, and its ability to bind tensin and talin.

224 mutants indicate that OPHN1 requires its Rho-GAP domain to control fusion pore dynamics.

225 However, regulation of Rho-GAP cellular localization and function is not fully unde

226 ions, its Rho-GTPase activating protein (Rho-GAP) function, and its ability to bind several ligands,

227 atalytically active arginine R185 in the RHO-GAP domain.

228 nformation by efficiently binding to the Rho-GAP domain.

229 erines in DLC1 located N-terminal to the Rho-GAP domain.

230 Loss of function of the Rho-GAP oligophrenin-1 is associated with cognitive impairme

231 ellular localization and function of the Rho-GAP Rga7 are regulated by a novel protein, Rng10, during

232 tein Rng10 and its relationship with the Rho-GAP Rga7 in fission yeast.

233 We recently reported that the Rho-GAP, GRAF1, was particularly abundant in muscles undergo

234 Rich2 was an uncharacterized Rho-GAP protein.

235 Here, we identify a critical role for a RhoA GAP, Cumberland GAP (C-GAP), which coordinates with a Rh

236 O3(-) group based on the structure of a RhoA/GAP-GDP-MgF3(-) TSA complex.

237 Molecular details for RhoA/GAP catalysis of the hydrolysis of GTP to GDP are poorly

238 Mechanistically, absence of RP2 GAP activity increases ARL3-GTP levels, forcing PDE6D to

239 386 does not switch the specificity of Mgc's GAP activity and is not required for successful cytokine

240 cells, both the target specificity of Mgc's GAP activity and the involvement of phosphorylation of M

241 Together these results indicate that Mgc's GAP activity down-regulates the active populations of Rh

242 We show that Mgc's GAP activity spatially restricts accumulation of both Rh

243 Serum GAP-43 levels were significantly higher in CD rats that

244 Several GAPs and GEFs have been shown to be present at the posts

245 rc homology 3 (SH3) domain of a Ras-specific GAP (p120RasGAP).

246 e catalytic activity of RhoGAP (Rho-specific GAP) on the 6-TGTP-Rac1 adduct to produce the biological

247 on induced by all self-resolving blood stage GAP infections.

248 ses over time, we report a novel blood stage GAP that lacks a secreted factor related to histamine-re

249 All such GAPs generated so far bear mutations in housekeeping gen

250 Together, these results suggest GAP-43 as a key factor promoting epileptogenesis, a poss

251 However, it is not known how synaptic GAP and GEF proteins are organized within the PSD signal

252 enic mice for endoplasmic reticulum-targeted GAP exhibited a robust long-term expression that correla

253 The crystal structure of the TBC1d5 GAP domain bound to VPS29 and complementary biochemical

254 typical of human AD in a mouse model termed GAP.

255 Physicians should be aware that GAP can occur without NSF or renal disease and is associ

256 We suggest that GAP activity cooperates with the GDI to counteract the d

257 The GAP complex has a striking molecular complexity.

258 ants carrying point mutations abolishing the GAP activity and/or the WPP-dependent subcellular locali

259 e we show that EGF stimulation activates the GAP activity of DLC1 through a concerted mechanism invol

260 Both the ADPRT and the GAP domain activities contribute to ExoT-induced apoptos

261 Together, the ADPRT and the GAP domains make ExoT into a highly versatile and potent

262 e signal suppression is a result of both the GAP (GTPase accelerating) and receptor binding functions

263 To further characterize the GAP activities of the three human ELMODs as GAPs we deve

264 this strategy with measuring changes in the GAP activity by bioluminescence resonance energy transfe

265 network of 20 hydrogen bonds, including the GAP Arg85' side chain, but neither phosphate torsional s

266 dence showing that the domains including the GAP, BoCCS and GRM are all important for normal MoGlo3 f

267 PA binds and inhibits the GAP activity of RGS1.

268 xamined the organizational principles of the GAP complex in ON-BCs.

269 of hierarchical assembly and function of the GAP complex that supports ON-BCs visual signaling.

270 nal data suggest that a distinct loop of the GAP domain may contact VPS35.

271 eracted with TBC1D10A, and expression of the GAP-insensitive Rab35(Q67A) mutant rescued the inhibitor

272 s to the noncatalytic (GAPex) portion of the GAP-related domain (GRD) of neurofibromin.

273 of Sst2, noise suppression requires only the GAP activity.

274 ense mutations, although located outside the GAP-related domain, may be an important risk factor for

275 both R9AP and RGS7 does not reconfigure the GAP complex and completely abolishes synaptic transmissi

276 ions of increasing severity and requires the GAP activity of RanGAP, while the subcellular positionin

277 In this study, we demonstrate that the GAP domain activity is both necessary and sufficient to

278 series of transgenic mice, we show that the GAP domain of plexins constitutes their key signaling mo

279 Here, we provide evidence that the GAP, RASA3, inhibits platelet activation and provides a

280 In contrast to the GAP domain mutants, Plexin-B2 transgenic mice defective

281 However, the mechanism underlying the GAP-induced apoptosis remains unknown.

282 ide genetic evidence that, unexpectedly, the GAP domain-mediated developmental functions of plexins a

283 To dissect whether the GAP activity and/or the subcellular localization of RanG

284 .0); difference in C index compared with the GAP gender, age, and physiology model of -0.4 (95% confi

285 have been shown to mainly interact with the GAP-related domain (GRD) of IQGAP1.

286 her modulates RGS proteins to increase their GAP activity.

287 or to exploration of the regulation of their GAP activities via agonists or antagonists of the S1R.

288 r direct contribution to modulation of their GAP activity.

289 ties of each interactome and show that these GAP/GEF proteins are highly associated with and cluster

290 Furthermore, we also show that these GAPs/GEFs associate with several proteins involved in ps

291 In this GAP procedure, the crude solids are washed with diethyl

292 xternal receptors or intracellularly through GAP junctions.

293 GTP-bound conformation and are resistant to GAP-mediated GTP hydrolysis.

294 X1 colocalized and coimmunoprecipitated with GAP-43, and NCX1 silencing prevented NGF-induced effects

295 equent recruitment of GATOR1, a complex with GAP activity toward RagA/B GTPases, can attenuate amino

296 as4B(Q61H)-GTP/GDP) and their complexes with GAP.

297 s binding of Ras and does not interfere with GAP activity.

298 We show that intoxication with GAP domain results in: (i) JNK1/2 activation; (ii) subst

299 Sites treated with GAPs resulted in coronal displacement of GM with RecRed

300 infection of naive C57BL/6 mice with a yopE GAP mutant (the R144A mutant), flow cytometry analysis o