ライフサイエンスコーパス: GAP

1 GAP activity, in turn, does not affect ER binding.

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

3 GAP-43 protein was primarily located in excitatory neuro

4 GAP-43 was measured using an enzyme-linked immunosorbent

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

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

7 Growth-associated protein 43 (GAP-43) exhibits induced expression during axonal growth

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

9 Growth-associated protein 43 (GAP-43) plays a central role in the formation of presyna

10 in addition to growth-associated protein-43 (GAP-43), Synapsin-I and thermo-sensitive transient recep

11 captured by structural determination, and a GAP mode that stimulates GTP hydrolysis by RagA but rema

12 we found that C9orf72-SMCR8-WDR41 acts as a GAP for the ARF family of small GTPases.

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

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

15 (NPR3-like GATOR1 complex subunit), and is a GAP for RagA.

16 These data reveal features of a GAP-GTPase interaction and the structure of a critical c

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

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

19 iled to alter NMII RLC localization, while a GAP-dead version of RN-tre partially restored phosphomyo

20 hibition of the kinase domain of ZAP-70, and GAP inhibition of the p21(ras)-ERK pathway.

21 e PH domain decreased [2-17]ARF1 binding and GAP activity.

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 ) = 0.995) for the deprotonation of DHAP and GAP, respectively.

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

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

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

28 how that G-actin contacts the RPEL motif and GAP domain sequences.

29 Reintroduction of Myo9b or Myo9b motor and GAP mutants revealed that local GAP activity rescues cel

30 own pathogens, class C acid phosphatases and GAP proteins are found in a variety of microbes that inh

31 ankle there is increased CGRP(+), TH(+), and GAP-43(+) fiber synovial innervation.

32 to 72% for sugars, 75% for organic acids and GAPs.

33 can also efficiently identify effectors and GAPs of Rho and Ras family GTPases such as Cdc42, RhoA,

34 GTPases identified many known effectors and GAPs, as well as putative novel effectors, with examples

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

36 egrin adhesions spatially segregate GEFs and GAPs to shape RAC1 activity zones in response to mechani

37 ARF signaling and its regulation by GEFs and GAPs will require the concerted effort of many laborator

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

39 Arf GAP with Src homology 3 domain, ankyrin repeat, and plec

40 AGAP2 (Arf GAP with GTP-binding protein-like domain, Ankyrin repeat

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

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

43 The Arf GTPase-activating protein (Arf GAP) with SH3 domain, ankyrin repeat and PH domain 1 (AS

44 pends on its highly-regulated and robust ARF GAP activity, requiring both the PH and the ARF GAP doma

45 activity, requiring both the PH and the ARF GAP domains of ASAP1, and is modulated by phosphatidylin

46 hem, and the GTPase-activating proteins (ARF GAPs) that have the ability to both propagate and termin

47 For the ZA domain of Arf-GAP ASAP1, with a global correlational time of 24 ns at

48 We previously showed that Arf-GAP with coil-coil, ANK repeat and PH domain-containing

49 G-actin inhibits ArhGAP12 GAP activity, and this requires the G-actin contacts ide

50 on is also found in RAS GTPases, we assessed GAP-stimulated GTP hydrolysis for KRAS and observed a si

51 B-GAP was an interventional study done in the city of Bula

52 testing and care for children in Zimbabwe (B-GAP) study, we investigated the uptake and yield of inde

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

54 ulation could not modify the balance between GAPs and primary metabolites or increase the concentrati

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

56 rol of regulatory GTPases by serving as both GAPs and effectors.

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

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

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

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

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

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

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

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

65 mor-promoting phorbol esters and a catalytic GAP domain that inactivates the small GTPase Rac.

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

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

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

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

70 al relay, p190RhoGAP uses a non-conventional GAP-independent mode to transiently suppress attraction

71 functions in parallel with the conventional GAP dehydrogenase, providing an alternative ferredoxin-d

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

73 CSF GAP-43 concentration was significantly lower in progress

74 However, DMTs did not alter CSF GAP-43.

75 Interestingly, in RRMS CSF GAP-43 levels were higher in patients with signs of acti

76 According to CSF GAP-43 concentrations, regeneration seems reduced in pro

77 at it has similar kinetic parameters K(m) (d-GAP) and K(m) (pyruvate) (54 +/- 3 and 11 +/- 1 mum, res

78 pyruvate and d-glyceraldehyde 3-phosphate (d-GAP) into 1-deoxy-d-xylulose 5-phosphate (DXP), an essen

79 During development, GAP-43 is found in axonal extensions of most neurons.

80 Mutant p53-enforced GAP isoforms lose cell membrane association, leading to

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

82 light key aspects of signaling by ARF family GAPs that contribute to previously underappreciated sour

83 tion of GTP (GEFs) or its hydrolysis to GDP (GAPs).

84 In doing so, it blocks all GEF, GAP, and effector interactions with KRAS, leading to inh

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

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

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

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

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

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

91 We aimed to evaluate if GAP-43 can serve as a biomarker of regeneration in relap

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

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

94 ion, altering GEF specificity, and impairing GAP function yet retaining key effector interactions.

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

96 urther showed that the E62K mutation impairs GAP activity for RAC2(E62K) As this disease mutation is

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

98 that the mutation plays a conserved role in GAP activation.

99 metabolites or increase the concentration in GAPs in the physiologically ripe grape.

100 appreciated sources of complexity, including GAPs acting from multiple sites in cells, working with m

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

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

103 0% developed chronic epilepsy with increased GAP-43 levels in their serum.

104 disease-modifying therapies (DMTs) influence GAP-43 concentration in cerebrospinal fluid (CSF).

105 residues 2-17 of ARF1 ([2-17]ARF1) inhibited GAP activity, and PIP(2)-dependently bound to a protein

106 the Ras activator GEF and the Ras inhibitor GAP.

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

108 by RN-tre is only partially dependent on its GAP activity as overexpression of constitutively active

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

110 ASAP1's PH domain and thereby regulates its GAP activity.

111 CGA) and IVY Glioblastoma Atlas Project (IVY GAP) databases had pre-operative imaging analyzed to cal

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

113 We also show that a mutant of ELMOD2 lacking GAP activity is capable of promoting fusion, suggesting

114 9b motor and GAP mutants revealed that local GAP activity rescues cell morphology and migration.

115 at the lagging pole by MglB due to its MglA GAP activity.

116 phylogenetically distinct from the monomeric GAP-oxidizing enzyme found previously in several Archaea

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

118 fusion, suggesting that ELMOD2 does not need GAP activity to influence mitochondrial morphology.

119 ncer cells are frequently comutated with NF1 GAP but NF1 is rarely mutated in cancers with KRAS codon

120 ce presynaptic recruitment and activation of GAP-43.

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

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

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

124 motifs that are functionally independent of GAP activity.

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

126 to uPAR induces not only the mobilization of GAP-43 from the axonal shaft to the presynaptic terminal

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

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

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

130 nic goblet cell-associated antigen passages (GAPs), which translocate enteric bacteria across the int

131 ofiles, named Pfr-B-Phos, Pfr-C-Phos and Pfr-GAP, to describe the three groups of acid phosphatases.

132 sphatases and (3) generic acid phosphatases (GAP).

133 ate (DHAP) and d-glyceraldehyde 3-phosphate (GAP) bound to wild-type triosephosphate isomerase (TIM),

134 a heterodimeric glyceraldehyde-3-phosphate (GAP) ferredoxin oxidoreductase (GOR) present not only in

135 roduce the sugar glyceraldehyde 3-phosphate (GAP), which is used for regeneration of RuBP and is the

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

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

138 PmxA is a cGAMP-specific phosphodiesterase (GAP) that promotes resistance to osmotic stress in M. xa

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

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

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

142 r families of glycosylated aroma precursors (GAPs) at the arrest of fruit phloem unloading of two whi

143 codons 12, 13, or 61 are thought to prevent GAP protein-stimulated GTP hydrolysis and render KRAS-mu

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

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

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

147 s through their GTPase-accelerating protein (GAP) activity, which is conferred by a conserved domain

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

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

150 t purified by its GTPase-activating protein (GAP) activity toward ARL2 and later shown to have unique

151 GATOR1 (GTPase-activating protein (GAP) activity toward Rags-1), a negative regulator of th

152 triphosphatase (GTPase) activating protein (GAP) activity toward the GTPase RagC.

153 factor (GEF) and GTPase-activating protein (GAP) activity, and effector binding of RAC2(E62K) Our fi

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

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

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

157 acting protein 2) GTPase activating protein (GAP) complex, and prevents Rag dimer activation during a

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

159 is a multidomain GTPase-activating protein (GAP) for ADP-ribosylation factor (ARF)-type GTPases.

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

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

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

163 FLCN-FNIP2, is a GTPase activating protein (GAP) for RagC/D, but despite its important role, how it

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

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

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

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

168 The cognate MglA GTPase activating protein (GAP) MglB, which localizes mainly to the lagging cell po

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

170 , we identify the GTPase-activating protein (GAP) Rasal1 as a novel TCR-ZAP-70 binding protein that n

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

172 the Rab-specific GTPase-activating protein (GAP) RN-tre as necessary for the assembly of NMII RLC in

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

174 C1 by acting as a GTPase-activating protein (GAP) towards the small GTPase Rheb.

175 YopE is a GTPase-activating protein (GAP) while YopT is a protease, and they inhibit RhoA by

176 is a synaptic Ras GTPase-activating protein (GAP) with four C-terminal splice variants: alpha1, alpha

177 nge factor (GEF), GTPase-activating protein (GAP), and effector-binding specificities in mixtures of

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

179 9orf72-SMCR8 is a GTPase-activating protein (GAP), and we found that C9orf72-SMCR8-WDR41 acts as a GA

180 t ELMOD2, an ARL2 GTPase-activating protein (GAP), is necessary for ARL2 to promote mitochondrial elo

181 osin Myo9b, a Rho GTPase-activating protein (GAP), negatively regulates Rho activity and deletion of

182 ofibromin 1 (NF1)-GTPase-activating protein (GAP), providing a mechanism for sustained activity of th

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

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

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

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

187 maerin family of GTPase-activating proteins (GAPs) and is encoded by the CHN2 gene, which also encode

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

189 ArhGAP32-family GTPase-activating proteins (GAPs) are RPEL proteins.

190 bility to act as GTPase-activating proteins (GAPs) for activated Galpha subunits.

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

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

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

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

195 are regulated by GTPase-activating proteins (GAPs), activating the hydrolysis of bound GTP.

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

197 factors (GEFs), GTPase activating proteins (GAPs), and in the Rho and Rab subfamilies, guanine nucle

198 ich exons within GTPase-activating proteins (GAPs), negative regulators of RAS family members.

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

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

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

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

203 (GEFs) and their GTPase-activating proteins (GAPs).

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

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

206 and several glideosome-associated proteins (GAPs).

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

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

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

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

211 ly promoting the expression of Armus, a RAB7-GAP required for autophagosome turnover and whose add-ba

212 Instead, retromer cooperates with the RAB7-GAP TBC1D5 to restrict late endosomal RAB7 into microdom

213 sGAP), and the alpha- and beta-Chimaerin Rac GAPs.

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

215 insights into the diversity of chimaerin Rac-GAP regulation and function and highlight a potential me

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

217 vity, which functions together with its Rac1-GAP activity to terminate arborization.

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

219 sassembly of the LFC and release of the RagC-GAP activity of FLCN enabled mTORC1-dependent regulation

220 The RagC-GAP activity of FLCN was inhibited within the LFC, owing

221 at neurofibromin, a tumor suppressor and Ras-GAP (GTPase-activating protein), is also an estrogen rec

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

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

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

225 ss of the RAS GTPase-activating protein (RAS-GAP) NF1 drives aberrant activation of RAS/MEK/ERK signa

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

227 N terminus that reduced binding also reduced GAP activity.

228 RF1 N terminus, which may partially regulate GAP activity.

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

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

231 sted multiple mutations representing all RGS GAP subfamilies and sampling both G protein interface an

232 cally assess the mutational landscape of RGS GAPs in cancer.

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

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

235 r the frequency of codon mutations of 10 Rho-GAP and experimentally tested biochemical and biological

236 down-regulates DLC1's tensin-binding and Rho-GAP activities.

237 , ERK1/2, and AKT kinases to reduce DLC1 Rho-GAP and tumor suppressor activities in cancer cells, whi

238 in the Rho-GAP domain were deficient for Rho-GAP activity and for suppressing cell migration and anch

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

240 findings indicate that point mutation of Rho-GAP genes is unexpectedly frequent in several cancer typ

241 Thus, mutation of Rho-GAP genes occurs frequently in some cancer types and the

242 o-specific GTPase-accelerating proteins (Rho-GAP), which negatively regulate RHOA and related GTPases

243 utants whose lesions were located in the Rho-GAP domain were deficient for Rho-GAP activity and for s

244 DLC1 was the Rho-GAP gene mutated most frequently, with 5%-8% of tumors i

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

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

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

248 migration and growth in agar, but their Rho-GAP activity was similar to that of wild-type DLC1.

249 ense mutations in at least one of the 10 Rho-GAPs.

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

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

252 he arginine finger that carries out GATOR1's GAP function.

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

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

255 s, we propose IqgC acting as a RasG-specific GAP in large-scale endocytosis.

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

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

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

259 , dioctanoyl-PIP(2) (diC8PIP(2)), stimulated GAP activity on an N terminus-containing variant, [L8K]A

260 The mechanistic basis of PIP(2)-stimulated GAP activity is incompletely understood.

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

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

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

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

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

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

267 The GAP complex has a striking molecular complexity.

268 Fusion inhibition by the GAP Gyp1-46 is not limited to Ypt7-tm with bound GTP, in

269 In kidney cell (HEK293-T) culture, the GAP activity toward RAG (GATOR1) protein complex suppres

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

271 hese residues, Lys-1155 and Lys-1230, in the GAP-related domain of IQGAP1 (termed IQGAP1 GRD-2K) redu

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

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

274 PA binds and inhibits the GAP activity of RGS1.

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

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

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

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

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

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

281 ents, and structural analysis, we probed the GAP mode and found that a critical residue on Nprl2, Arg

282 increased Ca(2+) concentration promotes the GAP activity of the RZ subfamily, leading to RZ-mediated

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

284 c42 and R-ras; this association required the GAP-related domain (1004-1237 aa) of IQGAP1.

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

286 ntains at least four major domains, with the GAP-related domain being the most well-studied.

287 her modulates RGS proteins to increase their GAP activity.

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 cells further revealed participation of this GAP in the regulation of both types of large-scale endoc

292 Ypt7-tm with bound GTP, indicating that this GAP has an additional mode of regulating fusion.

293 xternal receptors or intracellularly through GAP junctions.

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

295 9) destabilizes the LFC and thereby triggers GAP activity of FLCN:FNIP2 toward RagC.

296 The TSC2 GAP domain is found abutting the centre of the body on e

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

298 ormatics analysis of the 20 RGS domains with GAP activity revealed hundreds of low-frequency mutation

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

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