ライフサイエンスコーパス: GEF

1 GEF-H1 is further regulated by Src phosphorylation, acti

2 GEF-H1 was required for neutrophil polarization in respo

3 GEF-H1(-/-) leukocytes were deficient in in vivo crawlin

4 GEFs catalyze exchange of GDP for GTP; the GTP-bound, ac

5 GEFs play a key role in activation and membrane targetin

6 Our results have general implications: 1) GEF's targeting is independent of Sec7d, but Sec7d influ

7 Surprisingly, TIAM-1/GEF appears to function independently of Rac1 guanine nu

8 he guanine nucleotide exchange factor TIAM-1/GEF in a complex with act-4/Actin to pattern higher orde

9 y modulating F-actin dynamics through TIAM-1/GEF.

10 HGEF1), and dedicator of cytokinesis (DOCK)2 GEFs mediate CXCL12-induced LFA-1 activation in human pr

11 ng Rho guanine nucleotide exchange factor 2 (GEF-H1, ARHGEF2) and MRTF-A target genes tropomyosin 4.2

12 The mechanism of Ric-8A GEF activity differs considerably from that employed by

13 ir homologous complex, is likely to act as a GEF during activation of Rab GTPases involved in cilioge

14 pendent and mediated, at least in part, by a GEF-H1/Rho-dependent mechanism.

15 entire fusion cascade can be controlled by a GEF.

16 Here we identify a GEF-H1 autoinhibitory sequence and exploit it to produce

17 ependent kinase inhibitor P27 (P27KIP1) in a GEF-H1/RHOA-dependent manner.

18 s (GEFs), as well as the binding domain of a GEF Vav2.

19 Expression of a GEF-deficient P-Rex1 mutant effectively blocked Smads-de

20 of the GTPase Arf5 via the Ca(2+)-activated GEF IQSec1, and that both IQSec1 and Arf5 activation are

21 regulated by Src phosphorylation, activating GEF-H1 in a narrower band ~0-2 um from the cell edge, in

22 tion by the localization of their activating GEFs; and 3) effector association with membranes require

23 he auto-inhibited state to promote an active GEF.

24 In doing so, it blocks all GEF, GAP, and effector interactions with KRAS, leading t

25 However, some non-receptor proteins are also GEFs.

26 However, it does alter GEF specificity, as RAC2(E62K) is activated by the DOCK

27 by promoting RAC2 hyperactivation, altering GEF specificity, and impairing GAP function yet retainin

28 Simultaneous imaging of MT dynamics and GEF-H1 activity revealed that autoinhibited GEF-H1 is lo

29 tein Rap2A is the obligate effector for, and GEF substrate of, Epac2 in mediating growth arrest throu

30 identified 34 out of 186 Rab GTPase, GAP and GEF family members as potential autophagy regulators, am

31 owever, it is not known how synaptic GAP and GEF proteins are organized within the PSD signaling mach

32 Fs) or receptor tyrosine kinase-mediated and GEF-dependent RAS activation (such as by targeting the s

33 Several GAPs and GEFs have been shown to be present at the postsynaptic d

34 reclude the practical implementation of anti-GEF therapies.

35 lowed the generation of hypotheses about ARF GEF protein function(s) as well as a better understandin

36 An ARF GEF known as General receptor for 3-phosphoinositides 1

37 need to be coordinated in localizing an ARF GEF to an intracellular compartment to initiate a transp

38 the guanine nucleotide exchange factors (ARF GEFs) that activate them, and the GTPase-activating prot

39 We performed phylogenetic analyses of ARF GEFs in eukaryotes, defined by the presence of the Sec7

40 tion of a functionally diverse cohort of ARF GEFs to control it.

41 This role requires ARF GEFs to be recruited from the cytosol to intracellular m

42 adherens junctions recruit the cytohesin Arf-GEF Steppke, which down-regulates junctional tension and

43 ctor-guanine nucleotide exchange factor (ARF-GEF), to the Golgi.

44 one of the two SEC7 domains of the GNOM ARF-GEF dimer with its ARF1 substrate reduced the efficiency

45 the regulation of Sec7, the trans-Golgi Arf-GEF, through autoinhibition, positive feedback, dimeriza

46 rs of Arabidopsis (Arabidopsis thaliana) ARF-GEF GNOM, which is involved in polar recycling of the au

47 We show that ARF-GEF GNOM acts early, whereas BIG ARF-GEFs act at a later

48 cascade starts by the recruitment of the ARF-GEF cytohesins to the plasma membrane, which, in turn, b

49 indicate a division of labor within the ARF-GEF family in mediating differential growth with GNOM ac

50 gi-associated proteins revealed that the ARF-GEF GBF1 can selectively modulate the ER-Golgi trafficki

51 e done with monomeric proteins, although ARF-GEFs form dimers in vivo.

52 he evolutionary conservation of ARFs and ARF-GEFs, this initial regulatory step of membrane trafficki

53 hat ARF-GEF GNOM acts early, whereas BIG ARF-GEFs act at a later stage of apical hook development.

54 accharomyces cerevisiae, three conserved Arf-GEFs function at the Golgi: Sec7, Gea1, and Gea2.

55 ARF guanine-nucleotide exchange factors (ARF-GEFs), resulting in the recruitment of coat proteins by

56 The Golgi Arf-GEFs contain multiple autoregulatory domains, but the pr

57 ing of the regulation of the early Golgi Arf-GEFs Gea1 and Gea2.

58 ory mechanisms unique to the early Golgi Arf-GEFs.

59 The Arf-GEFs activate Arf GTPases and are therefore the key mole

60 ARF6 GTPase activity by positioning the ARF6-GEF EFA6 at the cell membrane.

61 ntaining complexes have been shown to act as GEFs for Rab7 subfamily GTPases [9-12].

62 GEF-H1 activity revealed that autoinhibited GEF-H1 is localized to MTs, while MT depolymerization su

63 Cumulatively, this work reveals a bacterial GEF within the multifunctional OtDUB that co-opts host R

64 cterial GEF fold shared with other bacterial GEF domains.

65 h a unique topology, on a V-shaped bacterial GEF fold shared with other bacterial GEF domains.

66 Collectively, these data show that the BCR GEF domain affects phenotypes associated with progressio

67 ymphoma syndrome and is regulated by the BCR GEF domain.

68 uantitatively probe the relationship between GEF-H1 conformational change, RhoA activity, and edge mo

69 Importantly, both GEF changes are expected to decrease neurite outgrowth,

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

71 nd that KRAS K104Q exhibited defects in both GEF-mediated exchange and GAP-mediated GTP hydrolysis, c

72 ctivation and inactivation of Rab GTPases by GEFs and GAPs promotes or terminates vesicle tethering t

73 exity of ARF signaling and its regulation by GEFs and GAPs will require the concerted effort of many

74 fector, Bem1, a scaffold, and Cdc24, a Cdc42 GEF.

75 To our surprise, FGD1, another Cdc42 GEF at the Golgi, was not required for Cdc42 regulation

76 discovered a domain in OtDUB with Rac1/Cdc42 GEF activity (OtDUB(GEF)), with higher activity toward R

77 duced the expression of Dock10, a Rac1/Cdc42 GEF, during EMT.

78 ified, GxcU (in Dictyostelium) and the Cdc42-GEF FGD1-related F-actin binding protein (Frabin) (in hu

79 increases the association of FLNa with Cdc42-GEF FGD6, promoting cell division cycle 42 (Cdc42) GTPas

80 activating proteins (GAPs), or the chaperone/GEF Ric-8A], while favoring high-affinity binding to all

81 strate how two TRAPP complexes with a common GEF core select distinct Rab substrates through a steric

82 When compared to a conventional GEF-stimulated nucleotide exchange assay in a proof-of-c

83 city, as RAC2(E62K) is activated by the DOCK GEF, DOCK2, but not by the Dbl homology GEF, TIAM1, both

84 The structurally-related DOCK1 and DOCK2 GEFs are specific for RAC, and require ELMO (engulfment

85 findings extend the family of longin domain GEFs and define a molecular activity linking Rab23-regul

86 ts, SH3-containing class I myosins, the dual-GEF Trio, and other adaptors and signaling molecules.

87 Here, we demonstrate that nuclear Ect2 GEF activity is required for Kras-Trp53 lung tumorigenes

88 SCLL context, the presence of the endogenous GEF motif leads to reduced leukemogenesis.

89 s chaperone and guanine nucleotide exchange (GEF) activity toward heterotrimeric G protein alpha subu

90 ator, the guanine nucleotide exchange factor GEF-H1.

91 confers guanine nucleotide exchange factor (GEF) activity in vitro and promotes G protein-dependent

92 rectly augments the guanine exchange factor (GEF) activity of Cdc24.

93 d by the guanine-nucleotide exchange factor (GEF) activity of GPCRs.

94 ired for guanine nucleotide exchange factor (GEF) activity of VAV proteins.

95 ing as a guanine nucleotide exchange factor (GEF) and a chaperone.

96 nce of a guanine nucleotide exchange factor (GEF) and a GTPase activating protein (GAP) is an efficie

97 ability, guanine nucleotide exchange factor (GEF) and GTPase-activating protein (GAP) activity, and e

98 in vitro guanine nucleotide exchange factor (GEF) assays revealed that I942 and, to a lesser extent,

99 n by the guanine-nucleotide exchange factor (GEF) Brag2, which controls integrin endocytosis and cell

100 cryptic guanine nucleotide exchange factor (GEF) domain in the OtDUB protein encoded by the pathogen

101 ited a guanidine nucleotide exchange factor (GEF) domain to the fusion kinase to facilitate activatio

102 ains two guanine nucleotide exchange factor (GEF) domains with distinct specificities: GEF1 activates

103 e RhoA guanidine nucleotide exchange factor (GEF) Ect2 to control local F-actin organization and cont

104 The guanine nucleotide exchange factor (GEF) epithelial cell transforming sequence 2 (Ect2) has

105 -8b is a guanine nucleotide exchange factor (GEF) expressed in the olfactory epithelium and in the st

106 s as a guanosine nucleotide exchange factor (GEF) for ARL3-GDP.

107 Daple, a guanine nucleotide exchange factor (GEF) for Galphai.

108 cts as a guanine nucleotide exchange factor (GEF) for its GTP-binding protein partner eIF2 via intera

109 mmalian Mon1-Ccz1 guanidine exchange factor (GEF) for Rab7, required for complex stability and functi

110 DOCK6, a guanine nucleotide exchange factor (GEF) for Rac1 and CDC42, as an independent biomarker for

111 ave as a guanine nucleotide exchange factor (GEF) for the RAB-A2a GTPase.

112 V, aka Girdin) is a guanine exchange factor (GEF) for the trimeric G protein Galphai and a bona fide

113 terminal guanine nucleotide exchange factor (GEF) module of Trio (TrioC) transfers signals from the G

114 fics the guanine nucleotide exchange factor (GEF) Rabin8 to the centrosome to activate Rab8, needed f

115 in (Ran) guanine nucleotide exchange factor (GEF) RCC1.

116 The guanine nucleotide exchange factor (GEF) Son of Sevenless (SOS) is a key Ras activator that

117 The guanine nucleotide exchange factor (GEF) Son of Sevenless (SOS) plays a critical role in sig

118 ast, Arf guanine nucleotide-exchange factor (GEF) Syt1p activates Arf-like protein Arl1p, which was a

119 ytosolic Guanine Nucleotide exchange Factor (GEF) that activates heterotrimeric G protein alpha subun

120 yet the guanine nucleotide exchange factor (GEF) that activates Rab11 in most eukaryotic cells is un

121 the CCZ1-MON1 RAB7 guanine exchange factor (GEF) that positively regulates RAB7 recruitment to LE/au

122 l-family guanine nucleotide exchange factor (GEF) that specifically activates the Rho-family GTPase R

123 RhoA Rho guanine nucleotide exchange factor (GEF) Trio as a critical component of the N-cadherin adhe

124 ated Rho guanine nucleotide exchange factor (GEF)), PDZ-RhoGEF, and p115RhoGEF augmented interaction

125 C by its guanine nucleotide exchange factor (GEF), eIF2B.

126 revealed guanine nucleotide exchange factor (GEF), GTPase-activating protein (GAP), and effector-bind

127 , a Rab8 guanine-nucleotide exchange factor (GEF), to the mother centriole, leading to Rab8 activatio

128 specific guanine nucleotide exchange factor (GEF), was identified in our prior global screen for cand

129 quires a guanine nucleotide exchange factor (GEF), which is Mon1-Ccz1 for Rab7.

130 rate of guanine nucleotide-exchange factor (GEF)-dependent and -independent nucleotide exchange and

131 sociated guanine nucleotide exchange factor (GEF)-H1, is required for the phosphorylation of IRF5 by

132 requires guanine nucleotide exchange factor (GEF)-mediated activation of downstream Ras family small

133 S1), rho guanine nucleotide exchange factor (GEF)1 (ARHGEF1), and dedicator of cytokinesis (DOCK)2 GE

134 Vam7), a guanine nucleotide exchange factor (GEF, Mon1-Ccz1), a Rab-GDP dissociation inhibitor (GDI)

135 DennD1C (guanine nucleotide exchange factor [GEF]) to the IL-17R/Act1 complex in ASMCs, resulting in

136 oupling guanine nucleotide exchange factors (GEF) to effectors, generating a positive feedback of GTP

137 Guanine nucleotide exchange factors (GEFs) activate and consequently stabilize Rab substrates

138 cognate guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs), which partn

139 ions of guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs).

140 by their specific guanine exchange factors (GEFs) and their GTPase-activating proteins (GAPs).

141 Guanine nucleotide exchange factors (GEFs) are the initiators of signaling by every regulator

142 ich are guanine nucleotide exchange factors (GEFs) for Rac, thereby stimulating Rac-Pak signaling.

143 idomain guanine nucleotide exchange factors (GEFs) for RHO GTPases that regulate intracellular actin

144 eceptor guanine-nucleotide exchange factors (GEFs) have emerged as critical signalling molecules and

145 ning of guanine nucleotide exchange factors (GEFs) in human bronchial epithelial cell monolayers, we

146 s (Rho) guanine nucleotide exchange factors (GEFs) Kalirin and Trio have emerged as central regulator

147 d its effector ARF-guanine-exchange factors (GEFs) of the Brefeldin A-inhibited GEF (BIG) family and

148 tion of guanine nucleotide exchange factors (GEFs) on the ADP-ribosylation factor (ARF) family of sma

149 ivating guanine nucleotide exchange factors (GEFs) or receptor tyrosine kinase-mediated and GEF-depen

150 roteins (GAPs) and guanine exchange factors (GEFs) play essential roles in regulating the activity of

151 ins are guanine nucleotide exchange factors (GEFs) that activate Rac and Cdc42, and are known to have

152 amily GTPases, and guanine exchange factors (GEFs), as well as the binding domain of a GEF Vav2.

153 eceptor guanine nucleotide exchange factors (GEFs), GIV/Girdin, Daple, NUCB1 and NUCB2 have revealed

154 lators; guanine nucleotide exchange factors (GEFs), GTPase activating proteins (GAPs), and in the Rho

155 ated by guanine nucleotide exchange factors (GEFs), GTPase-activating proteins (GAPs), and also post-

156 tion by guanine nucleotide exchange factors (GEFs), Rac1 associates with a variety of proteins in the

157 ors and guanine nucleotide exchange factors (GEFs), showed induction of RAB11B binding to the GEF SH3

158 f Rho guanosine nucleotide exchange factors (GEFs), the enzymes that stimulate Rho GTPases, can be a

159 ogether with their GDP-GTP exchange factors (GEFs), TRAPP-II and Rabin8, promote recruitment of the c

160 on is regulated by guanine exchange factors (GEFs).

161 trol by guanine nucleotide exchange factors (GEFs).

162 f Rab11 guanine nucleotide exchange factors (GEFs).

163 ivating guanine nucleotide exchange factors (GEFs).

164 ated by guanine nucleotide exchange factors (GEFs).

165 by Rho guanine nucleotide exchange factors (GEFs).

166 We find that lysine 104 is important for GEF recognition, because mutations at this position impa

167 lation and suggest a combinatorial model for GEF inhibition and activation of the Rac1 signaling path

168 B cells silenced for GEF-H1 or Exo70 display defective lysosome secretion, wh

169 a scaffold protein rather than a functional GEF under long-term flow conditions.

170 ne the interactomes of three interacting GAP/GEF proteins at the PSD, including the RasGAP Syngap1, t

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

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

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

174 kinase I phosphorylates a RhoA-specific GEF, GEF-H1, whose phosphorylation enhances its GEF activity.

175 regulators that promote acquisition of GTP (GEFs) or its hydrolysis to GDP (GAPs).

176 Guanine exchange factor H1 (GEF-H1), a RhoA activator, is thought to act as an integ

177 on of guanine nucleotide exchange factor H1 (GEF-H1), leading to Ras homolog family member A (RHOA) a

178 cific guanine nucleotide exchange factor-H1 (GEF-H1) and was abolished by HDAC6 down-regulation.

179 gout-like inflammation, we found that GEF-H1/GEF-H1/AHRGEF2, a microtubule-associated Rho-GEF, was ne

180 DOCK GEF, DOCK2, but not by the Dbl homology GEF, TIAM1, both of which activate the parent protein.

181 al epithelial cell monolayers, we identified GEFs that are required for collective migration at large

182 Our results identify GEF-H1 as a component of the shear stress response machi

183 c42, RhoA, Rheb, and N-Ras, and can identify GEFs by use of GDP-bound forms.

184 because mutations at this position impaired GEF-mediated nucleotide exchange.

185 ab substrates on membranes, thus implicating GEFs as the primary determinants of Rab localization.

186 d the synovium in wild-type mice, but not in GEF-H1(-/-) mice.

187 ons affecting the ARL13b G-domain inactivate GEF activity and lead to Joubert syndrome (JS) in humans

188 Bem1 also increases GEF phosphorylation by the p21-activated kinase (PAK), C

189 nding that inactivate the protein and induce GEF binding and protein mislocalization.

190 factors (GEFs) of the Brefeldin A-inhibited GEF (BIG) family and GNOM in ethylene- and auxin-mediate

191 ricts endothelial permeability by inhibiting GEF-H1, thereby limiting RhoA signaling at AJs and reduc

192 patterning of the small GTPase Rab5 and its GEF/effector complex Rabex5/Rabaptin5 on supported lipid

193 , GEF-H1, whose phosphorylation enhances its GEF activity.

194 path-DG synapse function is dependent on its GEF domain and identify a potential role for the auto-in

195 ineered proteins, using Src tyrosine kinase, GEF Vav2, and Rho GTPase Rac1 as examples.

196 thelial monolayers, whereas GEF-H1 knockout (GEF-H1(-/-)) neutrophils were unaffected by treatment wi

197 ears no obvious sequence similarity to known GEFs, crystal structures of OtDUB(GEF) alone (3.0 angstr

198 Down-regulation of the latter GEFs differentially enhanced front-to-back propagation o

199 The trimeric Mon1-Ccz1-C18orf8 (MCC) GEF therefore plays a central role in cellular cholester

200 opener (ARNO)/cytohesin-2, a plasma membrane GEF reported to activate all ARFs.

201 Because there are numerous GEFs and also a host of Ras family small GTPases, it is

202 coupled to the recruitment and activation of GEF-H1, which is required for assembly of the exocyst co

203 The deletion of GEF-H1 or dominant-negative variants of GEF-H1 prevent a

204 production by colchicine was independent of GEF-H1, supporting a neutrophil-intrinsic mode of action

205 1, in the absence of cAMP, and inhibition of GEF activity in the presence of cAMP.

206 d membrane recruitment and the initiation of GEF activity of individual SOS molecules on microarrays

207 The prevalence of GEF/effector coupling in nature suggests a possible univ

208 GEF assays to demonstrate that regulation of GEF activity is achieved through an intramolecular inter

209 ogates the scaffold-dependent stimulation of GEF activity, rendering Cdc24 insensitive to additional

210 n of GEF-H1 or dominant-negative variants of GEF-H1 prevent activation of IKKepsilon and phosphorylat

211 racterization of the functional behaviour of GEFs with single-molecule precision but without the need

212 GTPases is activated by distinct families of GEFs.

213 in OtDUB with Rac1/Cdc42 GEF activity (OtDUB(GEF)), with higher activity toward Rac1 in vitro.

214 y to known GEFs, crystal structures of OtDUB(GEF) alone (3.0 angstrom) and complexed with Rac1 (1.7 a

215 tially in cells, and expression of the OtDUB(GEF) alone alters cell morphology.

216 Thus, a Par3-GEF-Rac axis mediates both tissue-level and hair cell-in

217 tion subadjacent to the cell cortex promotes GEF-H1 activation in an ~5-um-wide peripheral band.

218 exchange factors/GTPase-activating proteins (GEF/GAP).

219 plexes are known to be Rab effectors and Rab GEFs (Guanine nucleotide Exchange Factors) that regulate

220 ation especially through the activity of Rab GEFs remains largely elusive.

221 amily of Rab7 GEFs and form a specific Rab23 GEF complex.

222 position Rabex5 but to also control its Rab5 GEF activity through allosteric structural alterations.

223 We further provide evidence that the Rab5 GEF activity of RIN1 regulates surface GluA1 subunit end

224 The Rab5 GEF, Rabex5, was previously proposed to be auto-inhibite

225 Strikingly, yeast lacking its two Rab5 GEFs (Muk1 and Vps9) or its three Rab5 paralogs (Vps21/Y

226 aracteristic of the Mon1-Ccz1 family of Rab7 GEFs and form a specific Rab23 GEF complex.

227 d to an increase in affinity for SOS Ras/Rac GEF 1 (SOS1), which appears to be the major mode of acti

228 RAKEC consisting of CaMKII and Tiam1, a Rac-GEF.

229 x1 interacting protein that promotes the Rac-GEF activity and membrane localization of P-Rex1.

230 Here, we identify the Rac-GEF Tiam1 as an important regulator of DG development an

231 By characterizing mice lacking the Rac-GEF Tiam1, we demonstrate that Tiam1 promotes the stabil

232 The Rac-GEF, P-Rex1, activates Rac1 signaling downstream of G pr

233 Rac guanine nucleotide exchange-factors (Rac-GEFs) were also up-regulated in TGF-beta-treated NSCLC c

234 We further identified FARP2 as the Rac1 GEF necessary for CRC collective invasion.

235 Furthermore, the postsynaptic Rac1-GEF kalirin-7 regulated spinule formation, elongation, a

236 suggest an unconventional mechanism for Rag GEF activity.

237 otein activation by a family of non-receptor GEFs containing a Galpha-binding and -activating (GBA) m

238 in VE-PTP-depleted endothelial cells reduced GEF-H1 activity and restored VE-cadherin dynamics at AJs

239 in recognition of factors that up-regulate (GEF) and down-regulate (GAP) RAS activity.

240 strate that the TRAPP complexes, two related GEFs that use the same catalytic site to activate distin

241 ata underscore the pros and cons of anti-Rho GEF therapies for cancer treatment.

242 ibitor for the catalytic activity of the Rho GEF Vav2 at the organismal level.

243 ntext, it is worth remembering that many Rho GEFs can mediate both catalysis-dependent and independen

244 of RhoA activity involves ICAM-1 and the Rho GEFs Ect2 and LARG.

245 GEF-H1/AHRGEF2, a microtubule-associated Rho-GEF, was necessary for the inhibitory effect of colchici

246 Type 2 nodes containing Blt1p, Rho-GEF Gef2p, and kinesin Klp8p remain intact throughout th

247 ent, thus suggesting different routes of rho-GEF triggering upon CXCR4 engagement.

248 inner nuclear placement relies on SPIKE1 Rho-GEF, SUPERCENTIPEDE1 Rho-GDI, and ACTIN7 (ACT7) function

249 bly and the nuclear sequestration of the Rho-GEF Pebble.

250 ing module, with at least four different rho-GEFs cooperating in the regulation of chemokine-induced

251 We show that Rgf1p (Rho1p GEF), participates in a delay of cytokinesis under cell

252 Here, we demonstrated that the RhoA GEF Arhgef1 is essential for Ang II-induced inflammation

253 The RhoA GEF Pebble (Dm ECT2) did not evidently tip-track, but ra

254 t large, such as SOS1 and beta-PIX, and RHOA GEFs that are implicated in intercellular communication.

255 development and stimulates its cryptic RhoA-GEF activity, which functions together with its Rac1-GAP

256 for effective collective migration, the RHOA-GEFs --> RHOA/C --> actomyosin pathways must be optimall

257 at through binding and inhibiting the RhoGEF GEF-H1 modulates RhoA activity and tension across VE-cad

258 that integrin adhesions spatially segregate GEFs and GAPs to shape RAC1 activity zones in response t

259 tein kinase I phosphorylates a RhoA-specific GEF, GEF-H1, whose phosphorylation enhances its GEF acti

260 Here, we show that SGEF, a RhoG-specific GEF, forms a ternary complex with Scribble and Dlg1, two

261 ases, it is important to know which specific GEF-small GTPase dyad functions in a given cellular proc

262 Specifically, GEF-H1 functions in a microtubule based recognition syst

263 Thus, Bem1 stimulates GEF activity in a reversible fashion, contributing to si

264 Our results indicate that CLDN-2 suppresses GEF-H1/RHOA.

265 of Lte1 is mediated by its N- and C-terminal GEF domains, which, we propose, directly activate the ME

266 ent between GBA proteins and GPCRs, and that GEF-mediated perturbation of nucleotide phosphate bindin

267 els of gout-like inflammation, we found that GEF-H1/GEF-H1/AHRGEF2, a microtubule-associated Rho-GEF,

268 The GEF-H1-IKKepsilon-IRF5 signaling axis functions independ

269 ty destabilizes MT and thereby activates the GEF-H1/Rho pathway, increasing both EC permeability and

270 al structure of unbound Brag2 containing the GEF (Sec7) and membrane-binding (pleckstrin homology) do

271 However, how the GEF activity of DENND3 toward Rab12 is regulated at the

272 ndependent of Sec7d, but Sec7d influence the GEF substrate specificity and downstream effector events

273 Loss of the GEF domain enhanced cell proliferation and invasion pote

274 Indeed, loss of the GEF domain suppressed activation of RHOA and PTEN, leadi

275 ilia [1, 7, 8]; however, the identity of the GEF pathway activating Rab23, a member of the Rab7 subfa

276 Previous studies indicate that the GEF activity of the TrioC module is autoinhibited, with

277 Our findings reveal that the GEF Mon1-Ccz1 is necessary and sufficient for stabilizin

278 , and we find that Abl also acts through the GEF Trio to stimulate the signaling activity of Rac GTPa

279 ), showed induction of RAB11B binding to the GEF SH3BP5, again similar to inactive RAB11B.

280 nd downstream effectors of signaling via the GEF Epac2 in the neuroendocrine NS-1 cell line.

281 the first non-receptor protein for which the GEF activity was ascribed to a well-defined protein sequ

282 cular interactions, and interaction with the GEF, Cdc24p, were defective for fMAPK pathway signaling.

283 ain Rabs by mediating interaction with their GEFs.

284 ne-induced tyrosine phosphorylation of these GEFs is fully mediated by JAK protein tyrosine kinases.

285 tumorigenesis and identified a role for this GEF in ribosomal RNA (rRNA) synthesis that is mediated b

286 Deletion of this GEF domain increased leukemogenesis, enhanced cell survi

287 However, the functional significance of this GEF in the olfactory neurons in vivo remains unknown.

288 While this GEF bears no obvious sequence similarity to known GEFs,

289 Notably, the three GEFs are all critically involved in chemokine-induced Rh

290 and Src signaling in RhoA activation through GEF-H1.

291 the inflamed vasculature and occurs through GEF-H1-dependent neutrophil stimulation by colchicine.

292 ht the role of the PHn-CC-Ex domain in Tiam1 GEF regulation and suggest a combinatorial model for GEF

293 how that the PHn-CC-Ex domain inhibits Tiam1 GEF activity by directly interacting with the catalytic

294 to relieve intramolecular repression of Trio GEF activity by the Trio N-terminal domain.

295 Understanding GEF-Rab interactions will be crucial to unravel the co-o

296 vation is shared by TRAPPII and an unrelated GEF that is metazoan specific.

297 These results define the VAV GEFs as effectors of ERBB4 activity in a signaling pathw

298 ance energy transfer, pulldown, and in vitro GEF assays to demonstrate that regulation of GEF activit

299 on activated endothelial monolayers, whereas GEF-H1 knockout (GEF-H1(-/-)) neutrophils were unaffecte

300 PTP cytosolic domain mutant interacting with GEF-H1 in VE-PTP-depleted endothelial cells reduced GEF-