ライフサイエンスコーパス: GEF

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

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

3 Ric-8 GEF activity clearly differs from the GEF activity of G

4 the same motif that allows it to serve as a GEF for Galphai.

5 PP) II complex has been proposed to act as a GEF for Rab11 based on genetic evidence, but conflicting

6 nism that one ciliopathy GTPase ARL-13, as a GEF, coordinates with UNC-119, which may act as a GTP-bi

7 entire fusion cascade can be controlled by a GEF.

8 s, acting as a negative regulator of ECT2, a GEF required for activation of Rho GTPases.

9 reas it regulated STAT3 phosphorylation in a GEF activity-dependent manner.

10 -driven process of wound repair in mice in a GEF-dependent manner.

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

12 ors for a variety of small GTPase-activating GEF reactions.

13 diffusion coefficients of the Ras activator GEF and the Ras inhibitor GAP.

14 via interaction with RhoA-specific activator GEF-H1.

15 ion, S100A4 and MACC1, and clustering of all GEFs together improved the prognostic accuracy of the in

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

17 We demonstrated that although GEF-H1 deficiency had little impact on the migratory pro

18 G proteins as both a molecular chaperone and GEF.

19 mplex, a multi-subunit tethering complex and GEF for RAB1, as an interactor of TBC1D14.

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

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

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

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

24 four distinct mutations within BRAG1, an Arf-GEF synaptic protein, each led to X-chromosome-linked in

25 he functional relevance of reduced BRAG1 Arf-GEF activity as seen in the XLID-associated human mutati

26 tic transmission, independently of BRAG1 Arf-GEF activity or neuronal activity, but dependently on it

27 ctor guanine nucleotide exchange factor (ARF-GEF) GNOM.

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

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

30 each of these mutations reduces BRAG1's Arf-GEF activity.

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

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

33 al DCB and HUS regulatory domains of the Arf-GEF Sec7 form a single structural unit.

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

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

36 Cytohesin Arf-GEFs are conserved plasma membrane regulators.

37 Arf guanine nucleotide exchange factors (Arf-GEFs) regulate virtually all traffic through the Golgi b

38 ylation factor-guanine exchange factors (ARF-GEFs).

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

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

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

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

43 with developmental upregulation of the ARF6 GEF ARNO enhancing retrograde transport.

44 Since a specific Arl3-GEF is postulated to reside inside cilia, the N-terminal

45 ls) domain-bearing proteins that function as GEFs (guanine nucleotide exchange factors) for the small

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

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

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

49 on, have focused on how RhoA is activated by GEFs to promote cell contractility, with little investig

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

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

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

53 c42 GEF Gef1, a homologue of mammalian Cdc42 GEF DNMBP/TUBA, to spatially control Cdc42 GTPase activi

54 in Rad24 modulates the availability of Cdc42 GEF Gef1, a homologue of mammalian Cdc42 GEF DNMBP/TUBA,

55 promotes interaction of DOCK4 with the CDC42 GEF DOCK9.

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

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

58 l function, yet the regulation of connecdenn GEF activity is unexplored.

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

60 OS1 with micromolar affinity, and disrupting GEF-Ras interaction.

61 ugh the intracellular activation of distinct GEFs and Rac GTPases.

62 epletion of DOCK10 or expression of a DOCK10 GEF-dead mutant led to a strong decrease in spine densit

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

64 e we report that elevated expression of each GEF in circulating tumor cells (CTCs) isolated from the

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

66 the ISR and its stimulatory effect on eIF2B GEF activity toward its substrate, the translation initi

67 his enables cells to grow with reduced eIF2B GEF activity but impairs activation of GCN4 targets in r

68 d by eIF5 (GAP and GDI functions) and eIF2B (GEF and GDF activities), while eIF2alpha phosphorylation

69 of interacting molecules: upstream enzymes (GEF/GAP) regulate Ras's ability to recruit multiple comp

70 Rgf3 is an essential GEF for Rho1 GTPase in fission yeast.

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

72 Here we show that TD-60 exhibits GEF activity, in vitro and in cells, for the small GTPas

73 s and that tumor cells engineered to express GEF-deficient GIV fail to transduce integrin signals int

74 ify the guanosine nucleotide exchange factor GEF-H1 as critical for shear stress-induced transendothe

75 on of the guanine nucleotide exchange factor GEF-H1, thereby stimulating its ability to activate the

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

77 1, a Rac-guanine nucleotide exchange factor (GEF) aberrantly expressed in breast cancer.

78 but its guanine-nucleotide exchange factor (GEF) activators seem dispensable for this process, which

79 c-8A has guanine nucleotide exchange factor (GEF) activity and is a chaperone for several classes of

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

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

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

83 ts DOCK8 guanine nucleotide exchange factor (GEF) activity while sparing protein expression also impa

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

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

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

87 y of the guanine nucleotide exchange factor (GEF) catalytic activity and of the presence of RAP1.

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

89 bunit of guanine nucleotide exchange factor (GEF) eIF2B.

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

91 -8b is a guanine nucleotide exchange factor (GEF) expressed in the olfactory epithelium and in the st

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

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

94 nctional guanine-nucleotide-exchange factor (GEF) for Rho GTPases that is characterized by its locali

95 X2) is a guanine nucleotide exchange factor (GEF) for the Ras-related C3 botulinum toxin substrate 1

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

97 hat GIV/Girdin, a guanidine exchange factor (GEF) for the trimeric G protein Galphai, is another majo

98 sociates with Cdc42 guanine exchange factor (GEF) Gef1, limiting Gef1 availability to promote Cdc42 a

99 receptor guanine nucleotide exchange factor (GEF) GIV (also known as Girdin), a metastasis-associated

100 hai proteins by the guanine exchange factor (GEF) GIV.

101 ARL-13 acts as a nucleotide exchange factor (GEF) of ARL-3, while UNC-119 can stabilize the GTP bindi

102 egulated guanine nucleotide exchange factor (GEF) of the Rac small GTPase, for its potential involvem

103 that the guanine nucleotide exchange factor (GEF) of Ypt7 (the Mon1-Ccz1 complex) and BLOC-1 both loc

104 r 1 (GDI1), but not guanine exchange factor (GEF) or GTPase-activating protein (GAP) enzymes, and is

105 is a Rac-guanine nucleotide exchange factor (GEF) overexpressed in a significant proportion of human

106 Ras/Rap guanine nucleotide exchange factor (GEF) PDZ-GEF1.

107 y resembles the Ran guanine exchange factor (GEF) RCC1, but has not previously been shown to have GEF

108 1 and the nuclear guanosine exchange factor (GEF) RCC1.

109 T-2, the guanine nucleotide exchange factor (GEF) required for RhoA activation, is activated by the c

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

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

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

113 ex1 is a guanine-nucleotide exchange factor (GEF) that activates the small G protein (GTPase) Rac1 to

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

115 alGDS, a guanine nucleotide exchange factor (GEF) that precipitated the assembly of the exocyst compl

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

117 The Rac1 guanine nucleotide exchange factor (GEF) Trio is essential for netrin-1-induced axon outgrow

118 io, as a guanine nucleotide exchange factor (GEF) upstream of both CED-10 and MIG-2.

119 ver, the guanine nucleotide exchange factor (GEF) which activates Arl3 is unknown.

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

121 specific guanine nucleotide exchange factor (GEF), displayed limited migration and recruitment of neu

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

123 the cAMP-dependent Rap1 GTP exchange factor (GEF), Epac, known to down-regulate RhoA activity through

124 cognate guanine nucleotide exchange factor (GEF), Rabin8 (by using the Ser111Glu phosphorylation mim

125 (GIV), a guanine-nucleotide exchange factor (GEF), transactivates Galpha activity-inhibiting polypept

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

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

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

129 ated Rho guanine nucleotide exchange factor, GEF-H1, participates in TRPC3-mediated RhoA activation i

130 taining guanine nucleotide exchange factors (GEFs) 1 and 2, regulator of G protein signaling (RGS)-ho

131 Guanine nucleotide exchange factors (GEFs) activate and GTPase-activating proteins (GAPs) inh

132 mily of guanine nucleotide exchange factors (GEFs) activates Rho GTPases, leading to important roles

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

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

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

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

137 uk1 are guanine nucleotide exchange factors (GEFs) in Saccharomyces cerevisiae that regulate membrane

138 -family guanine nucleotide exchange factors (GEFs) Muk1 and Vps9.

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

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

141 hat the guanine nucleotide exchange factors (GEFs) UNC-73/Trio and TIAM-1 promote anterior and poster

142 by Rho guanine nucleotide exchange factors (GEFs), are conserved molecular switches for signal trans

143 ated by guanine nucleotide exchange factors (GEFs), are essential regulators of polarized cell growth

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

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

146 related guanine nucleotide exchange factors (GEFs), PDZ-RhoGEF and leukemia-associated RhoGEF (LARG),

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

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

149 tion of guanine nucleotide exchange factors (GEFs), which activate these GTPases, in spine and synaps

150 h ROR2 and recruit guanine exchange factors (GEFs), which activated Rac1 and RhoA; siRNA-mediated sil

151 ated by guanine nucleotide exchange factors (GEFs).

152 by Rho guanine nucleotide exchange factors (GEFs).

153 f Rab11 guanine nucleotide exchange factors (GEFs).

154 ivating guanine nucleotide exchange factors (GEFs).

155 In this study we show that the Rho family GEF Asef2 is found at synaptic sites, where it promotes

156 initive evidence that TRAPPII is a bona fide GEF for the yeast Rab11 homologues Ypt31/32.

157 lanine scanning reveals residues crucial for GEF activity within that sequence.

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

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

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

161 mechanism of action of a nonreceptor Galpha GEF.

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

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

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

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

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

167 These results illuminate how GIV-GEF is turned on upon receptor activation, adds GIV to t

168 idence for such reversible regulation of GIV-GEF in skeletal muscles from patients with IR.

169 However, what turns on GIV-GEF downstream of growth factor RTKs remained unknown.

170 racellular matrix (ECM) also converge on GIV-GEF via beta1 integrins and that focal adhesions (FAs) s

171 We also provide evidence that GIV-GEF serves as therapeutic target for exogenous manipulat

172 Thus GIV-GEF serves as a unifying platform for integration and am

173 We found that mice lacking GEF-H1 (GEF-H1(-/-)), a RhoA-specific guanine nucleotide exchang

174 1, but has not previously been shown to have GEF activity.

175 ers; PFS was significantly lower in the high-GEFs versus the low-GEFs groups [H.R = 5, 20 (95% CI; 2,

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

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

178 3B Joubert-Syndrome patient mutations impair GEF activity and thus Arl3 activation.

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

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

181 Increased GEF-H1 association with cingulin was essential for down-

182 and RhoGEF-H1 protein expression, increased GEF-H1 activity, with a trend in increased p63RhoGEF act

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

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

185 f Nox2 attenuated mechanical stretch-induced GEF-H1 activation in cardiomyocytes.

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

187 y are capable of dose-dependently inhibiting GEF catalytic activity, binding to SOS1 with micromolar

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

189 s and phosphorylates GIV at Ser1674 near its GEF motif.

190 ponse and glucose uptake in myotubes via its GEF function.

191 on pattern due to the distinct action of its GEFs, Gef1 and Scd1, in fission yeast.

192 We found that mice lacking GEF-H1 (GEF-H1(-/-)), a RhoA-specific guanine nucleotide

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

194 omer with distinct VPS9 GEFs could thus link GEF-dependent regulatory inputs to the temporal or spati

195 These RhoA/B/C FRET sensors show localized GEF and GAP activity and reveal spatial activation diffe

196 cantly lower in the high-GEFs versus the low-GEFs groups [H.R = 5, 20 (95% CI; 2,15-12,57)].

197 Finally, we used these sensors to monitor GEF-specific differential activation of RhoA/B/C.

198 the balance of positive (GAP) and negative (GEF) regulators in the system.

199 evealed that expression of wild-type but not GEF-dead PREX1 resulted in the formation of larger tumor

200 restored by expression of wild-type but not GEF-dead-PREX1.

201 Expression of wild-type but not GEF-inactive PREX1 increased anchorage-independent cell

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

203 ystem depends on PI3K-mediated activation of GEF-H1 and p115 RhoGEF.

204 was associated with increased activation of GEF-H1 and RhoA detected in pulldown activation assays.

205 ults demonstrate the role for association of GEF-H1 with cingulin as the mechanism of RhoA pathway in

206 s and synapses is abrogated by expression of GEF activity-deficient Asef2 mutants or by knockdown of

207 of cingulin was required for inactivation of GEF-H1 and endothelial cell barrier preservation.

208 utively associated with STAT3 independent of GEF activity, whereas it regulated STAT3 phosphorylation

209 1, in the absence of cAMP, and inhibition of GEF activity in the presence of cAMP.

210 ays to identify small molecule inhibitors of GEF catalytic activity toward Ras.

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

212 rawling of neutrophils and relocalization of GEF-H1 to flotillin-2-rich uropods.

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

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

215 is required for Wnt5a-induced recruitment of GEFs to ROR1/ROR2.

216 o the traditional view focusing primarily on GEF distribution and exchange reaction.

217 d Gbetagamma, and further regulation of PREX GEF activity occurs by phosphorylation.

218 sphorylation also negatively regulates PREX1 GEF activity.

219 PREX1 and PREX2 GEF activity is activated by the second messengers PIP3

220 tes its own inactivation by decreasing PREX2 GEF activity.

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

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

223 Using physiological Rab-GEF reconstitution reactions, we now provide definitive

224 We show that Vps9 is the primary Rab5 GEF required for biogenesis of late endosomal multivesic

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

226 nsitive and require CD44s binding to the Rac GEF TIAM1.

227 Here we show that Tiam1 and P-Rex1, two Rac GEFs, promote Rac1 anti- and pro-migratory signalling ca

228 Rac-GEF activity assays with purified recombinant proteins s

229 e the possibility of cooperation between Rac-GEF families.

230 Therefore, PREX1-Rac-GEF activity is critical for PREX1-dependent anchorage-i

231 e basal, PIP3- and Gbetagamma-stimulated Rac-GEF activity of P-Rex1.

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

233 Therefore, platelet P-Rex and Vav family Rac-GEFs play important proinflammatory roles in leukocyte r

234 sociated with the N-terminal region and Rac1 GEF domain of Trio.

235 suggest an unconventional mechanism for Rag GEF activity.

236 platform established here for targeting Ras GEF enzymes could be broadly useful for identifying lead

237 xt of the multistep process by which the Ras GEF (guanine nucleotide exchange factor) activity of SOS

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

239 d ROR1/ROR2 heterooligomers, which recruited GEFs, and enhanced proliferation, cytokine-directed migr

240 AK-mediated phosphorylation of PREX2 reduced GEF activity toward Rac1 by inhibiting PREX2 binding to

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

242 Here we show that the mammalian Rho GEF homolog, ECT-2, functions through the conserved RAS/

243 Rho guanine nucleotide exchange factors (Rho GEFs) activate Rac GTPases to regulate cell migration, i

244 GTPases (Cdc42 and Rho1-Rho5) and seven Rho GEFs (Scd1, Rgf1-Rgf3, and Gef1-Gef3).

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

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

247 type guanine nucleotide exchange factor (Rho-GEF) homologous to Beta-PIX and Alpha-PIX in mammals.

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

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

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

251 e protein levels and localization of the Rho-GEF Rgf3, which in turn modulates active Rho1 levels dur

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

253 However, the regulation of Rho-GEFs themselves is not well understood.

254 d GAP (C-GAP), which coordinates with a RhoA GEF, RhoGEF2, to organize spatiotemporal contractility d

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

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

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

258 second phosphomodification terminates GIV's GEF function, triggers the assembly of GIV-Galphas compl

259 of GIV-Galphai complexes and activates GIV's GEF function; then a second phosphomodification terminat

260 ease in the expression of the Cdc42-specific GEF DOCK10.

261 e (6-TGDP)-Rac1 adduct, RhoGEF (Rho-specific GEF) cannot exchange the 6-TGDP adducted on Rac1 with fr

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

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

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

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 ngulin-truncated mutants, we determined that GEF-H1 interaction with the rod + tail domain of cinguli

268 The GEF activity of Arl13B is mediated by the G-domain plus

269 noviral rescue, we demonstrate that both the GEF (CDC25 homology domain) and RA2 domains of PLC are r

270 1 activity in platelets is controlled by the GEF CalDAG-GEFI and an unknown regulator that operates d

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

272 Ric-8 GEF activity clearly differs from the GEF activity of G protein-coupled receptors (GPCRs).

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

274 in Arl13B mutated in Joubert syndrome is the GEF for Arl3, and its function is conserved in evolution

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

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

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

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

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

280 The GEFs for Rho2-Rho5 have not been unequivocally assigned.

281 The GEFs were stronger prognostic markers than two other mar

282 Thus we define unique roles of the GEFs Gef1 and Scd1 in the regulation of distinct events

283 Rac subfamily GTPases act downstream of the GEFs; CED-10/Rac1 is activated by TIAM-1, whereas CED-10

284 teins, the poor prognosis conferred by these GEFs in CTCs implies that hyperactivation of G-protein s

285 eractivation of G-protein signaling by these GEFs is an important event during metastatic progression

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

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

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

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

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

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

292 t with CYK-4 RhoGAP activity contributing to GEF activation, the catalytic domains of CYK-4 and ECT-2

293 We also found that different Ras-to-GEF positive feedback mechanisms could reshape output dy

294 er static conditions, shear stress triggered GEF-H1-dependent spreading and crawling of neutrophils a

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

296 gly suggest that microtubule-localized TRPC3-GEF-H1 axis mediates fibrotic responses commonly in card

297 These two GEFs are further regulated by FAK/ERK and Src family kin

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

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

300 e interaction of retromer with distinct VPS9 GEFs could thus link GEF-dependent regulatory inputs to