ライフサイエンスコーパス: RhoGEF

1 RhoGEFs activate small molecular weight GTPases at the p

2 RhoGEFs are central controllers of small G-proteins in c

3 RhoGEFs promote formation of the active GTP-bound state

4 upting any component of the S1pr2/Galpha(13)/RhoGEF pathway impairs endoderm convergence during segme

5 trate for the first time that the Galpha(13)/RhoGEF-dependent pathway functions downstream of S1pr2 t

6 WD40, protein kinase, Src homology 2 and 3, RhoGEF, and pleckstrin homology domains involved in cell

7 Caenorhabditis elegans UNC-73 RhoGEF isoforms function in axon guidance, cell migratio

8 CV-mediated signaling defects, rescue unc-73 RhoGEF-2 and rab-2 lethargic movement phenotypes.

9 temporal and spatial requirements of UNC-73 RhoGEF-2 isoform function in mutant rescue experiments.

10 Together, these data suggest UNC-73 RhoGEF-2 isoforms are required for proper neurotransmitt

11 ent with peptidergic neuron function, unc-73 RhoGEF-2 mutants exhibit a decreased level of neuropepti

12 Although unc-73 RhoGEF-2 mutants have grossly normal synaptic morphology

13 The UNC-73E RhoGEF-2 isoform is activated by the G-protein subunit G

14 small interfering RNA against ARHGEF1 and a RhoGEF inhibitor prevented the effects of TGF-beta on Rh

15 Fgd1 contains a RhoGEF domain specific for Cdc42.

16 vergence of many ASD-related genes.Trio is a RhoGEF protein that promotes actin polymerization and is

17 Ect2 is a RhoGEF that plays a well-established role in formation o

18 eletion of the active site of the obscurin A RhoGEF domain in order to examine its functions in zebra

19 Light-mediated recruitment of a RhoGEF domain to the plasma membrane leads to rapid indu

20 ng-and also defines the essential roles of a RhoGEF-anillin module in septin architectural remodeling

21 rotein sequence contains in its C-terminus a RhoGEF domain followed by a pleckstrin domain.

22 2 to regulate myocardial migration through a RhoGEF-dependent pathway.

23 ng actin cytoskeleton organization through a RhoGEF/Rho-dependent pathway.

24 n dynamics, Rho GTPases and their activators RhoGEFs are implicated in various aspects of neuronal di

25 n, are dependent upon a catalytically active RhoGEF domain.

26 oguanosine diphosphate (6-TGDP)-Rac1 adduct, RhoGEF (Rho-specific GEF) cannot exchange the 6-TGDP add

27 sequential activation of Galpha(q)/alpha13, RhoGEF, and RhoA, and involve Rho kinase-mediated phosph

28 lyR beta subunit (GLRB), gephyrin (GPHN) and RhoGEF collybistin (ARHGEF9).

29 T is associated with increased p63RhoGEF and RhoGEF-H1 protein expression, increased GEF-H1 activity,

30 ts provide in vivo evidence that the Ras and RhoGEF domains of Sos are separable signaling modules an

31 Its N-terminus, central region and RhoGEF/pleckstrin domain are homologous to the recently

32 However, deletion of RhoGEF or SH3 and RhoGEF domains did not result in any phenotypic changes,

33 that oligomerization of leukemia-associated RhoGEF (LARG) functions to prevent nucleocytoplasmic shu

34 leotide exchange factor (leukemia-associated RhoGEF (LARG)) in human head and neck squamous carcinoma

35 Here we show that leukemia-associated RhoGEF (LARG), a RhoA-specific RGS-RhoGEF, is required f

36 activation: PDZ-RhoGEF, leukemia-associated RhoGEF (LARG), and p115RhoGEF.

37 hoA GEFs, PDZ-RhoGEF and leukemia-associated RhoGEF (LARG), link bombesin receptors to RhoA in a non-

38 s (GEFs), PDZ-RhoGEF and leukemia-associated RhoGEF (LARG), use their PDZ domains to bind class B ple

39 es cell motility through leukemia-associated RhoGEF (LARG)-dependent Rho GTPase activation.

40 des PDZ-RhoGEF (PRG) and leukemia-associated RhoGEF (LARG).

41 de exchange factor (GEF) leukemia-associated RhoGEF (LARG)/RhoA pathway in skin homeostasis.

42 y of both p115RhoGEF and leukemia-associated RhoGEF but not PDZ-RhoGEF.

43 but not of PDZ RhoGEF or leukemia-associated RhoGEF in human aortic smooth muscle cells (HASMCs).

44 ors p115RhoGEF and LARG (leukemia-associated RhoGEF), fails to stimulate Rho-dependent transcriptiona

45 in-containing RhoGEF and leukemia-associated RhoGEF), RGS3 and RGS12, spinophilin and neurabin-1, SRC

46 s (RhoGEFs) (p115RhoGEF, leukemia-associated RhoGEF, and PDZ-RhoGEF) contain an RH domain and are spe

47 ponses to p115RhoGEF and leukemia-associated RhoGEF.

48 at Ser-70, while only mutants unable to bind RhoGEFs also decreased cellular levels of Bcl-2.

49 previously been shown to interact with both RhoGEF (guanine nucleotide exchange factors) and RhoGAP

50 of direct and independent activation of both RhoGEFs as well as their co-recruitment due to heterodim

51 an-cultured blood vessels, we show that both RhoGEFs are activated by the physiologically and pathoph

52 RGS)-homology-RhoGEFs (PDZ domain-containing RhoGEF and leukemia-associated RhoGEF), RGS3 and RGS12,

53 of an essential role for the RGS-containing RhoGEF family in signaling to Rho by Galpha12/13-coupled

54 G protein signaling (RGS) domain-containing RhoGEFs (RGS-RhoGEFs) that link activated heterotrimeric

55 We hypothesized that RGS domain-containing RhoGEFs, especially LARG, participate in linking GPCR to

56 13 proteins via RH (RGS homology) containing RhoGEFs.

57 RGS-containing RhoGEFs (RGS-RhoGEFs) represent a direct link between th

58 blasts defective in all three RGS-containing RhoGEFs.

59 that the most active form of the cytokinetic RhoGEF involves complex formation between ECT-2, central

60 In this review, we summarize the role of Dbl RhoGEFs in development and disease, with a focus on Ect2

61 Silencing (siRNA) CD44, EphA2, PATJ, or Dbs (RhoGEF) expression blocked LMW-HA-mediated angiogenesis

62 that LARG is a novel and temporally distinct RhoGEF required for completion of abscission.

63 al. (2016) reveal how acute effects of DOCK6 RhoGEF depletion on RAC1 and CDC42 activation are revers

64 Here, we report that Kalirin9, a dual RhoGEF, binds p75 directly and regulates p75-Nogo recept

65 Pase reflects the very specific role of each RhoGEF in controlling distinct signaling mechanisms invo

66 eterotrimers, indicating that these effector RhoGEFs can engage Galpha13.R7-RGS complexes.

67 hoGEF domain that are predicted to eliminate RhoGEF activity inhibit RhoA activation.

68 anding of Galpha(s) activity and establishes RhoGEF coupling as a universal Galpha function.

69 the Rho guanine-nucleotide-exchange factor (RhoGEF) Bud3, and the anillin-like protein Bud4 exclusiv

70 functions of its RhoGTPase Exchange Factor (RhoGEF) domain have not been characterized.

71 specific guanine nucleotide exchange factor (RhoGEF) domain that is retained within p210 Bcr-Abl.

72 the Rho guanine nucleotide exchange factor (RhoGEF) Ect2 to the central spindle, abolishes RhoA GTPa

73 Rho guanine-nucleotide exchange factor (RhoGEF) proteins as powerful modulators of glutamatergic

74 specific guanine nucleotide exchange factor (RhoGEF) that regulates neurotrophin-3-induced cell migra

75 The Rho-guanine nucleotide exchange factor (RhoGEF) TRIO acts as a key regulator of neuronal migrati

76 The Rho guanine nucleotide exchange factor (RhoGEF) Trio promotes actin polymerization by directly a

77 specific guanine nucleotide exchange factor (RhoGEF) with in vitro exchange activity specific for Rho

78 ning Rho guanine nucleotide exchange factor (RhoGEF), has been studied primarily in tissue culture, w

79 RH) Rho guanine nucleotide exchange factors (RhoGEFs) (p115RhoGEF, leukemia-associated RhoGEF, and PD

80 Rho guanine-nucleotide exchange factors (RhoGEFs) activate Rho GTPases, and thereby regulate cyto

81 ify Rho guanine nucleotide exchange factors (RhoGEFs) activated during cardiac pressure overload in v

82 idomain guanine nucleotide exchange factors (RhoGEFs) and GTPase-activating proteins (RhoGAPs).

83 ily Rho guanine nucleotide exchange factors (RhoGEFs) can serve as the direct downstream effectors of

84 pecific guanine nucleotide exchange factors (RhoGEFs) PDZ-RhoGEF and LARG that stimulate the GDP-GTP

85 and Rho guanine nucleotide exchange factors (RhoGEFs) related to Trio, in a strikingly similar fashio

86 by Rho guanine nucleotide exchange factors (RhoGEFs), a family of proteins involved in the activatio

87 e activated by Rho guanine exchange factors (RhoGEFs), but the RhoGEF(s) required for LTP also remain

88 mily of guanine nucleotide exchange factors (RhoGEFs), which includes PDZ-RhoGEF (PRG) and leukemia-a

89 ous Rho guanine nucleotide exchange factors (RhoGEFs).

90 the Rho guanine nucleotide exchange factors (RhoGEFs).

91 family guanine nucleotide exchange factors (RhoGEFs).

92 ly of RhoGEFs is comprised of the Dbl family RhoGEFs with 70 human members.

93 Here we show that the protein Farp1 [FERM, RhoGEF (ARHGEF), and pleckstrin domain protein 1], a Rac

94 metaphase furrows, a function distinct from RhoGEF/Pebble and likely due to the absence of a RacGAP5

95 ss to separate the role of microtubules from RhoGEF activation.

96 G alpha12Q229L variants uncoupled from RhoGEFs (but not fully functional activated G alpha12Q22

97 Mutations in human FYVE, RhoGEF, and PH domain-containing 1 (FGD1) cause faciogen

98 a new endothelial specific gene named FYVE, RhoGEF, and PH domain-containing 5 (FGD5) that plays a c

99 There are three Rho-specific GEFs (RhoGEFs) in vascular smooth muscle that contain a bindin

100 ulator of G protein signaling (RGS)-homology-RhoGEFs (PDZ domain-containing RhoGEF and leukemia-assoc

101 lization, we reveal at the systems level how RhoGEFs and RhoGAPs contextualize and spatiotemporally c

102 There are at least 22 human RhoGEFs that contain SH3 domains, raising the possibilit

103 stiffening to Xlfc, a previously identified RhoGEF, which binds microtubules and regulates the actom

104 e findings reveal a dual role for Galphaq in RhoGEF activation, as it both recruits and allostericall

105 RhoGEF(619) to the plasma membrane increases RhoGEF activity towards RhoA, but full activation requir

106 During cytokinesis, RhoA is activated by its RhoGEF, ECT2.

107 or its Bud4-interacting domain, but not its RhoGEF domain, leads to a complete loss of the single fi

108 t splice form of the multifunctional Kalirin RhoGEF, includes a PDZ [postsynaptic density-95 (PSD-95)

109 ch in PRG-PH that is conserved among all Lbc RhoGEFs.

110 nlike the zygotic, central spindle-localized RhoGEF (Pebble), RhoGEF2 localizes to metaphase furrows,

111 The catalytic activity of membrane-localized RhoGEFs is not dependent on activated Galpha13.

112 Like many RhoGEF family members, the in vivo exchange activity of

113 of the importance of the obscurin A-mediated RhoGEF signaling in vertebrate organogenesis and highlig

114 Our resource enabled us to uncover a multi-RhoGEF complex downstream of G-protein-coupled receptors

115 e "Ras-binding domain." Syx is a multidomain RhoGEF that participates in early zebrafish development.

116 he utilization of this mechanism by multiple RhoGEFs suggests that this regulatory paradigm may be a

117 is requires the concerted effort of multiple RhoGEFs.

118 Thus, a novel RhoGEF(Pbl)-dependent input promotes the simultaneous as

119 s because of the ongoing combined actions of RhoGEF and RhoGAP.

120 a indicate that in addition to activation of RhoGEF(s), reduction of RhoGAP (p190) is a critical mech

121 However, deletion of RhoGEF or SH3 and RhoGEF domains did not result in any p

122 gf-1 and rga-5 genes, encoding homologues of RhoGEF and RhoGAP, respectively, as regulators of axon r

123 nd PH could play a key role in regulation of RhoGEF activity in vivo.

124 In this review, we focus on the ability of RhoGEFs and RhoGAPs to form complexes with diverse bindi

125 show that the recruitment and activation of RhoGEFs is the cause of a significant time lag between t

126 ignaling via Galphaq-dependent activation of RhoGEFs such as p63.

127 d are sufficient to modulate the activity of RhoGEFs by hormones via mediating their localization to

128 gical roles of this RGS-containing family of RhoGEFs in vivo.

129 The largest family of RhoGEFs is comprised of the Dbl family RhoGEFs with 70 h

130 is predicted to exist in a broader family of RhoGEFs that includes p115-RhoGEF, Lbc, Lfc, Net1, and X

131 even members of the homologous Lbc family of RhoGEFs which includes the RH-RhoGEFs.

132 s of the poorly characterized DOCK family of RhoGEFs, we performed gene expression profiling of fluor

133 be a common feature in the broader family of RhoGEFs.

134 isolated rat bronchioles, and inhibitors of RhoGEFs (Y16) and Rho-kinase (Y27632), but not the SrcFK

135 bling the well-known activation mechanism of RhoGEFs activated by Galpha12/13.

136 The multitude of RhoGEFs that activate a single Rho GTPase reflects the v

137 ding leading to a transcriptional program of RhoGEFs that facilitate nMRTF activity.

138 that PDZ-RhoGEF, a member of a subfamily of RhoGEFs that contain regulator of G protein signaling do

139 ion that is integral to the formation of one RhoGEF array.

140 atory mechanism that is likely used by other RhoGEF family members.

141 In contrast to studies of other RhoGEFs, particularly Ect2 and GEF-H1, LARG depletion do

142 lpha12-dependent Pyk2-mediated Gab1 and p115 RhoGEF interactions, leading to Rac1- and RhoA-targeted

143 sine phosphorylation of Pyk2, Gab1, and p115 RhoGEF, leading to Rac1- and RhoA-dependent Pak2 activat

144 PI3K-mediated activation of GEF-H1 and p115 RhoGEF.

145 12 negated thrombin-induced Pyk2, Gab1, p115 RhoGEF, Rac1, RhoA, and Pak2 activation, leading to atte

146 ombin-induced activation of Pyk2, Gab1, p115 RhoGEF, Rac1, RhoA, and Pak2, resulting in diminished TH

147 inhibition or depletion of Pyk2, Gab1, p115 RhoGEF, Rac1, RhoA, or Pak2 levels substantially attenua

148 In Galphaq, p115 RhoGEF, and RhoA-depleted human umbilical vein ECs, thro

149 i/o-Fyn signaling mediates MCP1-induced p115 RhoGEF and Rac1 GTPase activation.

150 servations, balloon injury (BI) induced p115 RhoGEF tyrosine phosphorylation in rat common carotid ar

151 Moreover, p115 RhoGEF inhibition suppressed MCP1-induced HASMC migratio

152 CP1 induced tyrosine phosphorylation of p115 RhoGEF but not of PDZ RhoGEF or leukemia-associated RhoG

153 Furthermore, depletion of p115 RhoGEF levels also abrogated MCP1- or BI-induced Rac1-NF

154 Src family kinases in the regulation of p115 RhoGEF.

155 tified phosphorylation of serine 240 on p115 RhoGEF by PKC to be the mechanistic link between PKC and

156 n cells surrounding a dying cell target p115 RhoGEF to the actin cortex to control where contraction

157 n neighboring cells reorient and target p115 RhoGEF to this site.

158 These findings suggest that p115 RhoGEF is critical for MCP1-induced HASMC migration and

159 1/CDK6 and upstream of CDK4-PAK1 in the p115 RhoGEF-Rac1-NFATc1-cyclin D1-CDK6-PKN1-CDK4-PAK1 signali

160 eam to Pyk2, Gab1 formed a complex with p115 RhoGEF involving their pleckstrin homology domains.

161 ciation with nucleotide exchange factor p115-RhoGEF, and myosin light chain phosphorylation, which wa

162 broader family of RhoGEFs that includes p115-RhoGEF, Lbc, Lfc, Net1, and Xpln, and identify regions w

163 G), leukemia-associated Rho GEF (LARG), p115-RhoGEF (p115), lymphoid blast crisis (Lbc), and Dbl.

164 Expression of dominant negative p115-RhoGEF or p115RhoGEF-specific siRNA inhibited both RhoA

165 Although the GEF activity of p115-RhoGEF (p115), an RGS-RhoGEF, can be stimulated by Galph

166 hosphorylation of p115 RhoGEF but not of PDZ RhoGEF or leukemia-associated RhoGEF in human aortic smo

167 PDZ-RhoGEF exists in cells as a dimer, raising the possibili

168 PDZ-RhoGEF is a member of the regulator family of G protein

169 PDZ-RhoGEF-deficient mice were protected from diet-induced o

170 Interestingly, while characterizing a PDZ-RhoGEF antiserum, we found that a transfected PDZ-RhoGEF

171 t focal adhesion kinase, which activates PDZ-RhoGEF and LARG, is required for bombesin-stimulated Rho

172 ble of linking GPCRs to RhoA activation: PDZ-RhoGEF, leukemia-associated RhoGEF (LARG), and p115RhoGE

173 specific interaction between plexin and PDZ-RhoGEF and to signaling by plexin in the cell.

174 We find that G12/13 and PDZ-RhoGEF are required for entotic invasion, which is drive

175 5RhoGEF, leukemia-associated RhoGEF, and PDZ-RhoGEF) contain an RH domain and are specific GEFs for t

176 DH/PH constructs of p115RhoGEF/ARHGEF1, PDZ-RhoGEF (PRG)/ARHGEF11, and LARG/ARHGEF12.

177 construct associated with the endogenous PDZ-RhoGEF.

178 cific guanine nucleotide exchange factor PDZ-RhoGEF (Arhgef11) in white adipose tissue biology.

179 -Rho guanine nucleotide exchange factor (PDZ-RhoGEF) that was associated with and inhibited by microt

180 tin cytoskeleton as a novel function for PDZ-RhoGEF, thus implicating actin interaction in organizing

181 anine nucleotide exchange factor (GEF)), PDZ-RhoGEF, and p115RhoGEF augmented interaction between act

182 nine nucleotide exchange factors (GEFs), PDZ-RhoGEF and leukemia-associated RhoGEF (LARG), use their

183 e also show that two of these RhoA GEFs, PDZ-RhoGEF and leukemia-associated RhoGEF (LARG), link bombe

184 nge factor for Rho family small GTPases, PDZ-RhoGEF.

185 define a novel actin-binding sequence in PDZ-RhoGEF with a critical amino acid motif of IIxxFE.

186 nce of a novel 25-amino acid sequence in PDZ-RhoGEF, located at amino acids 561-585, that is necessar

187 change factors (RhoGEFs), which includes PDZ-RhoGEF (PRG) and leukemia-associated RhoGEF (LARG).

188 ange factors (RGL-RhoGEFs) that includes PDZ-RhoGEF (PRG), p115RhoGEF, and LARG, thereby regulating c

189 12/13 GPCRs to Rho activation, including PDZ-RhoGEF (PRG), leukemia-associated Rho GEF (LARG), p115-R

190 On a whole organism level, PDZ-RhoGEF deletion resulted in an acute increase in energy

191 Mechanistically, PDZ-RhoGEF enhanced insulin/IGF-1 signaling in adipose tissu

192 Furthermore, overexpression of a minimal PDZ-RhoGEF fragment can down-regulate cAMP signaling, sugges

193 F and leukemia-associated RhoGEF but not PDZ-RhoGEF.

194 erization of the actin-binding region of PDZ-RhoGEF revealed a dimerization-dependent actin bundling

195 el mechanism controlling the activity of PDZ-RhoGEF, LARG, and p115RhoGEF, which involves homo- and h

196 exinB2 in complex with the PDZ domain of PDZ-RhoGEF.

197 licating actin interaction in organizing PDZ-RhoGEF signaling.

198 ne nucleotide exchange factors (RhoGEFs) PDZ-RhoGEF and LARG that stimulate the GDP-GTP exchange rate

199 Unique among the RGS-RhoGEFs, PDZ-RhoGEF contains a short sequence that localizes the prot

200 Our results demonstrate that PDZ-RhoGEF acts as a key determinant of mammalian metabolism

201 as a dimer, raising the possibility that PDZ-RhoGEF could influence actin structure in a manner indep

202 This report demonstrates that PDZ-RhoGEF, a member of a subfamily of RhoGEFs that contain

203 L that mediates its interaction with the PDZ-RhoGEF protein.

204 ted from Gbetagamma to interact with the PDZ-RhoGEF-RGS domain.

205 F antiserum, we found that a transfected PDZ-RhoGEF construct associated with the endogenous PDZ-RhoG

206 Unconventionally, PDZ-RhoGEF (PRG), a member of the RGS-RhoGEFs, binds tightly

207 While PDZ-RhoGEF was dispensable for a number of RhoA signaling-me

208 Taken together, results with PDZ-RhoGEF and frabin identify a novel actin-binding sequenc

209 rminus of the RhoGEF frabin, and as with PDZ-RhoGEF, mutagenesis and actin interaction experiments de

210 t the substrate utilization of a promiscuous RhoGEF family member.

211 using the multidomain protein RGBARG (RCC1, RhoGEF, BAR, and RasGAP-containing protein).

212 ediated inhibition of RhoA and also recruits RhoGEFs to directly stimulate RhoA activity.

213 We define two separable and redundant RhoGEF/Pebble-dependent inputs into Sticky recruitment t

214 each now known to directly bind and regulate RhoGEFs.

215 F) family; however, mechanisms that regulate RhoGEFs are not well understood.

216 n contrast, p63RhoGEF, a Galpha(q)-regulated RhoGEF, appears to be constitutively localized to the PM

217 PCRs and effectors such as G alpha-regulated RhoGEFs, but also novel conformational changes that are

218 , as opposed to other known Galpha-regulated RhoGEFs, which are instead sequestered in the cytoplasm,

219 e known G protein-coupled receptor-regulated RhoGEFs are found in the cytoplasm of unstimulated cells

220 ase Ras homolog family member J by releasing RhoGEF Tuba from direct binding to PlexinD1, thus mediat

221 skeleton reorganization via their respective RhoGEF effectors.

222 onal interaction between G alpha(13) and RGL-RhoGEFs based on the structure of RGL domains and their

223 Rho guanine nucleotide exchange factors (RGL-RhoGEFs) that includes PDZ-RhoGEF (PRG), p115RhoGEF, and

224 association results in the activation of RGL-RhoGEFs are still poorly understood.

225 2), which acts via the single C. elegans RGS RhoGEF (RHGF-1).

226 e GEF activity of p115-RhoGEF (p115), an RGS-RhoGEF, can be stimulated by Galpha(13), the exact mecha

227 ssociated RhoGEF (LARG), a RhoA-specific RGS-RhoGEF, is required for abscission, the final stage of c

228 into the mechanism of regulation of the RGS-RhoGEF and broadens our understanding of G protein signa

229 tor of G protein signaling (RGS) domain (RGS-RhoGEFs).

230 ct of this mutation in its regulation of RGS-RhoGEFs p115 or LARG.

231 RGS-containing RhoGEFs (RGS-RhoGEFs) represent a direct link between the G(12) class

232 gnaling (RGS) domain-containing RhoGEFs (RGS-RhoGEFs) that link activated heterotrimeric G protein al

233 nally, PDZ-RhoGEF (PRG), a member of the RGS-RhoGEFs, binds tightly to both nucleotide-free and activ

234 Unique among the RGS-RhoGEFs, PDZ-RhoGEF contains a short sequence that local

235 lpha13 is important for interaction with RGS-RhoGEFs and is critically involved in the regulation of

236 hological effects of expressing shortened RH-RhoGEF DH/PH constructs of p115RhoGEF/ARHGEF1, PDZ-RhoGE

237 RH-RhoGEFs are a family of guanine nucleotide exchange fact

238 leotide exchange factor (GEF) activity of RH-RhoGEFs, leading to activation of RhoA.

239 Galpha(13) stimulates the GEF activity of RH-RhoGEFs, such as p115RhoGEF, has not yet been fully eluc

240 em to rapidly control the localization of RH-RhoGEFs.

241 the RGS-homology (RH) domains of several RH-RhoGEFs allosterically activates these proteins, causing

242 lpha proteins might directly regulate the RH-RhoGEFs was not known.

243 Lbc family of RhoGEFs which includes the RH-RhoGEFs.

244 Because all three RH-RhoGEFs can localize to the plasma membrane upon express

245 nge factors for the monomeric G protein Rho (RhoGEFs) are well characterized as effectors of this G p

246 s-specific role is independent of ARHGEF17's RhoGEF activity in interphase.

247 Based on the homology of our protein's RhoGEF domain to the RhoGEF domains of Trio, Duo and Due

248 howed that this mechanism relies on the same RhoGEF-RhoGTPase cascade components that are up-regulate

249 of F-actin assembly, we uncovered a separate RhoGEF(Pbl)-dependent pathway that, at the normal time o

250 can facilitate increased activity of soluble RhoGEFs on vesicle-delimited substrate (RhoA-GDP).

251 essed UNC-73 isoforms contain a Rac-specific RhoGEF-1 domain, a Rho-specific RhoGEF-2 domain, or both

252 Rac-specific RhoGEF-1 domain, a Rho-specific RhoGEF-2 domain, or both domains.

253 provide evidence that developmentally staged RhoGEFs control assembly of two alternative forms of cle

254 WH2 domain, two SH3 domains and a C-terminal RhoGEF (DH)-PH domain.

255 RhoGAPs are more promiscuous than RhoGEFs to confine Rho activity gradients.

256 ese observations support the hypothesis that RhoGEFs, particularly LARG, participate in linking GPCR

257 The RhoGEF Ect2 controls cell division and exerts oncogenic

258 The RhoGEF FARP2, which binds to the KRK motif, shows identi

259 The RhoGEF mutant of p210 Bcr-Abl does not affect the tyrosi

260 equator of dividing cells by activating the RhoGEF Pebble.

261 rmal levels of tyrosine kinase activity, the RhoGEF mutant of p210 Bcr-Abl is impaired in transformin

262 vage furrow during cytokinesis, p190 and the RhoGEF Ect2 play opposing roles in cytokinesis, and sust

263 he RasGAP Syngap1, the ArfGAP Agap2, and the RhoGEF Kalirin, which includes a total of 280 interactio

264 guanine exchange factors (RhoGEFs), but the RhoGEF(s) required for LTP also remain unknown.

265 During cytokinesis, RhoA is activated by the RhoGEF ECT-2.

266 Galpha(12)/Galpha(13) or their effector, the RhoGEF protein LARG, RhoA-dependent SRF-regulation was b

267 tein that through binding and inhibiting the RhoGEF GEF-H1 modulates RhoA activity and tension across

268 oA observed by overexpression of five of the RhoGEF DH-PH domains.

269 nesis and involves precise activation of the RhoGEF ECT2.

270 actin-binding motif in the N-terminus of the RhoGEF frabin, and as with PDZ-RhoGEF, mutagenesis and a

271 re, we delineate a pathway downstream of the RhoGEF Pbl/Ect2 that directs this process in a model epi

272 estigate the synaptic regulatory role of the RhoGEF protein Tiam1, whose expression appears to be rem

273 PTTG1-dependent expression of the RhoGEF proto-oncogene ECT2 was observed in a number of c

274 ction of a contractile ring and requires the RhoGEF ECT-2, a RhoA activator also essential for cytoki

275 l mechanism by which Galpha13 stimulates the RhoGEF activity of these proteins has not yet been well

276 al, and imaging techniques, we show that the RhoGEF Kalirin and its paralog Trio play critical and re

277 Silencing studies show that the RhoGEF Trio is crucial for keeping active Rac1 at the do

278 210 Bcr-Abl to interact with XPB through the RhoGEF domain.

279 ain-of-function activity attributable to the RhoGEF domain of p210 Bcr-Abl that is required to suppor

280 mology of our protein's RhoGEF domain to the RhoGEF domains of Trio, Duo and Duet and its homology wi

281 Here we investigate whether the RhoGEF (Rho guanine-nucleotide exchange factor) protein

282 ne kinase activity, and mutations within the RhoGEF domain that are predicted to eliminate RhoGEF act

283 We found that, among the RhoGEFs tested, MCP1 induced tyrosine phosphorylation of

284 Here, we sought to identify the RhoGEFs involved in monocyte chemotactic protein 1 (MCP1

285 s not modulate the intrinsic activity of the RhoGEFs, activated RhoA associated with phospholipid ves

286 ecently been determined for several of these RhoGEFs and their G protein complexes, providing fresh i

287 ted Galpha13, cellular localization of these RhoGEFs has been proposed as a mechanism for controlling

288 can bind and regulate the activity of these RhoGEFs, thus providing a direct link from these heterot

289 nge factor (GEF) activity toward RhoA, these RhoGEFs also possess RGS homology (RH) domains that inte

290 This RhoGEF has an essential role in cytokinesis, but also pl

291 ave identified new, essential roles for this RhoGEF in ciliated epithelia during vertebrate developme

292 Three RhoGEF isoforms are produced by the gene ARHGEF25; p63Rh

293 e G12 family regulate the Rho GTPase through RhoGEFs that contain an amino-terminal regulator of G pr

294 rotein 90 (Hsp90) while retaining binding to RhoGEFs.

295 ons in both EGL-8 (PLCbeta) and UNC-73 (Trio RhoGEF) have strong synthetic phenotypes that phenocopy

296 Activated Galpha(q) and Trio RhoGEF appear to be part of a signaling complex, because

297 ic G protein Galphaq, and its effector, Trio RhoGEF.

298 ed C. elegans Galpha(q) synergizes with Trio RhoGEF to activate RhoA.

299 with F-actin and myosin II, which are under RhoGEF(Pbl)-dependent control themselves.

300 Together, these data reveal a unique RhoGEF-mediated molecular program of glutamatergic synap