ライフサイエンスコーパス: RhoGAP

1 RhoGAP also appears to function by stabilizing several r

2 RhoGAP proteins are key regulators of Rho family GTPases

3 RhoGAPs are more promiscuous than RhoGEFs to confine Rho

4 Defects resulting from loss of CYK-4 RhoGAP activity can be rescued by activating mutations i

5 Consistent with CYK-4 RhoGAP activity contributing to GEF activation, the cata

6 Thus, counterintuitively, CYK-4 RhoGAP activity promotes RhoA activation.

7 We suggest that ZEN-4/MKLP1 and CYK-4/RhoGAP regulate an early step in epithelial polarization

8 Centralspindlin kinesin-6/RhoGAP complex, a midbody component critical for both th

9 -phosphatase domain followed by an ASH and a RhoGAP-like domain.

10 results demonstrate that YopE functions as a RhoGAP to downregulate multiple Rho GTPases, leading to

11 ild type p190 appeared able to function as a RhoGAP.

12 family member c-ten requires R474 to bind a RhoGAP called DLC-1 (deleted in liver cancer).

13 The N-terminal domain comprises a RhoGAP activity, while the C-terminal domain comprises a

14 -activating proteins (GAPs), which contain a RhoGAP domain equipped with a characteristic arginine fi

15 otein 1 (MKLP1), and CYK-4, which contains a RhoGAP (GTPase-activating protein) domain.

16 er cancer 1) tumor suppressor gene encodes a RhoGAP protein that inactivates Rho GTPases, which are i

17 Now the generation of mice deficient for a RhoGAP suggests that this small G protein might also reg

18 Our study shows that GRAF1, a RhoGAP, is highly expressed in metabolically active tiss

19 of the genes identified in this screen is a RhoGAP protein, SH3-domain binding protein 1 (SH3BP1).

20 Depletion of myosin-IXA, a RhoGAP and actin motor protein, in collectively migratin

21 her DBL family Rho GEFs, Rho effectors, or a RhoGAP.

22 y: Ten-m binds to and negatively regulates a RhoGAP, thus activating the Rac1 small GTPases to promot

23 contributes to DLC1 tumor suppression via a RhoGAP-independent mechanism, and suggest that DLC1 inac

24 idomain protein with a RhoGTPase-activating (RhoGAP) domain and a StAR-related lipid transfer (START)

25 trameric complex consisting of kinesin-6 and RhoGAP (Rho-family GTPase-activating protein) subunits,

26 n cooperation between its tensin binding and RhoGAP activities, although neither activity depends on

27 EF (guanine nucleotide exchange factors) and RhoGAP (GTPase activating proteins), proteins that contr

28 otein RhoA complexed with MgF3(-) , GDP, and RhoGAP, which has the mutation Arg85'Ala.

29 e protein did inhibit both the intrinsic and RhoGAP-stimulated GTP hydrolysis rates of Cdc42 and Rac1

30 reveal that the binding sites for IQGAP1 and RhoGAP on the small G proteins overlap only partially.

31 gh multiple cellular targets for the PRR and RhoGAP have been identified, and their functions delinea

32 hat overexpression of a different RhoGEF and RhoGAP pair, RhoGEF2 and Cumberland GAP (C-GAP), resulte

33 a-5 genes, encoding homologues of RhoGEF and RhoGAP, respectively, as regulators of axon regeneration

34 f the ongoing combined actions of RhoGEF and RhoGAP.

35 reveal at the systems level how RhoGEFs and RhoGAPs contextualize and spatiotemporally control Rho s

36 impact of expressing sixty-seven RhoGEFs and RhoGAPs on the YAP1 dependent activity of a TEAD element

37 view, we focus on the ability of RhoGEFs and RhoGAPs to form complexes with diverse binding partners,

38 As RhoGAPs vastly outnumber Rho GTPases, this may represent

39 , Ses1 and Ses2, which interact with the ASH-RhoGAP-like (ASPM-SPD-2-Hydin homology and Rho-GTPase Ac

40 ed by the same missense mutations in the ASH-RhoGAP-like domain that also disrupt APPL1 binding.

41 allographic studies reveal a role of the ASH-RhoGAP-like domains in positioning the phosphatase domai

42 ion with APPL1, which is mediated by the ASH-RhoGAP-like domains of OCRL and is abolished by disease

43 recruitment of actomyosin and the associated RhoGAP Myo9b.

44 P190-B RhoGAP (p190-B, also known as ARHGAP5) has been shown to

45 he tyrosine-phosphorylation status of p190-B RhoGAP and its resulting subcellular relocalization.

46 trate-trapping mutants, we identified p190-B RhoGAP as a SHP-2 substrate.

47 ." Cells derived from embryos lacking p190-B RhoGAP exhibit excessive Rho activity, are defective for

48 When dephosphorylated, p190-B RhoGAP has been shown to stimulate the activation of Rho

49 ly inactive mutant of SHP-2 inhibited p190-B RhoGAP tyrosyl dephosphorylation, RhoA activity, and myo

50 During myogenesis, p190-B RhoGAP was tyrosyl dephosphorylated concomitant with the

51 e lacking the Rho-inhibitory protein, p190-B RhoGAP, are 30% reduced in size and exhibit developmenta

52 hat the Rho GTPase and its regulator, p190-B RhoGAP, are components of a critical switch in the adipo

53 y suggest that SHP-2 dephosphorylates p190-B RhoGAP, leading to the activation of RhoA.

54 In p190-B RhoGAP-deficient mice, CREB phosphorylation is substanti

55 we show that a signalling network of p190-B RhoGAP-ROS-TGF-beta-p38(MAPK) balances HSPC self-renewal

56 es, further suggesting a link between p190-B-RhoGAP and non-canonical TGF-beta signalling in HSPC dif

57 ant negative mutants of Cdc42 and Rac and by RhoGAP p190.

58 inger resembles the one within the canonical RhoGAP domains and inserts into the nucleotide-binding p

59 0RhoGAP (herein referred to as CRAD; catenin-RhoGAP association domain).

60 rmodynamic data pertaining to the Rac1/Cdc42-RhoGAP complexes.

61 n we identify "cold spots" in the Rac1/Cdc42-RhoGAP/IQGAP1 interfaces.

62 In addition to a conserved RhoGAP domain at the N terminus, multiple proline-rich m

63 logy-Bin-Amphiphysin-Rvs protein)-containing RhoGAP, Rgd3, that has activity primarily on Rho3, but a

64 f RGA-3/4, which functions as a conventional RhoGAP for RhoA.

65 which are predicted to encode three distinct RhoGAPs that share only the GAP domain.

66 Thus, distinct RhoGAPs, encoded by the same gene, regulate different ma

67 reveal the mechanism for inhibition of DLC1 RhoGAP activity by p120RasGAP and demonstrate the molecu

68 on occurred at mRNA level and relied on DLC1 RhoGAP function, leading to suppression of high level of

69 Hence, p120 associates with the DLC1 RhoGAP domain by targeting the catalytic arginine finger

70 on mode of the p120 SH3 domain with the DLC1 RhoGAP domain that is atypical and does not follow the c

71 the serines, located N-terminal to the DLC1 RhoGAP domain, induces strong binding of that N-terminal

72 p120RasGAP SH3 domain bound directly to DLC1 RhoGAP, at a site partially overlapping the RhoA binding

73 RhoA were increased upon depletion of either RhoGAP.

74 p190B mutant exhibits dramatically enhanced RhoGAP activity, consistent with a model whereby binding

75 SNX26, a brain-enriched RhoGAP, plays a key role in dendritic arborization durin

76 functions as a molecular mimic of eukaryotic RhoGAPs to inactivate Rho GTPases through RhoGDI.

77 Green fluorescent protein-RhoGDI and ExoS RhoGAP cooperatively stimulated actin reorganization and

78 ane inhibited the actions of RhoGDI and ExoS RhoGAP on the translocation of Cdc42 from membrane to cy

79 RhoA in vivo, the relationship between ExoS RhoGAP and the eukaryotic regulators of Rho GTPases is n

80 ation of actin cytoskeleton mediated by ExoS RhoGAP.

81 skeleton elicited by type III-delivered ExoS RhoGAP.

82 This indicates that ExoS RhoGAP and RhoGDI function in series to inactivate Rho G

83 n actin reorganization, suggesting that ExoS RhoGAP functions as a molecular mimic of eukaryotic RhoG

84 Although the ExoS RhoGAP inactivates Cdc42, Rac, and RhoA in vivo, the rel

85 Although ExoT RhoGAP stimulates actin reorganization through the inact

86 tumor suppressor and ubiquitously expressed RhoGAP protein; its activity is regulated in part by bin

87 onal interaction between RhoA and individual RhoGAP which involves distinct structural determinants o

88 nd structurally and show that they influence RhoGAP activity.

89 y competitively and very potently inhibiting RhoGAP activity.

90 ons as an autoinhibitory domain of intrinsic RhoGAP activity.

91 he tumor suppressor function of DLC1 that is RhoGAP-independent.

92 ulation of neurite outgrowth by exerting its RhoGAP activity and that its cellular activity may be re

93 vealed an allosteric regulation site for its RhoGAP activity.

94 regulation of neurite outgrowth through its RhoGAP activity.

95 screening Rho GTPase regulators, myosin-IXA RhoGAP was identified as a key requirement for cell-cell

96 p68RacGAP, a novel Vezf1-interacting 68-kDa RhoGAP domain-containing protein.

97 luding original data from a double-knockdown RhoGAP genetic screen, which likely reflects the redunda

98 is regulated by the asymmetrically localized RhoGAP Deleted in liver cancer (DLC1) in the cytoplasm a

99 of Myo9b (Myo9b-RhoGAP), a unique motorized RhoGAP that specifically targets RhoA for controlling ce

100 ntracellular domain interacts with the Myo9b RhoGAP domain and inhibits its activity; therefore, SLIT

101 missing in the RhoGAP domain of Myo9b (Myo9b-RhoGAP), a unique motorized RhoGAP that specifically tar

102 ers impaired the catalytic activity of Myo9b-RhoGAP and affected the Myo9b-mediated cell migration.

103 Here, we determined the structure of Myo9b-RhoGAP in complex with GDP-bound RhoA and magnesium fluo

104 Our data indicate that Myo9b-RhoGAP accelerates RhoA GTP hydrolysis by a previously u

105 Unexpectedly, Myo9b-RhoGAP contains two arginine fingers at its catalytic si

106 m, which may be shared by other noncanonical RhoGAP domains lacking the auxiliary asparagine.

107 A novel RhoGAP family member, p200RhoGAP, is cloned in human and

108 he conservation of the catalytic activity of RhoGAP (Rho-specific GAP) on the 6-TGTP-Rac1 adduct to p

109 ion of this interface relieves inhibition of RhoGAP activity by the SH3 domain.

110 ion to activation of RhoGEF(s), reduction of RhoGAP (p190) is a critical mechanism by which increased

111 ented by knowledge of the basic structure of RhoGAP/GTPase signaling, namely, that GAPs act directly

112 reflects the redundant network structure of RhoGAP/GTPase signaling.

113 xplain why, unique among the large family of RhoGAPs, p190A exhibits a significantly increased mutati

114 method makes mediocre predictions using only RhoGAP single-knockdown morphological data, yet achieves

115 h a large set of other representative SH3 or RhoGAP proteins.

116 Centralspindlin's own RhoGAP domain also contributes to furrow ingression.

117 p115 RhoGAP directly binds PRL-1 in vitro and in cells via it

118 l interaction between the SH3 domain of p115 RhoGAP and MEKK1 and results in activation of ERK1/2.

119 by inhibiting the catalytic activity of p115 RhoGAP.

120 hin the PxxP ligand-binding site of the p115 RhoGAP SH3 domain occupies a folded groove within PRL-1.

121 sults demonstrate that PRL-1 binding to p115 RhoGAP provides a coordinated mechanism underlying ERK1/

122 amino acids, has 86% homology with rat p122 RhoGAP gene, and was localized by fluorescence in situ h

123 P190 RhoGAP (GTPase activating protein) is a potent Rho regul

124 p190 RhoGAP is a 190-kDa protein that stably associates with

125 p190 RhoGAP, a GTPase regulatory protein, provides this coord

126 hesion molecules, the action of PKC and p190 RhoGAP leads to a modulation of Rho GTPase activity to d

127 The minimal regions of Syx and p190 RhoGAP that bind Rnd3 are not sequence-related but have

128 or in response to integrin engagement, p190 RhoGAP is rapidly translocated to regions of membrane ru

129 ates excessively, suggesting a role for p190 RhoGAP in the regulation of +Rho-mediated actin assembly

130 Mice lacking functional p190 RhoGAP exhibit several defects in neural development tha

131 phila using RNA interference identified p190 RhoGAP as essential for axon stability in mushroom body

132 Here we identify p190 RhoGAP (p190), the most abundant GAP for RhoA in cells,

133 ng Rac1 activation and RhoA inhibition, p190 RhoGAP is critical to the protective effects of Ang-1 ag

134 cells of the neural tube floor plate of p190 RhoGAP mutant mice, polymerized actin accumulates excess

135 ltinucleation phenotype is dependent on p190 RhoGAP activity, determine that the N-terminal GBDS1 reg

136 ion with their effectors such as Syx or p190 RhoGAP.

137 ng, the tyrosine phosphorylated protein p190 RhoGAP becomes associated with GRB2 in LA significantly

138 tor p190 Rho-GTPase-activating protein (p190 RhoGAP) also play an important regulatory role in fear m

139 ility effects of endotoxin but requires p190 RhoGAP to do so.

140 a FRET biosensor, we further show that p190 RhoGAP and RhoA act downstream of the PAR-6/aPKC complex

141 Herein, we report that p190 RhoGAP forms a high-affinity complex with Rho GTPases in

142 kinase C (PKC), and we have found that p190 RhoGAP is also a PKC substrate in vivo.

143 We have determined that p190 RhoGAP is specifically expressed at high levels througho

144 FII-I as a specific interactor with the p190 RhoGAP FF domains.

145 Inhibition of the p190 RhoGAP-downstream kinase ROCK in LA during fear conditio

146 Thus, the p190 RhoGAP/ROCK pathway, which regulates the morphology of d

147 revealed that RAFTK is associated with p190 RhoGAP (p190), RasGAP and ErbB-2, and plays an essential

148 s an abundant SH2-mediated complex with p190 RhoGAP in cells expressing activated tyrosine kinases.

149 Treatment with p190 RhoGAP small interfering RNA completely abolishes the ab

150 Our results identify p190 RhoGAPs as effectors of Rnd proteins and demonstrate a n

151 n the context of cell migration are the p190 RhoGAPs (p190A and p190B), which function to modulate Rh

152 The p190 RhoGAPs undergo complex regulation, including phosphoryl

153 ivating protein for Rho family members (p190(RhoGAP); p190) and membrane-protrusive activities at inv

154 ctin regulator ARHGAP35 (also known as p190A RhoGAP) to the basal body.

155 The ARHGAP35 gene encoding p190A RhoGAP (p190A) is significantly altered by both mutation

156 ative regulator of Rho family GTPases, p190A RhoGAP, is one of six mammalian proteins harboring so-ca

157 We identify p190A RhoGAP as a major target for ERK signaling in adhesion a

158 phosphorylation leads to inhibition of p190A RhoGAP activity in vitro and in vivo.

159 equired for the negative regulation of p190A RhoGAP activity.

160 itional regulatory mechanism unique to p190A RhoGAP that involves priming-dependent phosphorylation b

161 ted that IQGAP1 binds to both RhoA and p190A-RhoGAP, a GTPase-activating protein that normally inhibi

162 P1 acts as a scaffold that colocalizes p190A-RhoGAP and RhoA, inactivating RhoA and suppressing airwa

163 al sections revealed colocalization of p190A-RhoGAP and RhoA; however, these proteins did not colocal

164 ing of Rac1 relieves autoinhibition of p190B RhoGAP function.

165 p200 RhoGAP co-localizes with p120 RasGAP in cells and forms

166 p200 RhoGAP, a member of the Rho GTPase-activating protein (R

167 The morphology of the foci induced by p200 RhoGAP is distinct from that formed by Rac or Rho activa

168 uppresses the foci formation induced by p200 RhoGAP, suggesting that the Ras-ERK pathway is required

169 hat the Ras-ERK pathway is required for p200 RhoGAP-mediated cell transformation.

170 vity of the N-terminal RhoGAP domain in p200 RhoGAP is also required for its full transforming activi

171 region and the Src homology 3 domain of p200 RhoGAP and p120 RasGAP, respectively.

172 Expression of p200 RhoGAP results in a significant increase of Ras-GTP and

173 Here we show that ectopic expression of p200 RhoGAP stimulates fibroblast cell proliferation and cell

174 Mutations of p200 RhoGAP that disrupt interaction with p120 RasGAP abolish

175 he GDP- and GTP-bound states suppresses p200 RhoGAP transformation.

176 proliferation and provide evidence that p200 RhoGAP can mediate cross-talks between Ras- and Rho-regu

177 genic Ras, raising the possibility that p200 RhoGAP may engage Ras signaling.

178 ransferase, or the GTPase-activating protein RhoGAP p190 causes a marked reduction in the number of p

179 orms allowing Rho-GTPase-activating protein (RhoGAP) activity to be focused at a definite locus.

180 th N-terminal Rho GTPase-activating protein (RhoGAP) and C-terminal ADP-ribosyltransferase domains.

181 C-1 encodes a Rho GTPase-activating protein (RhoGAP) and negative regulator of specific Rho family pr

182 suppressor, a Rho GTPase-activating protein (RhoGAP) associated with focal adhesions.

183 1 (DLC-1) is a RhoGTPase-activating protein (RhoGAP) domain containing tumor suppressor that is often

184 9 include the Rho GTPase-activating protein (RhoGAP) domain, and residues 234-453 include the 14-3-3-

185 member of the Rho GTPase-activating protein (RhoGAP) family, was previously implicated in the regulat

186 , which encodes a GTPase activating protein (RhoGAP) for the RhoA and RhoC small GTPases.

187 e analyses of Rho GTPase activating protein (RhoGAP) function in Drosophila using RNA interference id

188 of the Rho family GTPase-activating protein (RhoGAP) MgcRacGAP/CYK-4 and the kinesin MKLP1/ZEN-4, is

189 (RhoGEF) and Rho GTPase activating protein (RhoGAP) pair required for actomyosin waves in egg chambe

190 codes a novel Rho GTPase-activating protein (RhoGAP) required for restricting the ROP1 activity to th

191 ene encodes a Rho GTPase-activating protein (RhoGAP) that functions as a tumor suppressor in several

192 BPGAP1 is a Rho GTPase-activating protein (RhoGAP) that regulates cell morphogenesis, cell migratio

193 ctly to p190B Rho GTPase-activating protein (RhoGAP), a major modulator of Rho signaling.

194 guanosine triphosphatase activating protein (RhoGAP), PAC-1, which mediates C. elegans radial polarit

195 pression of a Rho GTPase-activating protein (RhoGAP), RhoGAP7/DLC-1, via activation of the transcript

196 lant-specific ROP GTPase-activating protein (RhoGAP), which in turn deactivates the ROP GTPase OsRac1

197 values of the Rho GTPase-activating protein (RhoGAP)-catalyzed reactions were significantly increased

198 by Rho-selective GTPase-activating proteins (RhoGAP), which have generally been presumed to act as tu

199 The Rho GTPase-activating proteins (RhoGAPs) are a family of multifunctional molecules that

200 eins known as RhoGTPase Activating Proteins (RhoGAPs) that catalyse the conversion of RhoGTPases to t

201 C1-3) encode Rho-GTPase-activating proteins (RhoGAPs) whose expression is frequently down-regulated o

202 y inhibiting Rho GTPase activating proteins (RhoGAPs).

203 rs (RhoGEFs) and GTPase-activating proteins (RhoGAPs).

204 ode Rho-specific GTPase-activating proteins (RhoGAPs).

205 ted action of its proline-rich region (PRR), RhoGAP domain, and the BNIP-2 and Cdc42GAP homology (BCH

206 The number of potential Rac/RhoGAPs largely exceeds the number of Rac/Rho GTPases an

207 in other species, namely, mouse HSPE71, Rat RhoGAP protein, S cerevisiae leucyl tRNA synthetase and

208 Deletion of these domains reduces RhoGAP activity.

209 Our findings suggest that the REN1 RhoGAP controls a negative-feedback-based global inhibit

210 roliferation and that this function requires RhoGAP activity.

211 in, and this interaction enhances ARHGAP18's RhoGAP activity.

212 LC1 binding to S100A10 did not affect DLC1's RhoGAP activity, but it decreased the steady-state level

213 criptome revealed high expression of several RhoGAP genes in BLBC tumors, raising the possibility tha

214 We describe a brain-specific RhoGAP splice variant, BARGIN (BGIN), which comprises a

215 e have identified ARHGAP17, a Cdc42-specific RhoGAP, as a key regulator of invadopodia in breast canc

216 (DLC1), which encodes a protein with strong RhoGAP (GTPase activating protein) activity and weak Cdc

217 nteraction with p190B, modulates subcellular RhoGAP localization and activity, thereby providing a no

218 ExoS is bifunctional, with an amino-terminal RhoGAP and a carboxy-terminal ADP-ribosyltransferase dom

219 s a regulatory element for its COOH-terminal RhoGAP domain.

220 ti-internalization factor with an N-terminal RhoGAP domain and a C-terminal ADP-ribosyltransferase do

221 ingly, the RhoGAP activity of the N-terminal RhoGAP domain in p200 RhoGAP is also required for its fu

222 cal drivers of BLBC growth, and propose that RhoGAPs can act as oncogenes in cancer.

223 The RhoGAP (GTPase--activating protein toward Rho family sma

224 The RhoGAP activity is required for full DLC-dependent tumor

225 The RhoGAP activity, which is required for full DLC-dependen

226 The RhoGAP domain of p200RhoGAP stimulated the GTPase activi

227 The RhoGAP domains of Bcr and 3BP-1, which were thought to b

228 The RhoGAP-, but not the ADP-ribosyltransferase domain of th

229 ition, we present evidence that ROCK and the RhoGAP ARHGAP29 associate with caveolin-1 in a manner de

230 through the balance between RhoGEF2 and the RhoGAP C-GAP.

231 interaction between recombinant RhoA and the RhoGAP domains of p190, p50RhoGAP, Bcr, and 3BP-1.

232 utations in the 5-phosphatase domain and the RhoGAP-like domain.

233 aracterisation reveals that cv-c encodes the RhoGAP protein RhoGAP88C.

234 rface and a clathrin box protruding from the RhoGAP-like domain.

235 ed a set of chimeric molecules by fusing the RhoGAP domain of p190, a GTPase-activating protein that

236 ential for inhibiting tumor cell growth, the RhoGAP activities were significantly reduced in these mu

237 ses in both worm and fly have identified the RhoGAP-like protein Syd-1 as a key positive regulator of

238 Here, we identify the RhoGAP GRAF1 (Arhgap26) as a PINK1 substrate that regula

239 , the auxiliary asparagine is missing in the RhoGAP domain of Myo9b (Myo9b-RhoGAP), a unique motorize

240 SH3 domain of p120 selectively inhibits the RhoGAP activity of all three DLC isoforms as compared wi

241 Interestingly, the RhoGAP activity of the N-terminal RhoGAP domain in p200

242 e motility defect of macrophages lacking the RhoGAP (Rho GTPase-activating protein) myosin IXb (Myo9b

243 NA localization and local translation of the RhoGAP ARHGAP11A in the basal endfeet of RGCs control th

244 Transient expression of the RhoGAP domain and the full-length molecule, but not the

245 Expression of the RhoGAP domain of p200RhoGAP in Swiss 3T3 fibroblasts inh

246 o actin filaments, whereas expression of the RhoGAP domain partially rescued the cell scattering phen

247 he characterization of a novel member of the RhoGAP family, Rga8, identified from a two-hybrid screen

248 cally, depletion of the RhoGEF, Ect2, or the RhoGAP, RhoGAP15B, disrupted actomyosin wave induction,

249 tein 1, Rasip1, and its binding partner, the RhoGAP Arhgap29.

250 stretch of polybasic residues preceding the RhoGAP domain regulates CdGAP activity in vivo and is re

251 a small polybasic region (PBR) preceding the RhoGAP domain that mediates specific binding to negative

252 Consistent with the fact that the RhoGAP activity of DLC-1 is essential for inhibiting tum

253 Structural analyses revealed that the RhoGAP domain of Myo9b contains a unique patch that spec

254 We show that the RhoGAP PAC-1/ARHGAP21 inhibits CDC-42 activity at AJs, a

255 A new study reports that the RhoGAP SPV-1 senses membrane curvature and cell stretch

256 We show that the RhoGAP, ARHGAP18, is localized by binding active microvi

257 We have found that the RhoGAP, GRAF, inhibits actomyosin contractility during c

258 ong binding of that N-terminal region to the RhoGAP domain, converting DLC1 from an open, active dime

259 omeric state, Rac1 became insensitive to the RhoGAP stimulation, albeit maintaining the responsivenes

260 DLC-1 is a multi-domain protein, with the RhoGAP catalytic domain flanked by an amino-terminal ste

261 es with the interaction of RhoA-GTP with the RhoGAP domain, reduces the hydrolysis of RhoA-GTP, the b

262 , we show that brain Pyk2 interacts with the RhoGAP protein Graf1 to alter dendritic spine stability

263 ing, and genetic epistasis analysis with the RhoGAP spv-1 demonstrated that tension-dependent recruit

264 this, we examined the roles of two of these RhoGAPs, ArhGAP11A (also known as MP-GAP) and RacGAP1 (a

265 gical data from genetic screens, apply it to RhoGAP/GTPase regulation in Drosophila, and evaluate its

266 e a built-in arginine finger, in addition to RhoGAPs, for negative regulation.

267 monstrate that Moe interacts with an unusual RhoGAP, Conundrum (Conu), and recruits it to the cell co

268 we have developed a novel strategy utilizing RhoGAP-Rho chimeras to specifically down-regulate indivi

269 iological activity, as did a mutant that was RhoGAP-deficient.

270 ng both bound nucleotide and Mg(2+), whereas RhoGAP utilizes the Mg(2+) cofactor to achieve high cata

271 ngenetic mechanisms, encodes a protein whose RhoGAP and scaffolding activities contribute to its tumo

272 mor suppressor function but retains wildtype RhoGAP activity.

273 h RhoGAPArg85'Ala relative to wild-type (WT) RhoGAP.

274 troduction of the Y. pseudotuberculosis YopE RhoGAP protein could be bypassed by the overproduction o