ライフサイエンスコーパス: Rac GTPase

1 ultiple cellular functions by activating the Rac GTPase.

2 s involving the Abl tyrosine kinases and the Rac GTPase.

3 ide exchange factor (GEF) that activates the Rac GTPase.

4 ses cell motility and prevents activation of Rac GTPase.

5 de exchange factors (GEFs) that activate the Rac GTPase.

6 irectly to the active, GTP-bound form of the Rac GTPase.

7 on of core chemotactic effectors such as the Rac GTPase.

8 of c-myc transcription is independent of the Rac GTPase.

9 wn to exhibit one-to-one correspondence with Rac GTPase.

10 ng cell motility downstream of activation by Rac GTPase.

11 ronal apoptosis induced by the inhibition of Rac GTPase.

12 ctase suppresses MYC phosphorylation through Rac GTPase.

13 nces association with the active form of the Rac GTPase.

14 of Nox1, -2, and -3 requires the action of a Rac GTPase.

15 ptor B type I (SR-BI)-mediated activation of Rac GTPase.

16 dent cytoskeleton organization downstream of Rac-GTPase.

17 ciated mechanism for coordination of Rho and Rac GTPases.

18 ntracellular activation of distinct GEFs and Rac GTPases.

19 of PLC-beta2 as a putative effector site for Rac GTPases.

20 1, a GTPase-activating protein for CDC42 and Rac GTPases.

21 d oxidative burst by binding to and blocking Rac GTPases.

22 a is associated with increased activation of Rac GTPases.

23 lar localization and downstream signaling of Rac GTPases.

24 was found to also associate physically with Rac GTPases.

25 lated exchange factors that activate Ras and Rac GTPases.

26 of small Rho family of GTPases including the Rac-GTPases.

27 The Cdk5-p35 complex interacts with the Rac GTPase, a protein required for growth cone motility

28 Trio to stimulate the signaling activity of Rac GTPase: Abl gates the activity of the spectrin repea

29 iscuss here the current molecular models for Rac GTPase action in the control of the phagocytic leuko

30 Downstream of dAbl, Rac GTPases activate two distinct MAPK pathways: c-Jun N

31 Multiple Rac GTPase activating proteins are present in neutrophil

32 er receptors include chimaerins (a family of Rac GTPase activating proteins), RasGRPs (exchange facto

33 These Rac-GTPase activating proteins are regulated by the lipi

34 nhibition of the small G protein Rac1 by the Rac GTPase-activating protein (GAP) beta2-Chimaerin (bet

35 in-like protein 1 (MKLP1) and male germ cell Rac GTPase-activating protein (MgcRacGAP) and converts t

36 oading caused by depletion of male germ cell Rac GTPase-activating protein (MgcRacGAP), a component o

37 requires both the diacylglycerol-binding and Rac GTPase-activating protein activity of alpha1-chimaer

38 re, inactivation of Rac by expression of the Rac GTPase-activating protein beta2-chimerin inhibited H

39 glial:neuron adhesion protein contactin, the Rac GTPase-activating protein tumbleweed, and the planar

40 cruitment of Aurora B kinase, male germ cell Rac GTPase-activating protein, and RhoA to the cortex wa

41 TP very slowly and were unresponsive to p190 Rac GTPase-activating protein.

42 The chimaerin family of Rac GTPase-activating proteins (GAPs) has been implicate

43 in vivo model for the chimerins, a family of Rac GTPase-activating proteins (Rac-GAPs) that are uniqu

44 The unexpected pro-oncogenic functions of Rac GTPase-activating proteins also challenged the dogma

45 The members of the chimaerin family of Rac-GTPase-activating proteins possess a single C1 domai

46 or approach, we investigated the dynamics of Rac GTPase activation during chemotaxis of live primary

47 he DOCK180-related protein superfamily, as a Rac GTPase activator that is asymmetrically distributed

48 Importantly, genetic interaction data with Rac GTPase activators and effectors suggest that CACN-1

49 In addition, TLR4 stimulation enhanced Rac GTPase activity and promoted sustained Rac activatio

50 ruffling, but not cell contraction, requires Rac GTPase activity and the formation of a CAS/Crk compl

51 o dissect the complex upstream regulation of Rac GTPase activity in HSPC, we investigated the role of

52 Rac GTPase activity is needed for syncytium formation, w

53 he wave-pinning reaction-diffusion model for Rac GTPase activity.

54 is to suppress SFK and FYN, and to regulate RAC-GTPase activity after alpha(v) integrin stimulation.

55 Furthermore, we find that the CED-10(Rac) GTPase acts genetically downstream of these protein

56 ologic inhibition or genetic deletion of all Rac GTPases altered the distribution of F-actin and pMRL

57 The cycling of Rac GTPases, alternating between an active GTP- and an i

58 with ced-2 Crkll, ced-5 DOCK180, and ced-10 Rac GTPase and acting upstream of ced-10 Rac.

59 Ark promotes migration of GnRH neurons via Rac GTPase and concomitantly suppresses GnRH gene expres

60 ating PtdIns(3,4,5)P(3) levels that modulate Rac GTPase and F-actin reorganization through Vav1 excha

61 C that are associated with the activation of Rac GTPase and its cytoskeletal targets.

62 hat the apoptotic machinery of p75 comprises Rac GTPase and JNK.

63 We show that PKCalpha inhibits Rac GTPase and that c-Jun is a target of Rac.

64 as well as with actin regulators, including Rac GTPases and integrins, and have been thought to unde

65 cell function by interacting primarily with Rac GTPases and may play an integral role in breast canc

66 valuation of the direct interactions between Rac GTPases and PLC-beta isozymes and define a novel rol

67 ially redundant signaling pathways involving Rac GTPases and the adaptor protein Nck, which stimulate

68 enic Vav1 stimulates sustained activation of Rac GTPases and the biologic effects of oncogenic Vav1 a

69 Rac GTPases and their effectors control cellular morphog

70 nhibits, whereas H89 restores, activation of Rac-GTPase and abolishes morphine's inhibitory effect, i

71 resent study, we explored the involvement of Rac-GTPase and Rac-specific nucleotide exchange factor T

72 man CrkII protein), CED-5 (DOCK180), CED-10 (Rac GTPase), and CED-12 (ELMO), possibly through direct

73 ase, which is regulated by protein kinase C, Rac GTPase, and intracellular Ca(2+) signaling within th

74 WAVE activity is controlled by Rac GTPases, and data are presented here that suggest WV

75 actor coupling tyrosine kinase receptors and Rac GTPases, and has been implicated in transformation o

76 -P-enhanced TER occurred in conjunction with Rac GTPase- and p21-associated kinase-dependent endothel

77 Rac GTPases are also required for development of the rev

78 Here we demonstrate that endogenous Rac GTPases are caspase 3 substrates that are cleaved in

79 The Rac GTPases are currently being subjected to intensive s

80 Rac GTPases are key regulators of cell shape and cytoske

81 Rac-GTPases are major regulators of cytoskeletal remodel

82 il Vav 1 and 3, guanine exchange factors for Rac GTPases, are required for IgG/FcgammaR-mediated hemo

83 odulated by coactivation of Trk, identifying Rac GTPase as one of the key molecules whose activity is

84 tic anemia with reticulocytosis, implicating Rac GTPases as dynamic regulators of the erythrocyte cyt

85 orted here reveal a novel function for these Rac GTPases as regulators for ubiquitin/26S proteasome-m

86 PAKc contains a Rac-GTPase binding (CRIB) and autoinhibitory domain, a P

87 concept that some Rac-GEFs not only activate Rac GTPases but also participate in the selection of Rac

88 ely interact with the active versions of the Rac GTPases, but not with other similar Rho GTPases.

89 ration and function with UNC-73/Trio and the rac GTPases (CED-10 and MIG-2).

90 ance of the VCCMNs, PAK-1 also acts with the rac GTPases, CED-10 and MIG-2, and is completely redunda

91 dence that, in Caenorhabditis elegans, three Rac GTPases, CED-10, RAC-2, and MIG-2, define three redu

92 Rac GTPases control cell shape by regulating downstream

93 recently reported the critical importance of Rac GTPase-dependent cortical actin rearrangement in the

94 r (EGF)- and heregulin-induced activation of Rac GTPase, extracellular signal-regulated kinase (ERK)

95 dies indicate that SWAN-1 is an inhibitor of Rac GTPase function in cellular morphogenesis and cytosk

96 hat impairment of geranylgeranylated Rho and Rac GTPase function is most likely responsible for lovas

97 neurons (CGNs) principally via inhibition of Rac GTPase function.

98 pathway, such as Neurexin-IV, Syndecan, and Rac GTPases, further confirm that Cno functionally inter

99 RNA interference-mediated knockdown of Rac GTPases greatly reduced Fas-dependent, TCR-induced a

100 Activation of the Rac GTPase has been linked to regulation of actin polyme

101 Rac GTPases have been implicated in the regulation of di

102 activated by Toll-like receptors (TLRs) and Rac GTPases, how their strengths are controlled in quies

103 cluster of 6-10 cells, where the role of the Rac GTPase in migration was first established.

104 Numerous studies indirectly implicate Rac GTPases in cancer.

105 er, our results reveal an essential role for Rac GTPases in coordinating cell adhesion, cell prolifer

106 the accumulation of nonisoprenylated Rho and Rac GTPases in cytosolic fraction.

107 yse the loss-of-function phenotypes of three Rac GTPases in Drosophila mushroom body neurons.

108 To explore the involvement of the Rho and Rac GTPases in lovastatin-mediated effects, changes in d

109 hese results demonstrate the central role of Rac GTPases in multiple aspects of axon development in v

110 istically, Htl regulates the activity of Rho/Rac GTPases in nascent myotubes and effects changes in t

111 he canonical Crk-p130Cas complex to activate Rac GTPases in numerous contexts.

112 However, the function of Rac GTPases in otic development is largely unexplored.

113 factor with the ability to activate RAS and RAC GTPases in response to elevated calcium levels.

114 These studies identify Pak and Rac GTPases, including Vav1, as potential therapeutic ta

115 inhibition of the CD81 downstream molecule, Rac GTPase, inhibited IFN-alpha production.

116 llular superoxide scavenger) or NSC 23766 (a Rac GTPase inhibitor) completely inhibited Siglec-8-medi

117 olymerization, findings highly suggestive of Rac GTPase involvement.

118 proteins, as well as impaired activation of Rac GTPase is also observed in the absence of FAK.

119 ent apoptosis, indicating that activation of Rac GTPase is required for JNK activation and apoptosis

120 These data establish that Rac GTPase is spatially and temporally regulated to coor

121 We have shown previously that a subset of Rac GTPases is activated by auxin, and they in turn stim

122 ucleotide exchange factor (Rac GEF) Vav3 and Rac GTPases is required for leukemogenesis mediated by t

123 at TIAM1, a guanidine exchange factor of the Rac GTPase, is a direct target of both miR-21 and miR-31

124 Arp2/3 complex, but can be stimulated by the Rac GTPase, kinases and phosphatidylinositols.

125 t accelerates the hydrolysis of GTP from the Rac GTPase, leading to its inactivation.

126 lted in p130Cas tyrosine phosphorylation and Rac GTPase loading.

127 cient adhesion-induced activation of Akt and Rac GTPase, major contributors to the integrin-dependent

128 oxygen.This two-step model of regulation by Rac GTPase may provide a means of more effectively contr

129 Biphasic activation of Cdc42 or Rac GTPases may be a general mechanism for spatial cue-d

130 a cellular process whereby auxin induces and Rac GTPases mediate the recruitment of nucleoplasmic Aux

131 at is independent of the previously reported Rac GTPase-mediated Jun amino (N)-terminal kinase (JNK)

132 een implicated in the negative regulation of Rac GTPase-mediated signaling in hematopoietic cells.

133 s phosphatidylinositol 4,5-bisphosphate, the Rac GTPase MIG-2, and F-actin further indicate that INA-

134 UNC-34 (Ena/VASP), the Rac GTPases MIG-2 and CED-10 and the actin binding prote

135 rrent mutations in components of the Rho and Rac GTPase network, indicating a role for noncanonical W

136 ype C2 domains and functionally linked CDC42/Rac GTPases occurred independently in eukaryotes that ev

137 ive signaling proteins, we show that Ras and Rac GTPases, PI-3K, and PKC participate in cell migratio

138 These data demonstrate that Rac GTPases play an important role in the integrity of p

139 is not known whether Rac1, the prototype of Rac GTPase, plays a role in neuronal CREB activation ind

140 t closely related to the mammalian Cdc42 and Rac GTPases, plays an important role in the regulation o

141 we show that quiescent MuSCs have elaborate, Rac GTPase-promoted cytoplasmic projections that respond

142 Rac-GTPase promotes fibrotic TGF-beta1 signaling and chr

143 er is associated with impaired activation of Rac GTPases, reduced proliferation, increased apoptosis,

144 Rac GTPases regulate a wide variety of cellular processe

145 Rac GTPases regulate actin polymerization and extension

146 A Rac GTPase-regulated multiprotein NADPH oxidase is criti

147 e of phagocytes and nonphagocytic cells is a Rac GTPase-regulated system that generates reactive oxyg

148 The Rac GTPase regulates Rho signaling in a broad range of p

149 Thus, proteolytic inactivation of Rac GTPases represents a novel, irreversible mechanism o

150 /CED-5 protein complex, CED-12 regulates Rho/Rac GTPase signaling and leads to cytoskeletal reorganiz

151 ry for chemoattractant-induced activation of Rac GTPase signaling and Vav1 phosphorylation, suggestin

152 evolutionarily conserved module controlling Rac GTPase signaling during cell migration, phagocytosis

153 Selective activation of Rac GTPase signaling pathways requires the specific rele

154 As a mechanistically detailed example of Rac GTPase signaling, the NADPH oxidase provides a poten

155 hreonine phosphatase, PP5, as an effector of Rac GTPase signaling.

156 rallel to this PAK-1 pathway, independent of rac GTPase signaling.

157 ith function-altering mutations in canonical Rac GTPase-signaling-pathway members demonstrated a robu

158 first-generation small-molecule inhibitor of Rac GTPase targeting Rac activation by GEF.

159 KA-mediated recruitment of effectors such as Rac GTPases that impact the actin cytoskeleton.

160 ay be a shared kinase target of both Rho and Rac GTPases that mediates their effects on rearrangement

161 rough mTORC2-dependent activation of Akt and Rac GTPase, the activities of which are inhibited in the

162 Rac GTPases, the cytoskeletal signaling molecule Enabled

163 autonomous and non-autonomous functions for Rac GTPases, the latter manifesting itself as a strong c

164 Vav works as a GDP/GTP exchange factor for Rac GTPases, thereby facilitating the transition of thes

165 x1) catalyzes the exchange of GDP for GTP on Rac GTPases, thereby triggering changes in the actin cyt

166 Treatment with inhibitors of MMPs or Rac GTPase to abolish mesenchymal migration, suppresses

167 Although the ability of Cdc42 and Rac GTPases to activate PAK is well established, relativ

168 Although the ability of Cdc42 and Rac GTPases to activate Pak is well established, relativ

169 d support a direct regulatory interaction of Rac GTPases to promote activation of these NADPH oxidase

170 leotide exchange factors (Rho GEFs) activate Rac GTPases to regulate cell migration, invasion, and me

171 studies in other cell types have shown that Rac GTPases transduce signals leading to cell migration

172 d by loss-of-function mutations in ced-10 (a Rac GTPase), unc-34 (an Enabled homolog), and unc-115 (a

173 Furthermore, Rac GTPase was necessary for p27-dependent migration but

174 Furthermore, the recognition site for Rac GTPases was localized to the pleckstrin homology (PH

175 In macrophages, Vav regulation of Rac GTPases was required specifically in FcgammaR-mediat

176 effects, changes in distribution of Rho and Rac GTPases were analyzed by Western blot analysis, and

177 y specific CD81 tetraspanin ligands, such as Rac GTPase, were detected.

178 Here, we report that p75 activates Rac GTPase, which in turn activates c-jun N-terminal kin

179 axis, ROS production, and stimulation of the Rac GTPases, which control chemotaxis and ROS.

180 oring proteins inhibited the activity of the Rac GTPase within pseudopodia.