ライフサイエンスコーパス: Rac GTPase

1 on of core chemotactic effectors such as 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 de exchange factors (GEFs) that activate the Rac GTPase.

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

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

7 ronal apoptosis induced by the inhibition of Rac GTPase.

8 ctase suppresses MYC phosphorylation through Rac GTPase.

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

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

11 ses cell motility and prevents activation of Rac GTPase.

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

13 ultiple cellular functions by activating the Rac GTPase.

14 dent cytoskeleton organization downstream of Rac-GTPase.

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

16 1, a GTPase-activating protein for CDC42 and Rac GTPases.

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

18 a is associated with increased activation of Rac GTPases.

19 lar localization and downstream signaling of Rac GTPases.

20 ciated mechanism for coordination of Rho and Rac GTPases.

21 ntracellular activation of distinct GEFs and Rac GTPases.

22 was found to also associate physically with Rac GTPases.

23 lated exchange factors that activate Ras and Rac GTPases.

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

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

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

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

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

29 Multiple Rac GTPase activating proteins are present in neutrophil

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 Rac GTPase activity is needed for syncytium formation, w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Rac GTPases and their effectors control cellular morphog

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

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

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

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

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

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

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

73 Rac GTPases are also required for development of the rev

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

75 The Rac GTPases are currently being subjected to intensive s

76 Rac GTPases are key regulators of cell shape and cytoske

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

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

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

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

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

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

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

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

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

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

87 Rac GTPases control cell shape by regulating downstream

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

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

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

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

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

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

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

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

96 Rac GTPases have been implicated in the regulation of di

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

98 Numerous studies indirectly implicate Rac GTPases in cancer.

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

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

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

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

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

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

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

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

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

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

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

110 olymerization, findings highly suggestive of Rac GTPase involvement.

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

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

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

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

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

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

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

118 lted in p130Cas tyrosine phosphorylation and Rac GTPase loading.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Rac GTPases regulate a wide variety of cellular processe

135 Rac GTPases regulate actin polymerization and extension

136 A Rac GTPase-regulated multiprotein NADPH oxidase is criti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 Rac GTPases, the cytoskeletal signaling molecule Enabled

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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