ライフサイエンスコーパス: Rho protein

1 enylcysteine of CAAX proteins (e.g., Ras and Rho proteins).

2 e transcription events are terminated by the Rho protein.

3 bility and function of this GTPase-deficient Rho protein.

4 effects of insulin on prenylation of Ras and Rho proteins.

5 of GEF is to displace bound Mg(2+) from the Rho proteins.

6 thelial actin cytoskeleton and functional EC Rho proteins.

7 t interact with ARL2.GDP or activated ARF or RHO proteins.

8 egulator essential to control homeostasis of Rho proteins.

9 and characterized the five different mutant Rho proteins.

10 /or coordinate the activities of the Rac and Rho proteins.

11 nse to agonist was partly due to the loss of Rho proteins.

12 be highly conserved and unique among various Rho proteins.

13 (ArhGAP29), a GTPase activating protein for Rho proteins.

14 T surface availability via the activation of Rho proteins.

15 ented geranylgeranyl-enhanced degradation of Rho proteins.

16 o enhance the endogenous synthesis of latent Rho proteins.

17 nhanced the degradation of newly synthesized Rho proteins.

18 P2 acts by engaging a host ligand other than Rho proteins.

19 escent protein-conjugated Ras, Rab, Arf, and Rho proteins.

20 f farnesylated Ras but not geranygeranylated Rho proteins.

21 factors (GEFs) responsible for activation of Rho proteins.

22 are able to bypass the requirement for these Rho proteins.

23 ack signal for Bni1p activation, possibly by rho-proteins.

24 nown to produce dominant negative mutants of Rho proteins abolished the interaction with both of thes

25 Like all other GTPases, Rho proteins act as molecular switches, with an active G

26 such as T17NRac1, that block the endogenous Rho protein activation by sequestering upstream guanine

27 en unclear how the bacteria may benefit from Rho protein activation.

28 Some Yersinia spp. also secrete the Rho protein activator cytotoxic necrotizing factor-Y (CN

29 These results suggest that Rho protein activities have cell type-specific effects o

30 ho proteins, and specifically down-regulated Rho protein activities in cells depending on which Rho G

31 ymerization is independent of PI3-kinase and rho protein activity and requires Arp2/3 complex and cof

32 gens have developed strategies to manipulate Rho protein activity so as to enhance their own survival

33 H1, a guanine nucleotide exchange factor for Rho proteins, affects vesicle trafficking.

34 rminators, one that depends on the bacterial Rho protein and a second that depends on the HK022-encod

35 tumorigenesis have evolved naturally in this Rho protein and have similar consequences for catalytic

36 suppressing RhoGDI2 promotes activity of the Rho proteins and cell migration.

37 H domain involved in binding or catalysis of Rho proteins and demonstrate that maintaining a threshol

38 erase C3 from Clostridium botulinum modifies Rho proteins and inhibits their function.

39 nockout of GGTase-I in macrophages activates RHO proteins and proinflammatory signaling pathways, lea

40 f-life of RhoE is shorter than that of other Rho proteins and that its expression levels are regulate

41 ic effectors including activators of Rac and Rho proteins and the receptor protein-tyrosine phosphata

42 is limited by the rate of GTP binding to the Rho protein, and this, in turn, depends on the rate that

43 of ExoS targeted Ras and RalA but not Rab or Rho proteins, and Ral binding protein 1-GST pull-down as

44 tro, co-localized with the respective active Rho proteins, and specifically down-regulated Rho protei

45 These results from studies of the rho protein are likely to be general to hexameric helica

46 Active GTP-bound RHO proteins are down-regulated by RHO GTPase-activating

47 on of small intestinal crypt cells, and that Rho proteins are essential elements of a mechanism by wh

48 We proposed previously that farnesylated Rho proteins are important targets for alternation by FT

49 ing evidence indicates that the small GTPase Rho proteins are involved in a variety of important proc

50 ltiple signaling components regulated by the Rho proteins are involved in these processes.

51 The mutant Rho proteins are proposed to interfere with bacteriophag

52 Rho proteins are small GTP/GDP-binding proteins primaril

53 represents a novel mechanism by which active Rho proteins are targeted to the proteasome for degradat

54 lls contain abnormally high levels of active Rho protein, are reduced in size, and exhibit defects in

55 t spots in the interface between RHOGAPs and RHO proteins as critical determinants for binding and ca

56 Rho proteins as well as RhoA-mediated contractile mechan

57 rlying the transforming potential of Ras and Rho proteins, as well as the numerous morphological and

58 Concentration of Rho proteins at the division site is a general feature o

59 gest a functional cross-talk between Ras and Rho proteins at the level of regulatory proteins.

60 We discover that lysine acetylation impairs Rho protein binding and increases guanine nucleotide exc

61 To terminate transcription in E. coli, Rho protein binds an RNA loading site on the nascent tra

62 We previously showed that the hexameric Rho protein binds three molecules of ATP in active sites

63 re-function relationship between RHOGAPs and RHO proteins by combining our in vitro data with in sili

64 ly alters the lifecycle of newly synthesized Rho proteins by facilitating their membrane translocatio

65 act as an intermediary in the regulation of Rho proteins by G13 and G12.

66 stood, posttranslational modification of the Rho proteins by geranylgeranylation is required for thei

67 In cultured cells, toxin A inactivates Rho proteins by monoglucosylation.

68 The Rho protein Cdc42 induces a significant conformational c

69 From the six yeast Rho proteins (Cdc42p and Rho1-5p), we have determined th

70 In a similar way, the mutant Rho proteins containing these mutations are very resista

71 Previously, we have demonstrated that the Rho proteins contribute to the cell proliferation, gene

72 The small GTP-binding Rho proteins control a variety of biological activities,

73 Once activated, Rho proteins control cell signaling through interactions

74 Rho proteins cycle between an inactive, GDP-bound state

75 The E. coli Rho protein disengages newly transcribed RNA from its DN

76 Inactivation of Rho proteins disturbs the organization of the cytoskelet

77 transferase C3, which specifically inhibits Rho proteins, enhanced the activity of p21(WAF1/CIP1).

78 All three His-tagged mutant Rho proteins exhibited similar Km values for ATP; howeve

79 luding several syntaxins, and members of the Rho protein family, including Cdc 42.

80 ch I domain and an insert region distinct to Rho proteins for binding to Cdc42.

81 he subcellular redistribution of accumulated Rho proteins from cytosol to membrane and increasing Rho

82 pression of Rnd3, an endogenous inhibitor of Rho protein function.

83 s that have been attributed to inhibition of RHO protein geranylgeranylation in inflammatory cells.

84 The primary regulators of Rho proteins, guanine nucleotide dissociation inhibitors

85 e expression of GTPase-defective versions of Rho proteins has been shown to induce a transformed phen

86 C-terminal domains in the interactions with RHO proteins has remained obscure.

87 exchange factor for Rho1p and Rho2p GTPases; Rho proteins have been implicated in control of actin cy

88 esentative set of the Dbl proteins toward 12 Rho proteins; (iii) grouping the Dbl family into functio

89 of complex formation on the concentration of Rho protein in the presence and absence of various nucle

90 Little is known about the role of Rho proteins in apoptosis produced by stimuli evolved sp

91 Moreover, GEF-H1 binds to Rac and Rho proteins in both the GDP- and guanosine 5'-3-O-(thio

92 t the indirect pharmacological inhibition of Rho proteins in brain EC by statins can inhibit a key st

93 obtunded cells, the authors found activated Rho proteins in fully functional macrophages that hypers

94 icrodomains, suggesting an important role of Rho proteins in maintaining the association of TJ protei

95 the available information on the function of Rho proteins in malignant transformation is based on the

96 ral recent studies have suggested a role for Rho proteins in mediating tumor metastasis independent o

97 We will discuss the diverse roles played by Rho proteins in membrane trafficking and focus on the bi

98 ents that mediate changes in the activity of Rho proteins in response to the extracellular matrix rem

99 Although the involvement of Rho proteins in the pathogenesis of vascular diseases is

100 Recent findings suggest that certain Rho proteins, including RhoA, Rac1 and Cdc42, can also p

101 leotide exchange factor (GEF) that activates Rho proteins, inducing cytoskeletal rearrangement in neu

102 Rho protein inhibitor C3 dramatically inhibited both NT

103 The Rho protein inhibitor increased tPA production and rescu

104 delta siRNA, ROKalpha siRNA, and C3 toxin (a Rho protein inhibitor), suggesting that the PKC-delta an

105 The effect of a Rho protein inhibitor, exoenzyme C3 transferase, on tPA

106 d amino acids as fingerprints of the Dbl and Rho protein interaction; and (v) defining amino acid seq

107 on of a constitutively activated recombinant Rho protein into four-cell blastomeres induced cortical

108 s of Rho and Cdc42, TAT-mediated delivery of Rho proteins into osteoclasts was performed.

109 region; hence the availability of the active Rho protein is an important aspect of the centrosomally

110 g indicates that, in the absence of RNA, the Rho protein is structurally distinct from the Rho hexame

111 ly members to modulate the activity of other Rho proteins is also intrinsic to these processes.

112 that the ability of IQGAP1 to interact with RHO proteins is based on a multiple-step binding process

113 Abnormal activation of the Rho proteins is known to play a crucial role in cancer,

114 BC lesions, the populated RhoC but not other Rho proteins is likely to be a primary target for 6-TPs

115 We will describe how the activity of Rho proteins is regulated downstream from growth factor

116 However, the exact contribution of Rho proteins is unclear.

117 Although the activation of formins by Rho proteins is well characterized, its inactivation is

118 We found that the dendrite destabilizer Rho protein kinase 2 (Rock2), which accumulates in the b

119 gration by controlling a potent inhibitor of Rho proteins known as the Rho-GDP dissociation inhibitor

120 rganization and protein production including Rho protein levels and tyrosine phosphorylation with Wes

121 ransfection with antisense oligonucleotides, Rho protein levels were decreased more than 80%, and tyr

122 These data indicate that activation of the Rho proteins may change the activation status of LXR.

123 ese results demonstrate that ARF rather than Rho proteins mediate the activation of PLD by PDGF and p

124 nding of the relative differences of various Rho protein members in nucleotide exchange; (ii) compari

125 However, Rho proteins might also affect microtubules (MTs).

126 Macrophages lacking Rho proteins migrate faster in vitro, which, in the case

127 and overexpression of one dominant negative Rho protein mutant may affect the activity of other memb

128 When the endogenous Rho proteins of the cells were inactivated by treatment

129 Decreasing Rho protein or blocking its function inhibited ECM-stimu

130 affect the structure or conformation of the rho protein or the binding of rho to single-stranded RNA

131 to interfere with signaling by pro-oncogenic Rho proteins, possibly by sequestering common exchange f

132 on of a farnesyl-independent form of RhoB, a Rho protein previously implicated as a critical target f

133 nce many Rho GEFs can interact with multiple Rho proteins promiscuously, and overexpression of one do

134 findings suggesting a role for farnesylated Rho proteins prompted by studies on RhoB, and suggest a

135 As Rho proteins require post-translational modification wit

136 consistent with a model that states that the rho protein requires approximately 70-80 nucleotide resi

137 rnesylation on Ras proteins or vice versa on Rho proteins reversed the differential sensitivities to

138 ligonucleotides to the RNA-binding domain of Rho protein (rho130).

139 ey epithelial cell line, 293T, Cdc42 and all Rho proteins, RhoA, RhoB, and RhoC, but not Rac or Ras c

140 We have identified a human Rho protein, RhoE, which has unusual structural and bioc

141 d residues of the Q-loop region, four mutant Rho proteins, S281A, K283A, T286A and D290A, were isolat

142 ho-dependent terminator in vitro, all mutant Rho proteins show decreased termination compared with wi

143 mmon catalytic domain capable of terminating RHO protein signaling by stimulating the slow intrinsic

144 an function as both an assembly platform for Rho protein signaling complexes and a regulatory protein

145 apter to connect receptor-mediated events to Rho protein signaling.

146 olesterol biosynthetic pathway that regulate Rho protein signaling.

147 ibitors of geranylgeranyl transferase or the Rho proteins significantly increased the expression and

148 with C3 transferase, a specific inhibitor of Rho proteins, significantly inhibited the transmonolayer

149 consistent with their in vivo activation of Rho proteins, stimulation of cyclin D1 transcription is

150 wo unusual structural features of this novel Rho protein suggest a striking evolutionary divergence f

151 ), a protein which interacts with prenylated Rho proteins, suggest that the GDI is in direct contact

152 discerned the conformational changes in the Rho protein that occur upon nucleotide and nucleic acid

153 his process appears to be RhoB, an endosomal Rho protein that regulates receptor trafficking.

154 To identify specific Rho proteins that may regulate this process, we analyzed

155 ial toxins that target the small GTP-binding Rho proteins that regulate the actin cytoskeleton.

156 e coordinated activation and deactivation of Rho proteins, thereby controlling cell motility and ulti

157 orm of Rac1 but not by a dominant a negative Rho protein; this suggested that Rac functions downstrea

158 sults from the cross-linking of the modified Rho proteins to a series of lambda cro RNA derivatives s

159 at SifA may use a similar mode of action via Rho proteins to alter yeast peroxisomal and mammalian en

160 ore, we provide evidence that signaling from Rho proteins to JNK in 293T cells does not involve Pak1.

161 ctions with RhoGDI1, regulates activation of Rho proteins to promote GBM cell invasiveness.

162 o be related to decreased targeting of these Rho proteins to the plasma membrane and could be partial

163 we demonstrate that IQGAP1 interactions with RHO proteins underlie a multiple-step binding mechanism:

164 permits termination of transcription by the Rho protein upstream of mgtA, whereas slow or incomplete

165 The Escherichia coli Rho protein uses the energy of ATP binding and hydrolysi

166 FLAIR (fluorescence activation indicator for Rho proteins) was developed to quantify the spatio-tempo

167 Determinants of membrane targeting of Rho proteins were investigated in live cells with green

168 Like Ras, the Rho proteins (which include Rho, Rac, and CDC42) interac

169 oteins are atypical constitutively GTP-bound Rho proteins, whose regulation remains elusive.

170 ATP hydrolysis is coupled to interactions of Rho protein with RNA 3' of the rut region.

171 Inhibition of Rho proteins with C3 exoenzyme or of Rho kinase with Y27

172 l(-1)) inactivated 50-90% of all endothelial Rho proteins within 60-90 min.

173 ng via a process that involves inhibition of Rho proteins without significantly effecting parallel mo