ライフサイエンスコーパス: GTP-bound form

1 enomic null, and the third was an engineered GTP-bound form.

2 se activity and remains always in its active GTP-bound form.

3 cifically with the rab GTPase, Sec4p, in its GTP-bound form.

4 and consequently is restricted mostly to the GTP-bound form.

5 ass I ARFs, especially ARF1, but only in the GTP-bound form.

6 from an inactive GDP-bound form to an active GTP-bound form.

7 een an inactive GDP-bound form and an active GTP-bound form.

8 that is more similar to the GDP than to the GTP-bound form.

9 ir "inactive" GDP-bound form to the "active" GTP-bound form.

10 a3 was shown to activate Cdc42 to its active GTP-bound form.

11 und form and an active, membrane-associated, GTP-bound form.

12 m its inactive, GDP-bound state to an active GTP-bound form.

13 tes with purified ribosomal particles in the GTP-bound form.

14 oting efficient ribosomal recruitment of its GTP-bound form.

15 % of total endogenous Rab3D was found in the GTP-bound form.

16 t PI3-K may preferentially interact with the GTP-bound form.

17 B's G protein domain may exist mostly in the GTP-bound form.

18 t Sec3p directly interacts with Cdc42 in its GTP-bound form.

19 e non-guanine nucleotide-bound state and the GTP-bound form.

20 DP-ribosylation factor (ARF5) in its active, GTP-bound form.

21 tching between inactive GDP-bound and active GTP-bound forms.

22 Rac and Cdc42 are similarly active in their GTP-bound forms.

23 gh its alternation between the GDP-bound and GTP-bound forms.

24 gulates RHEB shuttling between GDP-bound and GTP-bound forms.

25 y to populate Ras in its biologically active GTP-bound form after the dissociation of GDP.

26 ect effector of Rab26 and binds Rab26 in its GTP-bound form, albeit only with low affinity.

27 t M(3) mAChR activation converts Rac1 to the GTP-bound form, alters interactions between Rac1, IQGAP1

28 ation between Ffh and FtsY 400-fold in their GTP-bound form, analogous to its 200-fold catalytic effe

29 ns act as molecular switches, with an active GTP-bound form and an inactive GDP-bound form.

30 nter mitosis, Spg1 accumulates in an active, GTP-bound form and binds the Cdc7 protein kinase to caus

31 e activity of its downstream effector in its GTP-bound form and inactivating the effector upon GTP hy

32 EF-G binds to the ribosome in a GTP-bound form and subsequently catalyzes GTP hydrolysis

33 hes, cycling between the biologically active GTP-bound form and the inactive GDP-bound state.

34 formational changes are observed between the GTP-bound form and the transition state intermediate, ma

35 Cycling between the GDP- and GTP-bound forms and the accessory proteins that regulate

36 ease in the proportion of Ras present in the GTP-bound form, and 2) introduction of neutralizing anti

37 ion and fusion by cycling between an active, GTP-bound form, and an inactive, GDP-bound form.

38 RhoA(Val-14) is predominantly in the [(32)P]GTP-bound form, and negligible levels of [(32)P]GDP or [

39 Like Ras, ARFs are active in their GTP-bound form, and their duration of activity is contro

40 cycle between inactive GDP-bound and active GTP-bound forms, and it is the active form that interact

41 y interacts with Cdc24 and Bem1: Bud1 in its GTP-bound form associates preferentially with Cdc24, whe

42 in specifically binds Rac and Cdc42 in their GTP-bound forms both in vitro and in cell samples.

43 l act as molecular switches, active in their GTP-bound form but inactive when GDP-bound.

44 ting or immunocytochemistry, but reduced the GTP-bound form by 78.6 +/- 3.3%.

45 aintained >10% of the total Gq in the active GTP-bound form by catalyzing GTP binding at a rate of at

46 The elimination of the Rac1-GTP-bound form from the cell by the introduction of the

47 R activation converts endogenous Rac1 to the GTP-bound form in cells expressing HA-Rac1 but not in ce

48 he ratio of inactive (GDP-bound) and active (GTP-bound) forms in the cell.

49 at Ypt31/32 in their guanosine triphosphate (GTP)-bound form interact directly with Myo2-GTD.

50 egative regulator of exocytosis and that its GTP-bound form interacts with Rabphilin3, a possible eff

51 Rab11, in its GTP-bound form, interacts with Rabin8 and kinetically st

52 Conversion from the GDP- to GTP-bound form is catalyzed by guanine nucleotide exchan

53 Arf GTPases, the switch from the GDP- to the GTP-bound form, is thought to be crucial for their funct

54 nt KRAS is persistently frozen in its active GTP-bound form may not be accurate.

55 e, the start codon, fMet-tRNA(fMet), and the GTP bound form of initiation factor 2 bound to the 30S s

56 The GTP bound form of the g-protein alpha-subunit and in som

57 binding sites may be the mechanism by which GTP bound forms of other small GTPases function in corre

58 The cycling between GDP- and GTP- bound forms of the Ras protein is partly regulated

59 ing of a human kidney cDNA library using the GTP-bound form of a class II ADP-ribosylation factor (AR

60 A GTP-bound form of a Ran mutant that cannot bind NTF2 was

61 n act on its membrane-restricted target, the GTP-bound form of ARF1.

62 Arfophilin bound only to the active, GTP-bound form of ARF5 and did not bind to GTP-ARF3, whi

63 The GTP-bound form of ARF5 with amino acid residues in the N

64 , Exo70, and Sec5 bind preferentially to the GTP-bound form of Arl13b, consistent with the exocyst be

65 1, the activity of which is regulated by the GTP-bound form of Cdc42 and Rac and by sphingosine, is p

66 are known to be activated by binding to the GTP-bound form of Cdc42 or Rac1, which are small GTPases

67 CIP4 interacts with the GTP-bound form of cdc42, with the Wiscott Aldrich Syndro

68 Nap1, the Clb2-Cdc28 kinase complex, and the GTP-bound form of Cdc42.

69 Cla4p kinase was activated in vivo by the GTP-bound form of Cdc42p.

70 ed membrane tubule formation, suggesting the GTP-bound form of DLP1 deforms liposomes into tubules as

71 Recent evidence suggests that the GTP-bound form of dynamin may recruit factors that execu

72 on the N-acylation, but does not require the GTP-bound form of Galpha(t1).

73 oth decreased the affinity of Gz GAP for the GTP-bound form of Galphaz by at least 90 percent and dec

74 mulator (ralGDS), factors that interact with GTP-bound form of H-Ras.

75 the disordered switch II in the uncomplexed GTP-bound form of H-Ras.

76 the "off" and "on" allosteric states of the GTP-bound form of H-Ras.

77 The GTP-bound form of IF2 accelerates subunit joining, where

78 ar tyrosine kinase which associates with the GTP-bound form of p21cdc42Hs.

79 eotide exchange factor (GEF) to generate the GTP-bound form of Rab10, but this GEF has not hitherto b

80 ab10 and thereby leads to an increase in the GTP-bound form of Rab10, which in turn triggers movement

81 hat SH3TC2 interacts preferentially with the GTP-bound form of Rab11, identifying SH3TC2 as a novel R

82 EPI64B almost completely abolished the GTP-bound form of Rab27B, without affecting GTP-Rab3D.

83 lasmic and high nuclear concentration of the GTP-bound form of Ran provides directionality for both n

84 RASSF1A promotes the accumulation of the GTP-bound form of RAN via the MST2-induced phosphorylati

85 anBP2, which specifically interacts with the GTP-bound form of Ran.

86 ad us to suggest that the interaction of the GTP-bound form of Ran/TC4 with p97 is linked to an early

87 mplex process involving association with the GTP-bound form of Ras (Ras-GTP), membrane translocation

88 gnificantly increased the level of activated GTP-bound form of Ras in these cells.

89 To examine the localization of the GTP-bound form of Ras, we used a FRET assay that exploit

90 rapidly promote accumulation of the active, GTP-bound form of Ras.

91 Gef3p interacts physically with the GTP-bound form of Rho3p.

92 to cognate eukaryotic effectors, as only the GTP-bound form of RhoA family members stimulates enzymat

93 d an increase in the levels of the activated GTP-bound form of RhoA, but not Rac1 or Cdc42, in vivo.

94 The GTP-bound form of Sar1p recruits Sec23/24p to the liposo

95 Expression of the constitutively active GTP-bound form of TC10 (TC10Q/75L), but not the inactive

96 The GTP-bound form of TC10 directs the trafficking of CFTR f

97 ic and strong interaction of BLOC-3 with the GTP-bound form of the endosomal GTPase, Rab9.

98 A concentration gradient of the GTP-bound form of the GTPase Ran across nuclear pores is

99 essing in a manner dependent upon the active GTP-bound form of the GTPase.

100 in vesicular transport requires not only the GTP-bound form of the protein but also the interaction o

101 exin B (PlexB) binds directly to the active, GTP-bound form of the Rac GTPase.

102 h interacts in the two-hybrid assay with the GTP-bound form of the Rho-type Cdc42 GTPase, a key regul

103 The active, GTP-bound form of the small GTPase RhoA activates a seri

104 The active, GTP-bound form of the small GTPase RhoA is a key regulat

105 ab effector, interacts specifically with the GTP-bound form of the synaptic vesicle-associated protei

106 and physically interacts with the activated, GTP-bound form of Vps21p, a Rab GTPase that functions in

107 o phosphorylated Pho4 in the presence of the GTP-bound form of yeast Ran in vitro.

108 up to 54-fold, has a higher affinity for the GTP-bound form of Ypt1p than for the GDP-bound form, and

109 ions as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required for the fu

110 inities for SNAREs, vacuolar lipids, and the GTP-bound form of Ypt7p; each of these affinities contri

111 the MAP3K protein MRK directly binds to the GTP-bound forms of both RhoA and RhoC in vitro.

112 g RhoGDI to distinguish between the GDP- and GTP-bound forms of Cdc42 and holds important implication

113 GTP-bound forms of Cdc42 and Rac bind to the regulatory

114 t that the GDI can bind to the GDP-bound and GTP-bound forms of Cdc42Hs equally well.

115 hilin, suggesting it is a target protein for GTP-bound forms of class II ARFs.

116 entified to be well conserved in the GDP and GTP-bound forms of EF-Tu structures, as well as in the s

117 Binding constants for the interaction of the GTP-bound forms of Rab3a, Rab3b, Rab3c, and Rab3d with R

118 JNK kinases, and increases the levels of the GTP-bound forms of Ral and Ras.

119 assembly, although the roles of the GDP- and GTP-bound forms of Ran in the recruitment of precursor v

120 import is likely a gradient of the GDP- and GTP-bound forms of Ran, a small GTPase.

121 , a striking exception to the rule that only GTP-bound forms of Ras-superfamily GTPases have active c

122 Recently, mammalian kinases that bind to the GTP-bound forms of Rho p21s have been isolated.

123 thesis that the balance between the GDP- and GTP-bound forms of spi1p mediates the host of nuclear pr

124 ain arrangement in the apo form and GDP- and GTP-bound forms of the factor, raising the question of h

125 Proteins that associate with the GTP-bound forms of the Ras superfamily of proteins are p

126 ange of MeaB must occur between the GDP- and GTP-bound forms of this protein.

127 to the affinity observed for the activated (GTP-bound) form of Cdc42 and that beryllium (Be) can rep

128 g-inactive (GDP-bound) and signaling-active (GTP-bound) forms of Cdc42 in solution, we show that when

129 t MLK2 and MLK3 interact with the activated (GTP-bound) forms of Rac and Cdc42, with a slight prefere

130 hat, unusually, it is the GDP-bound, not the GTP-bound, form of the GTGs that actively relays the sig

131 ated with Golgi membranes are in the active, GTP-bound form or are bound to some other unidentified p

132 Ras GTPase cycles between its active GTP-bound form promoted by GEFs and its inactive GDP-bou

133 In their active GTP-bound form, Rab proteins interact with proteins term

134 tion with 5HT stabilizes Rab4 in its active, GTP-bound form, Rab4-GTP.

135 form (RanGDP) and a guanosine triphosphate (GTP)-bound form (RanGTP) and plays important roles in nu

136 Remarkably, Arf6 in its GTP-bound form recruited ARNO to the PM and the two prot

137 GEF cascades, in which one Rab in its GTP-bound form recruits the GEF that activates the next

138 In its GTP-bound form, Ryh1, an evolutionarily conserved Rab GT

139 , ARF6-Q67L, which is predicted to be in the GTP-bound form, stimulates endocytosis exclusively at th

140 RhoA, in its active GTP-bound form, stimulates transcription through activat

141 y with the GDP-bound form of Rab but not the GTP-bound form, suggesting that the apparent Km effect i

142 In vivo, RhoE is found exclusively in the GTP-bound form, suggesting that unlike previously charac

143 addition, the interaction of TDalpha in its GTP-bound form (TDalphaGTPgammaS), the transition state

144 ARF6 was expressed in the GTP-bound form that localizes at the plasma membrane, re

145 e GTGs exhibits greater ABA binding than the GTP-bound form, the GTPase activity of the GTGs is inhib

146 In their GTP bound form, these proteins interact with downstream

147 ase, but differ in their ability to regulate GTP-bound forms; these functional differences are attrib

148 ed that strongly impaired the ability of the GTP-bound form to interact with Rabphilin3.

149 forms of rap1B demonstrated that the active GTP-bound form translocates to the nucleus whereas inact

150 Active Rap1 (GTP-bound form) was present in anergic cells.