ライフサイエンスコーパス: p21(ras)

1 nin mutations or nonmutational activation of p21ras.

2 ty of lineages requires signals conveyed via p21ras.

3 herefore, may facilitate the localization of p21ras.

4 of SOS to catalyze the association of GTP on p21RAS.

5 ine phosphorylation of Shc and activation of p21ras.

6 n cells, leading to constitutively activated p21RAS.

7 uanosine triphosphate (GTP)-binding protein, p21ras.

8 the block results from a failure to activate p21ras.

9 to Rat-1 cells stimulated the GTP loading of p21ras.

10 conditions, yet expressed similar levels of p21ras.

11 ation of GAP and decreases in GTP loading of p21ras.

12 ion path of the intrinsic GTPase reaction in p21ras.

13 nylation of protein in whole cells including p21ras.

14 r gene, NF1, a GTPase-activating protein for p21ras.

15 understanding of the biological functions of p21ras.

16 d guanine nucleotide exchange of recombinant p21ras.

17 e latter also prevented S-glutathiolation of p21ras.

18 from the classic GTPases, such as EF-Tu and p21(ras).

19 common pathway involving the small G protein p21(ras).

20 ion is a function of NF1 GRD GAP activity on p21(Ras).

21 vation of protein kinase Czeta (PKCzeta) and p21(ras).

22 ivate MAP kinase, despite its stimulation of p21(ras).

23 ween the Switch I region of NtrC and that of p21(ras).

24 ogous transforming Gly42 --> Val mutation in p21(ras).

25 olves oxidant modification and activation of p21(ras).

26 via modulation of the mevalonate pathway and p21(ras).

27 the ability of Sos to catalyze activation of p21(ras).

28 idylinositol 3-kinase pathways downstream of p21(RAS).

29 GAP that permits insulin to activate Sos and p21(ras).

30 ta suppression in cells containing activated p21(RAS).

31 eting of tumor cells containing an activated p21(RAS).

32 event apoptosis in the presence of activated p21(RAS).

33 hway activated by ANCA F(ab')(2) upstream of p21(ras).

34 [F(ab')(2)] fragment can activate the GTPase p21(ras).

35 mocysteine decreased carboxyl methylation of p21(ras) (a G1 regulator whose activity is regulated by

36 ichment also reduced the membrane content of p21ras (a low molecular weight G-protein requiring farne

37 p21(ras), a guanine nucleotide binding factor, mediates

38 ester significantly decreased ET-1dependent p21(ras) activation and suggested the involvement of the

39 ls resulted in essentially no enhancement of p21(ras) activation despite marked enhancement after tre

40 autophosphorylation mediated ET-1-dependent p21(ras) activation, adenovirus-mediated transfer was em

41 egion of the signaling cascade antecedent to p21(ras) activation, downstream of phosphatidylinositol

42 bited ANCA IgG-induced PIP(3) generation and p21(ras) activation.

43 ential for B cell Ag receptor (BCR)-mediated p21ras activation and calcium mobilization.

44 Whereas p21ras activation and desensitization by receptor tyrosi

45 provide evidence that ET-1-induced biphasic p21ras activation causes sequential stimulation of diver

46 he unique ability of BCR ligation to trigger p21ras activation in CD45+ cells.

47 en extensively investigated, the kinetics of p21ras activation induced by engagement of G-protein-cou

48 ors (18 of 70) that had significantly higher p21ras activation levels (8.0 +/- 0.9%; n = 18) compared

49 ing K-ras mutations had significantly higher p21ras activation levels (8.8 +/- 1.5%; n = 13) compared

50 ly sensitive method was then used to measure p21ras activation levels.

51 These observations suggest that p21ras activation plays a role in the HRG pathway.

52 act on ERK-2 directly, as it also inhibited p21ras activation, an effector molecule upstream from ER

53 on of B cell antigen receptor (BCR)-mediated p21ras activation, though the basis of this inhibition i

54 noted that this pathway might also regulate p21ras activation.

55 eam events, such as calcium mobilization and p21ras activation.

56 -protein-linked signaling systems, including p21ras activation.

57 s/Grb2 interaction can be dispensed with for p21Ras activation.

58 IP(3), activated protein kinase B (PKB), and p21(ras); activation of each mediator was inhibited with

59 Thus, therapies designed to decrease p21(ras) activity and up-regulate Fas antigen expression

60 ylinositol 3 kinase activity is required for p21(ras) activity and, in the current studies, we show t

61 protein encoded by NF1, negatively regulates p21(ras) activity by accelerating the conversion of Ras-

62 Increasing p21(ras) activity by expressing v-ras or by treatment wi

63 and activity in cells, whereas inhibition of p21(RAS) activity decreased the expression of the PKCdel

64 Fe(2+)-induced p21(ras) activity is abrogated with the Src inhibitor PP

65 on of p21(ras) is therefore sustained, while p21(ras) activity is not.

66 p21(ras) activity was reduced and p38 mitogen-activated

67 is transient on a time scale consistent with p21(ras) activity.

68 activating protein that negatively regulates p21(ras) activity.

69 hiolation of p21ras Cys-118, which increases p21ras activity and mediates downstream signaling.

70 d low-density lipoproteins (oxLDL) increases p21ras activity in bovine aortic endothelial cells.

71 F1 (nf1+/-) appear to be caused by excessive p21Ras activity leading to impairments in long-term pote

72 ts a negative feedback mechanism, modulating p21ras activity through ERK-dependent Sos1 phosphorylati

73 d the expression of iNOS, that activation of p21(ras) alone was sufficient to induce the expression o

74 Inhibition of farnesylation of p21ras also blocked the ability of insulin to activate m

75 with a 66% reduction in membrane-associated p21(ras) and a 67% reduction in extracellular signal-reg

76 nd align with conserved sequence elements of p21(Ras) and adenylate kinase.

77 A (5'-N-ethylcarboxamidoadenosine) activated p21(ras) and both p42 and p44 isoforms of extracellular

78 d that, by analogy to the GTPase activity of p21(ras) and by examining the crystallographic structure

79 The formation of a complex between p21(ras) and GAP accelerates the GTPase reaction of p21(

80 a cascade of intracellular signals involving p21(ras) and MAP kinase, culminating in transcription fa

81 Fos kinase activation is dependent on p21(ras) and mitogen-activated protein kinase/ERK kinase

82 tivation resulted in transient activation of p21(ras) and mitogen-activated protein/ERK kinase 1, whi

83 y, simvastatin attenuated activation of both p21(ras) and NF-kappaB in MPP(+)-stimulated microglial c

84 ncentrations of AGE-albumin, which activated p21(ras) and NF-kappaB.

85 First, MPP(+) induced the activation of p21(ras) and nuclear factor-kappaB (NF-kappaB) in mouse

86 tein is closely reminiscent of that found in p21(ras) and other GTPases.

87 ication that is required for the function of p21(ras) and other proteins.

88 analogous to the switch I effector region of p21(ras) and other purine nucleotide-binding proteins; r

89 there are no changes in association between p21(ras) and p110 delta in stimulated basophils.

90 Inhibition of both p21(ras) and p21(rac) activation by NaPB in microglial c

91 tration of NaPB reduced nigral activation of p21(ras) and p21(rac), protected nigral reduced glutathi

92 Consistently, we found activation of both p21(ras) and p21(rac)in vivo in the substantia nigra of

93 ediated apoptosis, may be interconnected via p21(ras) and perhaps Jun NH2-terminal kinase/JUN.

94 tial to signal through G(alphai) to activate p21(ras) and phosphatidylinositol 3-kinase, through G(al

95 ytes, despite an inhibition of activation of p21(ras) and Raf-1 by lovastatin, insulin continued to s

96 strate that Fe(2+)-generated O(2)() mediates p21(ras) and TAK1 activation via PTP inhibition and Lys(

97 ) and GAP accelerates the GTPase reaction of p21(ras) and terminates the signal for cell proliferatio

98 g to the possible activation of Ras protein (p21ras) and phosphatidylinositol kinase.

99 tivated T cells (NFAT) is a major target for p21ras and calcium signalling pathways in the IL-2 gene

100 a fold related to one found in the proteins p21ras and elongation factor EF-Tu.

101 Subsequent to p21ras and ERK deactivation, Sos1 reverts to the non-pho

102 arachidonic acid mediates Ang II's effect on p21ras and if so, to ascertain the signaling mechanism(s

103 ed in an approximately 50% reduction in both p21Ras and IL-1beta protein levels.

104 PtdIns 3-kinase signals cannot mimic p21ras and induce the Rac mediated responses of AP-1 tra

105 sitive-leukemic cells leads to activation of p21ras and phosphatidylinositol 3'-kinase (PI 3-Kinase).

106 Both p21ras and phosphatidylinositol 3-kinase (PI 3-k) are cr

107 or 2 second-tier kinases represented in the p21ras and phosphatidylinositol-3-kinase (PI-3-kinase) p

108 tivation of at least two signaling pathways, p21ras and PI 3-kinase.

109 s recipients of p210BCR-ABL, which activated p21ras and PI-3-kinase pathways, including raf/erk and a

110 n raf/erk and akt, unambiguous components of p21ras and PI-3-kinase pathways, to induce p65 NFkappaB

111 induced a transient and rapid activation of p21ras and preferentially activated c-Jun NH2 terminal k

112 emonstrate that inhibition of prenylation of p21ras and Rho-A arrests insulin-stimulated adipogenesis

113 chidonic acid induced an association between p21ras and Shc.

114 kinase cascades) prevents the activation of p21Ras and strongly suppresses the activation of c-Raf a

115 We observed that Ang II activated p21ras and that mepacrine, a phospholipase A2 inhibitor,

116 This activates p21(ras), and hence, the MAP kinase cascade.

117 on of neurofibromin, a negative regulator of p21(Ras), and increases Ras signaling.

118 ediate growth factor-dependent activation of p21Ras, and requires the presence of intact SH2 and SH3

119 eceptors, the GTP-binding regulatory protein p21Ras, and stimulated mitogen-activated protein (MAP) k

120 apk)/p44(mapk) are not well defined although p21ras- and protein kinase C (PKC)-dependent pathways ha

121 increases interactions of TAK1 and PI3K with p21ras as demonstrated by co-immunoprecipitation and co-

122 phosphatase-1, but does result in increased p21ras-associated phosphatidylinositol 3-kinase activity

123 The Bcl-2/p21Ras association cannot be competed by exogenous gluta

124 Bcl-2/p21Ras association is coincident with new phosphorylatio

125 wever, the resulting secondary activation of p21ras at 30 min does not lead to ERK activation, correl

126 The first peak of activation of p21ras, at 2-5 min, is mediated by immediate association

127 into the nigra, reduced nigral activation of p21(ras), attenuated nigral activation of NF-kappaB, inh

128 ominant-negative mutant of p21(rac), but not p21(ras), attenuated the production of ROS from activate

129 n assay, farnesylthiosalicylic acid inhibits p21(ras) binding to its substrate at comparable concentr

130 l line inhibits, while constitutively active p21ras both enhances and sustains, subsequent TCR-trigge

131 sixfold higher ratio of p21ras-bound GTP to p21ras-bound GDP as compared with parental NIH 3T3 cells

132 tor cDNA had about a sixfold higher ratio of p21ras-bound GTP to p21ras-bound GDP as compared with pa

133 The activation of p21(ras) by ANCA and its F(ab')(2) is prevented by inhib

134 It is also shown that activation of p21(ras) by ANCA is transient, peaking at 5 to 10 min an

135 nts but rather is due to direct targeting of p21ras by reversible S-glutathiolation of cysteine thiol

136 , upregulation of stretch response proteins (p21ras, c-fos, and p38 alpha/beta mitogen-activated prot

137 , we demonstrate that hyperactivation of the p21(ras)-class I(A) PI-3K pathway is the mechanism for t

138 In contrast, in the absence of p21ras, coexpression of JAK2 and Raf-1 resulted in an ov

139 n tumors with mutated or activated wild-type p21ras, compared with their nonactivated counterparts.

140 ariant stably expressing a dominant-negative p21(ras) construct (PC12-N17) or in cells pretreated wit

141 s oxLDL triggers direct S-glutathiolation of p21ras Cys-118, which increases p21ras activity and medi

142 Oncogenic p21(ras) decreases surface Fas antigen expression and re

143 examined with wild-type ras and nonactivated p21ras demonstrated these alterations.

144 orylation of CREB, indicating a role for the p21(ras)-dependent and phosphatidylinositol 3-kinase sig

145 t short-term local delivery of inhibitors of p21(ras)-dependent mitogenic signal transduction prevent

146 and PKC-independent activation of endogenous p21(ras), did not alter cell cycle progression, nor did

147 Given the inability to target p21RAS directly, here we performed an shRNA library scre

148 Given the inability to target p21RAS directly, here we performed an shRNA library scre

149 Haras, which expresses an activated form of p21ras, effected a modest stimulation of basal hANP-chlo

150 The p21(RAS) effector molecule responsible for the initiatio

151 r, identification of alterations in specific p21(ras) effector pathways that control proliferation in

152 Thus, the same p21(RAS) effector, PI3K, is responsible for delivering b

153 NF1 loss leads to deregulation of p21(ras)-effector pathways, which control myeloid cell s

154 onstitutively activated GTP-bound isoform of p21ras (EJ-Ras) produces morphogenic changes characteriz

155 The protein product (p21ras) encoded by the Kras2 gene must be post-translati

156 mediator of cross-talk between PI-3K and the p21(ras)-ERK pathway which functions to alter the cellul

157 domain of ZAP-70, and GAP inhibition of the p21(ras)-ERK pathway.

158 enesis by increasing CD1K activity through a p21(ras)/ERK/activator protein 1 pathway.

159 inases, causing sequential signaling via the p21ras/extracellular signal-regulated kinase pathway.

160 ular proteins, which includes members of the p21ras family, undergoes posttranslational farnesylation

161 hermore, we demonstrate that an inhibitor of p21(ras) farnesyl protein transferase suppressed the exp

162 The alpha subunit of p21(RAS) farnesyltransferase (FNTA), which is also share

163 For peroxynitrite-treated p21ras, five oxidized methionines, five nitrated tyrosin

164 ontrast, signaling was blocked by preventing p21(ras) from associating with the plasma membrane or mu

165 coprecipitated both RhoA and Rac-1, but not p21(ras), from Triton-soluble HeLa cell extracts.

166 The oncoprotein p21ras further activates transcription of the cyclin D1

167 ha i3, and G beta) or monomeric (p21rhoA and p21ras) G-protein or protein kinase C but may be related

168 nodetectable content of G-proteins (p21rhoA, p21ras, G alpha q/11, G alpha i3, and G beta) or protein

169 d the guanine nucleotide exchange factor for p21Ras (GRB-2/SOS), which are in turn required for insul

170 M-CSF-stimulated p21(ras)-GTP and Akt phosphorylation was elevated in Nf1

171 ate (TPA) did not affect the basal amount of p21(ras).GTP but significantly reduced insulin-induced i

172 cell lines, insulin significantly increased p21(ras).GTP loading (1.5-2-fold) and MAP kinase activit

173 For example, the p21(ras).GTP loading, p44 MAPK activity, and induction o

174 activates GAP and reduces insulin-stimulated p21(ras).GTP loading.

175 icantly reduced insulin-induced increases in p21(ras).GTP.

176 ations in the gene encoding Neurofibromin, a p21Ras GTPase Activating Protein (GAP).

177 sine kinases and tyrosine phosphorylation of p21(ras)-guanine nucleotide activating protein.

178 ail, the post-translational modifications of p21ras (H-ras) exposed to oxidants by combining bottom-u

179 rmed with a constitutively active isoform of p21(Ras), H-RasV12 (v-H-Ras or EJ-Ras), produced large a

180 The proto-oncogene product, p21(ras), has been implicated in the cellular mechanism

181 Point mutations of p21ras have been identified in various tumor types and l

182 The expression of oncogenic p21(ras) in a number of cell types, including Jurkat (a

183 ET-1 (100 nm) induced a rapid activation of p21(ras) in human glomerular mesangial cells (HMC).

184 S, and that NaB suppressed the activation of p21(ras) in microglia.

185 nt of p21(ras), supported the involvement of p21(ras) in MPP(+)-induced microglial activation of NF-k

186 AGE-albumin, a prototypic ligand, activated p21(ras) in rat pulmonary artery smooth muscle cells tha

187 To further investigate the role of p21(ras) in the regulation of apoptosis, the cellular me

188 M1311 cells, further supporting the role of p21(ras) in UV-mediated JNK activation.

189 stently, we found a very rapid activation of p21(ras) in vivo in the substantia nigra pars compacta o

190 Expression of a dominant negative form of p21ras in a thymocyte cell line inhibits, while constitu

191 Altering insulin signaling by overexpressing p21ras in adipocytes of transgenic mice results in incre

192 w that ET-1 induces a biphasic activation of p21ras in rat glomerular mesangial cells.

193 increase in the relative level of GTP-bound p21ras in response to OSM.

194 To examine the role of p21ras in the development of B lymphocytes, we generated

195 the observed LFER for the GTPase reaction of p21ras in the presence of GAP and discuss its relevance

196 ng Bronsted slope for the GTPase reaction of p21ras in the presence of GTPase Activating Protein (GAP

197 has been proposed that the sole function of p21(Ras )in Raf activation is to recruit Raf to the plas

198 -induced post-translational modifications of p21ras including S-nitrosation and S-glutathiolation hav

199 adding the COOH-terminal 9 amino acids from p21(ras), including the CAAX motif, to IRS-1 (IRS-CAAX)

200 red for IFNgamma activation of Raf-1 that is p21(ras)-independent.

201 tion and further emphasize the importance of p21ras-independent signaling pathways in growth factor-m

202 ion of myeloid cells in disease states where p21(ras) is hyperactivated.

203 b2/son of sevenless pathway to activation of p21(ras) is therefore sustained, while p21(ras) activity

204 p21ras is a potent regulator of myogenic cell growth and

205 p21ras is activated by the T cell antigen receptor (TCR)

206 t to the anti-Ras injection, indicating that p21Ras is required for pRb inactivation but also has oth

207 hich encodes a GTPase activating protein for p21(ras), is frequently inactivated in juvenile myelomon

208 Injection of antibodies to p21ras itself, or a recombinant Raf-1 protein domain whi

209 icromol/L) concentration-dependently reduced p21(ras) levels in porcine coronary artery smooth muscle

210 abolish ET-1-mediated increases in GTP-bound p21(ras) levels.

211 ion of key cell signalling pathways, such as p21ras, MAP kinases, NF-kappaB and cdc42/rac, thereby re

212 ses have been implicated in cell growth, the p21(ras)-MAP kinase pathway may represent one of the mec

213 that lovastatin decreased the enhanced brain p21Ras-MAPK activity of the nf1+/- mice, rescued their L

214 In response to various death stimuli, p21(ras) may act as a common intermediate regulator in t

215 suggested that the proliferative effects of p21(ras) may depend on signaling outputs from the small

216 or its role in signaling to the small GTPase p21(ras), mediated through its interaction with the SOS

217 rated that PKCdelta plays a critical role in p21(RAS)-mediated apoptosis.

218 p21Ras mediates mitogenic responses and also renders cel

219 ynthesis requires both p70 S6 kinase and the P21ras/MEK pathway.

220 of EPO via AT1R-mediated Egr-1 activation by p21Ras-mitogen-activated protein kinase/ERK kinase-ERK1/

221 phosphatidylinositide (PI) 3-kinase and the p21(ras)/mitogen-activated protein (MAP) kinase cascade.

222 identify lovastatin as a potent inhibitor of p21Ras/Mitogen Activated Protein Kinase (MAPK) activity

223 athways emanating from the IR, e.g., Shc/SOS/p21Ras/mitogen-activated protein kinase.

224 We demonstrate that Bcl-2 and p21Ras molecules can be co-immunoprecipitated in Jurkat

225 s abrogated by dominant-negative and Cys-118 p21ras mutants, and the latter also prevented S-glutathi

226 vating the GTPase reaction of many oncogenic p21ras mutants.

227 An activating p21(RAS) mutation, or activation of the phosphatidylinos

228 he MAPK cascade and the presence of specific p21ras mutations in this model.

229 ts of the MAPK cascade independent of common p21ras mutations.

230 Hence p21ras normally regulates early development of B lymphoc

231 ate the pro-apoptotic pathway induced by the p21(RAS) oncoprotein, we first identified the specific P

232 in synergy with T cell mitogens and with the p21ras oncoprotein.

233 old, and dominant-negative mutants of either p21(ras) or ERK reduced AII-stimulated cyclin D1 promote

234 transferase, suggests that farnesylation of p21(ras) or other proteins regulates the induction of iN

235 Our molecular dynamics simulations of the p21ras-p120GAP-GTP complex suggest that the local struct

236 e, and five markers, including CD34MVD, EMA, p21ras, p21WAF1, and tissue inhibitors of metalloprotein

237 rix metalloproteinases (MMP) -2, MMP-9, p16, p21ras, p21WAF1, p27kip1, p53, TIMP-1, TIMP-2, vascular

238 omoter, mRNA, and protein expression via the p21(RAS) pathway.

239 ism by which Ag receptors are coupled to the p21ras pathway in J558Lmicrom3.

240 al agents to link the hyperactivation of the p21(Ras)-phosphatidylinositol 3-kinase (PI3K) pathway to

241 n in hepatic macrophages and TAK1, PI3K, and p21ras physically interact in caveolae to initiate signa

242 These studies identify the p21(Ras)-PI3K pathway as a major regulator of the gain i

243 The small guanine nucleotide binding protein p21(Ras) plays an important role in the activation of th

244 ies provide in vivo confirmation of the role p21(ras) plays in JNK activation by UV irradiation.

245 se inhibitor III (FPTIII) is an inhibitor of p21(ras) processing and that when it is given locally in

246 The pathway involving the signalling protein p21Ras propagates a range of extracellular signals from

247 modes for GDP and GTP bound to the c-Harvey p21(ras) protein have been determined using 18O isotope

248 Oncogenic p21ras proteins can only exert their stimulation of cell

249 hibit the post-translational modification of p21ras proteins with a terminal CAAX motif.

250 Using dominant-negative constructs of p21(Ras), Raf-1 kinase, and mitogen-activated protein (M

251 inositide 3-kinase (PI-3K) and the classical p21(ras)-Raf-Mek-ERK pathway to confer a distinct prolif

252 n components of the Jak/STAT cascade and the p21(ras)/Raf-1/MAPK cascade are unexplored.

253 togen-activated protein kinase (MAPK) in the p21(ras)/Raf-1/MEK2 pathway and induced expression of th

254 Moreover, blocking p21Ras/Raf-1/MEK/ERK cascade by the expression of a tran

255 report here that OGD preconditioning induces p21(ras) (Ras) activation in an N-methyl-D-aspartate rec

256 AP are GTPase-activating proteins (GAPs) for p21(Ras) (Ras) and negatively regulate output by acceler

257 n essential downstream effector of activated p21(Ras) (Ras) in transducing proliferation or different

258 p21(ras) (Ras) proteins and GTPase-activating proteins (

259 sor gene, negatively regulates the output of p21(ras) (Ras) proteins by accelerating the hydrolysis o

260 receptor stimulation leads to activation of p21(ras) (Ras) through generation of nitric oxide (NO) v

261 its core the canonical alpha-beta domain of p21(ras) (Ras).

262 ls from activated growth factor receptors to p21Ras (Ras) and other signaling molecules.

263 e on the critical cellular signaling protein p21Ras (Ras) by S-nitrosylation of a redox-active thiol

264 p21Ras (Ras) proteins cycle between active GTP-bound and

265 mmon structural core, exemplified by that of p21ras (Ras), and significant sequence identity, suggest

266 romin, a GTPase-activating protein (GAP) for p21ras (Ras).

267 (Draf) activation in the complete absence of p21(Ras) (Ras1).

268 downstream events linked to Shc/Grb2/Sos and p21ras rather than protein kinase C as reported previous

269 d cells and tumor cells containing activated p21(RAS) results in apoptosis.

270 n by dominant negative mutants of PKCzeta or p21(ras) results in loss of RelA transcriptional activit

271 This initial activation of p21ras results in activation of the extracellular signal

272 onally, "top-down" analysis was conducted on p21ras S-glutathiolated by oxidized glutathione and iden

273 Moreover, p21ras S-glutathiolation and activation can be reversed

274 The time course of p21ras S-glutathiolation following peroxynitrite corresp

275 activation as well as directly activate the p21(ras) signaling pathway, did not restore the prolifer

276 dermal growth factor receptor (EGFR), to the p21ras-signaling pathway.

277 pathways in the IL-2 gene and is induced by p21ras signals acting in synergy with calcium/calcineuri

278 In contrast, p21ras signals are unable to induce Akt/PKB activity in

279 Deltap21(ras), a dominant-negative mutant of p21(ras), supported the involvement of p21(ras) in MPP(+

280 ce for a plasma membrane binding protein for p21(ras) that can recognize the isoprenoid substituent a

281 functional studies have demonstrated that in p21ras the substrate of the reaction, GTP itself, plays

282 P21ras, the translation product of the most commonly mut

283 ollectively, these findings demonstrate that p21(RAS), through its downstream effector PI3K, induces

284 th the plasma membrane or mutating Cys118 on p21(ras) to Ser.

285 ical Rac-1 signaling pathways and can couple p21ras to cell survival mechanisms via the serine/threon

286 nduces the translocation of the small GTPase p21Ras to GM1- and cholesterol-rich membrane areas.

287 ppaB in HM via activation and interaction of p21(ras), transforming growth factor beta-activated kina

288 Constitutively active p21ras (v-H-Ras) activated NF- kappa B-dependent transcr

289 s linkage of a G protein-coupled receptor to p21ras via Shc tyrosine phosphorylation and association

290 more, the ratio of GTP/GDP bound to cellular p21ras was consistently higher in the hSos1-Isf II-trans

291 noprecipiation experiments demonstrated that p21Ras was constitutively bound to the AT1R; this associ

292 The activity of p21Ras was decreased and Raf-1 abundance increased in PC

293 A neutralizing antibody directed against p21Ras was microinjected into cells derived from mutant

294 our tumors examined with activated wild-type p21ras, we observed increased c-erbB-2 receptor expressi

295 Mutations in p21ras were analyzed using an enzyme-linked immunosorben

296 d the guanosine triphosphate-binding protein p21ras were found to remain unactivated upon stimulation

297 Mutations in p21ras were not detected in this experimental model of H

298 nt effector of apoptosis, activates cellular p21(ras), which may be required for completion of the ce

299 tides corresponding to amino acids 96-110 on p21(ras), which were shown to block Ras-JNK association,

300 s participate in the specific association of p21ras with plasma membranes is the subject of this repo