ライフサイエンスコーパス: Ras protein

1 tively with the stress elicited by oncogenic Ras protein.

2 ed to glutathione beads to isolate activated ras protein.

3 uman intrabodies which bind to the oncogenic RAS protein.

4 vularia lunata, which is homologous with the Ras protein.

5 antigenic sites, or the presence of a mutant RAS protein.

6 luster formation by crosslinking constituent Ras proteins.

7 molecule inhibitors that directly target the Ras proteins.

8 d for optimal plasma membrane association of RAS proteins.

9 utations in RAS genes or otherwise activated RAS proteins.

10 s recently been proposed for the H-Ras and M-Ras proteins.

11 n cells partially dependent on expression of RAS proteins.

12 tochondria in the subcellular trafficking of Ras proteins.

13 been considered representative of all three Ras proteins.

14 mbrane attachment and biological activity of Ras proteins.

15 tes expressing the oncogenic forms of Raf or Ras proteins.

16 be feasible to develop direct inhibitors of RAS proteins.

17 ion of Ras-GAP and thereby the activation of Ras proteins.

18 could lead to increased potency of oncogenic Ras proteins.

19 stem for the plasma membrane localization of Ras proteins.

20 lmitoylation and subcellular localization of Ras proteins.

21 involved in the plasma membrane targeting of Ras proteins.

22 terminal proteolytic processing of the mouse Ras proteins.

23 eotide exchange factors (GEFs) that activate Ras proteins.

24 quate subcellular distribution of S-acylated Ras proteins.

25 potential binding partners for farnesylated Ras proteins.

26 gies and well-defined binding pockets on the Ras proteins.

27 roaches under investigation to target mutant RAS proteins.

28 llular distribution and activity of K- and H-Ras proteins.

29 inhibit the post-translational processing of RAS proteins.

30 We identified dexamethasone-induced Ras protein 1 (Dexras1) as a negative regulator of prote

31 is similar to those of GDP or GTP analogs in ras proteins, a prototype GTPase.

32 Ras proteins accelerate GTP hydrolysis by a factor of 10

33 Ras proteins activate Raf and PI-3 kinases, as well as e

34 Given that oncogenic Ras proteins activate the transcription factor NF-kappaB

35 re unsolved, and it is unknown precisely how Ras proteins activate their downstream targets.

36 Ras proteins activate three primary classes of effectors

37 were correlated with increased Rap1, but not Ras, protein activation following PMA and calcium ionoph

38 The Ras protein acyltransferase (PAT) consists of a complex

39 ccharomyces cerevisiae is palmitoylated by a Ras protein acyltransferase (Ras PAT) encoded by the ERF

40 One of the loci is zDHHC9, a gene encoding a Ras protein acyltransferase.

41 tion leads to a constitutively active mutant Ras protein and activation of downstream signaling event

42 Total H-ras protein and cyclin D1 were found to increase during

43 s of guanosine triphosphate-bound (active) H-ras protein and cyclin E were increased during the putat

44 tein kinase C that is activated by oncogenic Ras protein and is required for K-Ras-induced transforma

45 f YAP were associated with activation of the RAS protein and its downstream AKT and ERK.

46 Mx1-Cre, LSL-Nras(G12D) mice show much lower Ras protein and Ras-GTP levels.

47 rase reporter and strikingly increased the K-ras protein and the downstream effectors ERK1/2 and B-Ra

48 Ras proteins and cAMP-dependent protein kinase (protein

49 s in the extreme C terminus of the different Ras proteins and farnesylation of the CaaX box cysteine

50 These activations were mediated through Ras proteins and GPR40, a receptor expressed on the surf

51 a functional relationship between endogenous RAS proteins and identify a dynamic physical interaction

52 Proliferation of cells lacking both Ras proteins and p53 can be prevented by reexpression of

53 04 also inhibits the activities of wild-type Ras proteins and Ras oncoproteins.

54 s terminating with a CAAX motif, such as the Ras proteins and the nuclear lamins, undergo post-transl

55 One such pathway, whose components include Ras proteins and the PAK kinase Ste20, allows the human

56 n interactions, including the interaction of RAS proteins and their effectors, may provide chemical p

57 p21(ras) (Ras) proteins and GTPase-activating proteins (GAPs) tigh

58 en in the context of mutation of the cognate Ras protein, and only relatively weak effects are detect

59 in the post-translational processing of the RAS protein, and were developed initially as a therapeut

60 Despite extensive efforts to target mutated RAS proteins, anticancer agents capable of selectively k

61 The Ras proteins are aberrantly activated in a wide range of

62 riginates in differences in the way in which Ras proteins are activated by ligands of varying potency

63 f intracellular cAMP and the active forms of Ras proteins are also elevated in the ubp3Delta mutant.

64 ns that result in constitutive activation of RAS proteins are associated with approximately 30% of al

65 Here we report that Ras proteins are associated with lipid rafts in resting

66 Ras proteins are binary switches that, by cycling throug

67 RAS proteins are binary switches, cycling between ON and

68 mice have provided evidence that H-Ras and K-Ras proteins are bioequivalent.

69 Oncogenic mutant Ras proteins are commonly expressed in human tumors, wit

70 Whereas both Ras proteins are constitutively activated, 32D cells exp

71 Ras proteins are critical nodes in cellular signaling th

72 RAS proteins are critical regulators of mitosis and are

73 RAS proteins are difficult to target pharmacologically;

74 Ras proteins are essential components of signal transduc

75 The Ras proteins are essential GTPases involved in the regul

76 ctural and biochemical properties, oncogenic Ras proteins are exceedingly difficult targets for ratio

77 Ras proteins are founding members of a large superfamily

78 Ras proteins are highly conserved signaling molecules th

79 RAS proteins are important direct activators of p110alph

80 Dynamic clusters of lipid-anchored Ras proteins are important for high-fidelity signal tran

81 Ras proteins are important signalling hubs frequently dy

82 Ras proteins are key regulators of cell growth and diffe

83 Ras proteins are major regulators of chemotaxis in Dicty

84 Ras proteins are members of a superfamily of related sma

85 Ras proteins are membrane bound signalling hubs that ope

86 Ras proteins are modified by farnesyltransferase (FTase)

87 B-Raf and N-Ras proteins are often activated in melanoma, yet their

88 Although RAS proteins are often said to be "undruggable," there i

89 Ras proteins are organized into membrane nanoclusters, w

90 Most Ras proteins are posttranslationally modified by a palmi

91 Understanding how Ras proteins are regulated is important for elucidating

92 RAS proteins are signal transduction gatekeepers that me

93 Ras proteins are small GTPases that act as signal transd

94 RAS proteins are small GTPases that play a central role

95 Ras proteins are small GTPases that regulate cellular gr

96 Ras proteins are small GTPases with well known functions

97 Ras proteins are synthesized as cytosolic precursors, bu

98 In general, Ras proteins are thought to promote cardiac hypertrophy,

99 hibiting conditions, indicating that RasC or RasD proteins are essential for GSK3-mediated PKBR1 inhi

100 ression of both wild-type Harvey and Kirsten Ras proteins as contributors to rat mammary carcinogenes

101 Ras proteins associate with cellular membranes as a cons

102 the G12D and G13D oncogenic mutants of the K-Ras protein bound to a negatively charged lipid bilayer.

103 ine that contains high levels of wild-type H-ras protein but no H-rasV(12) mutation), introduction of

104 cells, G protein-coupled receptors activate Ras proteins, but it is unclear how Ras-associated pathw

105 Plants do not have Ras proteins, but they contain Rho-like small G proteins

106 njugates), and ISG15, in turn, stabilizes Ki-Ras protein by inhibiting its targeted degradation via l

107 icancer agents developed to target oncogenic Ras proteins by inhibiting Ras farnesylation.

108 therapeutic dilemma, as direct targeting of Ras proteins by small molecules has proved difficult.

109 Ras proteins can bring about activation of MEK1 and p42

110 However, a current model suggests that Ras proteins can compartmentalize to regulate different

111 Activation of RAS proteins can lead to multiple outcomes by virtue of

112 In vitro studies also suggest that WT Ras proteins can suppress the tumorigenic properties of

113 c42 GTPase, a member of the Rho subfamily of Ras proteins, can signal to the cytoskeleton through its

114 In the case of the Ras proteins, carboxyl methylation is important for targ

115 factor 1 (Ras-GRF1), a neuronal activator of Ras proteins, causes a specific loss of HFS-LTP in the m

116 lucidate the regulatory mechanism of the key Ras protein Clg2p in C. lunata.

117 ore stable complexes with Rap2 and classical Ras proteins compared with Rap1.

118 RAS proteins conduct signaling from surface receptors to

119 Using chimeric Ras proteins containing all combinations of Ras backgrou

120 Experiments have shown that homologous Ras proteins containing different lipid modification, wh

121 K-Ras proteins containing this tandem duplication or a sim

122 Active Ras proteins contribute to breast carcinogenesis and pro

123 Structural dynamics of Ras proteins contributes to their activity in signal tra

124 The Saccharomyces cerevisiae Ras proteins control cell growth by regulating the activ

125 us to the dual-signal targeting mechanism of Ras proteins, cooperate to target heterotrimeric G prote

126 Moreover, IDabs selected for binding to the RAS protein could inhibit RAS-dependent oncogenic transf

127 Similarly, we found that mutant Ras proteins could be detected and quantified in clinica

128 Ras proteins cycle between GDP-bound and GTP-bound state

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

130 Mutant K-Ras proteins demonstrate a range of gain-of-function eff

131 RAS proteins directly activate PI3-kinases.

132 is provided, using a dominant-negative N17 H-Ras protein (dn-H-Ras) and MEK inhibitor U0126, that act

133 Phosphorylation of R-Ras proteins does not affect their subcellular localizat

134 Oncogenic activation of Ras proteins due to missense mutations is frequently det

135 HDX provides a means of evaluating Ras protein dynamics, which may be useful for understand

136 distinct lipid compositions, indicating that Ras proteins engage in isoform-selective lipid sorting a

137 tial to inactivate both wild-type and mutant Ras proteins expressed in malignancies.

138 12D) expression results in markedly elevated Ras protein expression and Ras-GTP levels in Mac1(+) cel

139 MIC-dependent tumor growth through promoting RAS protein expression and that cancer therapies targeti

140 These results show that the level of K-ras protein expression is a major determinant of prolife

141 own of HAGE led to a significant decrease in RAS protein expression with a concomitant decrease in ac

142 KRAS, a key member of the RAS protein family, is an attractive cancer target, as f

143 n was blocked by the structurally dissimilar Ras protein farnesyl transferase inhibitors manumycin-A

144 e molecular mechanism by which full-length H-ras proteins form nanoclusters in a model membrane.

145 t experiments have shown that membrane-bound Ras proteins form transient, nanoscale signaling platfor

146 analyze the nature of the pool of endogenous Ras proteins found in the cytosol.

147 Although vesicular transport of the H-Ras protein from the Golgi to the plasma membrane is wel

148 egion, modulates the effector selectivity of RAS proteins from H-RAS to E-RAS features.

149 l known, but the precise mechanisms by which RAS proteins function are less clear.

150 Ras proteins function as signaling hubs that are activat

151 tical for beta(2)-integrin adhesion and that Ras-protein functions as the common regulator for cytoki

152 Unlike Ras proteins, Gbetagamma contains a single targeting sig

153 Here, we found that Ras proteins (H-Ras and R-Ras) enhance SF-mediated activ

154 lved in the IGF-1 signaling, because another Ras protein, H-ras localized to the plasma membrane inde

155 Mammalian cells encode three closely related Ras proteins, H-Ras, N-Ras, and K-Ras.

156 Although both Sos1 and Ras-GRF1 activate the Ras proteins Ha-Ras, N-Ras, and Ki-Ras, only Ras-GRF1 al

157 ammalian cells express three closely related Ras proteins: Ha-Ras, K-Ras, and N-Ras.

158 Posttranslational processing of Ras proteins has attracted considerable interest as a po

159 region (residues 166-189), of H-, N-, and K-Ras proteins has sequence determinants necessary for ful

160 Ras proteins have a key role in the regulation of severa

161 ular and nonvesicular transport pathways for Ras proteins have been proposed, but the pathway is not

162 Unlike Ras, few activating mutations of R-Ras proteins have been reported in human cancer, and ver

163 Oncogenic Ras proteins have been shown to stimulate macropinocytos

164 The Ras proteins have been termed "undruggable," based on fa

165 lso highlight our previous observations that Ras proteins have functions in the absence of acute mito

166 However, Ras proteins have proven difficult to target directly.

167 Ras proteins have to undergo a series of posttranslation

168 Recently, the structure of the full-length H-ras protein in a DMPC bilayer has been computationally c

169 Here, the structure of the full-length H-Ras protein in complex with a 1,2-dimyristoylglycero-3-p

170 To analyze the functions of RAS protein in granulosa cells during ovarian follicular

171 tic domain, due to the prominent role of the Ras protein in signaling pathways that control cell prol

172 emonstrate that sp-Erf2/zDHHC9 palmitoylates Ras proteins in a highly selective manner in the trans-G

173 high affinity, thereby displacing prenylated Ras proteins in cells.

174 ing the differential properties of oncogenic Ras proteins in primary cells, for identifying candidate

175 terns evoked by ectopic production of Myc or Ras proteins in primary tissue culture cells properly pr

176 Several studies have implicated Ras proteins in the development and function of synapses

177 approach to this question, we activated all Ras proteins in vivo by genetic deletion of the RasGAP p

178 Post-translational modification of Ras proteins includes prenylcysteine-directed carboxyl m

179 bations that are propagated throughout the H-Ras protein including increased flexibility of the centr

180 construct to the same loci as the endogenous Ras protein, indicating that Ras distribution is a conse

181 Activated Ras proteins interact with a broad range of effector pro

182 The RAS proteins interact with a common set of activators an

183 two-hybrid assay revealed a p204-cytoplasmic Ras protein interaction.

184 We transduced dominant negative (dn) HIV TAT-Ras protein into mature human eosinophils to determine t

185 The lateral segregation of Ras proteins into transient plasma membrane nanoclusters

186 intensively studied due to the finding that Ras protein is farnesylated coupled with the observation

187 urate measurement of activity of wild-type K-ras protein is important due to its tumor suppressor act

188 ing between GDP- and GTP- bound forms of the Ras protein is partly regulated by the binding of Sos.

189 ung tumors than in normal lung tissue, while RAS protein is significantly higher in lung tumors, prov

190 ecognized that the functional versatility of Ras proteins is accomplished through their differential

191 Plasma membrane (PM) localization of Ras proteins is crucial for transmitting signals upon mi

192 the aberrant biochemical output of oncogenic Ras proteins is one of the great challenges in cancer th

193 In the case of Ras proteins, it has been suggested that the differentia

194 pecificity of Ras isoforms is defined by the Ras protein itself and not by differential gene expressi

195 Thus, among four Ras proteins, K-Ras4A is unique in possessing a dual mem

196 Ins(4,5)P(2), resulting in the activation of Ras, protein kinase C and Ca(2+) flux.

197 s a filamentation program dependent upon the Ras-protein kinase A (PKA) pathway.

198 strong genetic interaction of DASH with the Ras/protein kinase A (PKA) pathway.

199 ce of interactions between the Nrd1-Nab3 and Ras/protein kinase A (PKA) pathways.

200 apping signaling networks--those centered on Ras/protein kinase A, AMP-activated kinase, and target o

201 d that several signaling pathways, including Ras/protein kinase A, AMP-activated kinase, the high-osm

202 localization, it selectively downregulated H-Ras protein levels at the post-translational level.

203 -, N-, or HRAS genes that encode an abnormal RAS protein locked in a constitutively activated state t

204 Therefore, differential ubiquitination of Ras proteins may control their location-specific signali

205 Ras proteins mediate PI3K activation through direct bind

206 Ras proteins mediate the proliferative effects of G-prot

207 FTI inhibited farnesylation of Ras protein more significantly in MIA PaCa-2 than BxPC-3

208 E-RAS protein most remarkably revealed a different mode of

209 Ras proteins move between membrane compartments in part

210 r amphiphiles such as indomethacin influence Ras protein nanoclustering in intact plasma membrane.

211 expression of ERAS, a constitutively active RAS protein normally expressed only in embryonic stem ce

212 Like all RAS proteins, NRAS must undergo a series of post-transla

213 Mutations in RAS proteins occur widely in human cancer.

214 t signaling by oncogenic mutant rat sarcoma (Ras) proteins occurs in approximately 15% of all human t

215 mitochondrial defects and an accumulation of Ras proteins on mitochondrial membranes.

216 -PKB signaling mediates effects of activated Ras proteins on the cytoskeleton and cell migration.

217 Ras proteins on the inner leaflet of the plasma membrane

218 ctivated protein kinases (MAPK) by an active Ras protein or TGF-beta treatment significantly increase

219 ing geranylgeranylation for farnesylation on Ras proteins or vice versa on Rho proteins reversed the

220 Ras protein over-expression has been observed in human b

221 cal and functional studies of three mutant K-Ras proteins (P34R, D153V, and F156L) found in individua

222 y proliferation through dysregulation of the RAS protein pathway can lead to within-testis expansion

223 were an average of 1.3 million molecules of Ras protein per cell, and the ratio of mutant to normal

224 in the RAS genes or their regulators render RAS proteins persistently active.

225 Ras proteins play a central role in transducing signals

226 Ras proteins play a major role in human cancers but have

227 The RAS proteins play a role in cell differentiation, prolif

228 Ras proteins play vital roles in numerous biological pro

229 Post-translational lipid modification of Ras proteins plays an important role in their recruitmen

230 o quantify the number and fraction of mutant Ras protein present in cancer cell lines.

231 The activated Ras proteins produced by these mutations can, among othe

232 Only the RalGDS 37G-N-Ras protein protected the N-Ras knockout cells from apop

233 per cell, and the ratio of mutant to normal Ras proteins ranged from 0.49 to 5.6.

234 study Ras signaling because it has a single Ras protein, Ras1, that regulates two distinct pathways:

235 Like other Ras proteins, Ras1 is activated upon guanine triphosphat

236 e front of migrating cells downstream of the Ras protein RasC, controlling F-actin dynamics and cAMP

237 ry for membrane attachment and maturation of Ras proteins, recent studies suggest that farnesyltransf

238 Ras proteins regulate a wide range of biological process

239 Ras proteins regulate cellular growth and differentiatio

240 Ras proteins regulate signal transduction processes that

241 Ras proteins regulate signaling pathways important for c

242 y activated in human cancers, but the mutant Ras proteins remain largely "undruggable" through the co

243 As Ras proteins require the membrane localization for the t

244 Unlike Ras proteins, RERG lacks a known recognition signal for

245 in antibody fragment (scFv) directed against Ras proteins results in radiosensitization.

246 Ras proteins share ~85% amino acid identity, are activat

247 Recombinant V14I and T58I K-Ras proteins show defective intrinsic GTP hydrolysis and

248 signaling cascade proteins (GO: 0007242) and Ras protein signal transduction (GO: 0007265), and conta

249 Ras proteins signal through direct interaction with a nu

250 Ras proteins signal to a number of distinct pathways by

251 we initially hypothesized a role for active Ras protein signaling in exosome biogenesis, we found th

252 bited specific genetic interactions with the Ras protein signaling pathway.

253 at was developed as a potential inhibitor of Ras protein signaling, with antitumor activity in precli

254 t-negative or an S-nitrosylation-site mutant Ras protein significantly abrogates the effects of NO.

255 Expression of a dominant-negative Ras protein significantly inhibited MMP-2 transcription,

256 hearts arose from up-regulated expression of Ras protein-specific guanine nucleotide releasing factor

257 At Rasgrf1 (encoding RAS protein-specific guanine nucleotide-releasing factor

258 e kinase, mitochondrial 2) and RASGRF2 gene (Ras protein-specific guanine nucleotide-releasing factor

259 impairs the ability of CARD9 to complex with Ras protein-specific guanine nucleotide-releasing factor

260 The p21 Ras proteins, such as K-Ras4B, K-Ras4A, H-Ras, and N-Ras

261 familiar farnesylated proteins belong to the Ras protein superfamily, well-known oncoproteins.

262 ll mammalian cells express 3 closely related Ras proteins, termed H-Ras, K-Ras, and N-Ras, that promo

263 Myogenesis is blocked by all Ras proteins tested, yet only in the case of H-Ras G12V

264 neated a unique ligand-binding pocket on the Ras protein that is adjacent to the switch I/II regions

265 that IEC-6 cells expressing an oncogenic Ha-Ras protein that no longer binds PI 3-kinase are greatly

266 ory nucleotide analogues, respectively, of K-Ras proteins that covalently and selectively bind G12C-m

267 nd reveal unexpected plasticity in oncogenic Ras proteins that has diagnostic and therapeutic implica

268 , resulting in mixed heterotypic clusters of Ras proteins that normally are separated spatially.

269 ate cellular transformation by the classical Ras proteins, the mechanisms through which TC21 induces

270 views the properties of normal and oncogenic Ras proteins, the prevalence and likely pathogenic role

271 Nf1 and examined mice doubly deficient in a Ras protein to determine its requirement in formation of

272 e endomembrane and that in order for a given Ras protein to fully transform cells, multiple compartme

273 The localization of oncogenic Src and Ras proteins to cellular plasma membranes is critical fo

274 tiation, and survival signals from activated RAS proteins to downstream effectors, most often by indu

275 h reduced the ability of cytosolic GTP-bound Ras proteins to inhibit Elk-1 activation and to induce c

276 that efficient cell transformation requires Ras proteins to interact with Cdc42 on the endomembrane

277 nase as well as for the correct targeting of Ras proteins to lipid rafts and non-raft membranes.

278 can be any amino acid) is required to target Ras proteins to the cytosolic surface of the plasma memb

279 Subcellular localization of Ras proteins to the plasma membrane is accomplished in p

280 C-terminal targeting sequences or the entire Ras proteins to Venus fluorescent protein.

281 Ras proteins traffic between the plasma membrane and end

282 Ras proteins transduce extracellular signals to intracel

283 Oncogenic Ras proteins transform cells via multiple downstream sig

284 Activation of Ras proteins underlies functional decisions in diverse c

285 compound, termed 3144, was found to bind to RAS proteins using microscale thermophoresis, nuclear ma

286 Redistribution of the two Ras proteins was monitored with confocal microscopy or w

287 ng in erythroid differentiation, different H-ras proteins were expressed in CFU-E progenitors and ear

288 In MEFs lacking Rce1 or Icmt, farnesylated Ras proteins were mislocalized.

289 t heterologously expressing mammalian mutant Ras proteins were used to immunize mice in a carcinogen-

290 Common substrates include oncogenic Ras proteins, which are implicated in up to 30% of all h

291 study, we demonstrate that unlike oncogenic Ras proteins, which are primarily activated by mutations

292 ation and activation of endogenous wild-type Ras proteins, which are required throughout tumorigenesi

293 However, the specific Ras proteins, which integrate in vivo with TGF-beta sign

294 Ras proteins-which are activated by many upstream pathwa

295 show that RasDM is the first structure of a Ras protein with identical GDP- and GTP-bound structures

296 ought to be important for the association of Ras proteins with membranes.

297 Directly targeting Ras proteins with small molecules may rely on the moveme

298 Remarkably, K-Ras proteins with switch 2 insertions are impaired for P

299 nds capable of inhibiting the interaction of RAS proteins with their effectors that transduce the sig

300 Using an activated Ha-Ras protein (Y64G/Y71G/F156L) that fails to interact wit