ライフサイエンスコーパス: ras

1 mal membrane anchor of the GTPase, N-Ras (tN-Ras).

2 encode a GTPase activating protein (GAP) for Ras.

3 ansduction (GO: 0007265), and contain active Ras.

4 al role in signal transduction by activating Ras.

5 cover synthetic lethal partners of oncogenic Ras.

6 e immunological processes leading to BOS and RAS.

7 anchorage independence similarly to mutant H-Ras.

8 cell proliferation signaling by oncogenic K-Ras.

9 n K27, which inhibits nucleotide exchange of Ras.

10 = 0.15 [BOS]; 60.5 vs 69.5 months, P = 0.80 [RAS]).

11 pattern of asexual conidiation similar to a ras-1 mutant that is used in circadian studies in N. cra

12 At 8 weeks, 4HT-treated K14.ROCK(er)/HK1.ras(1205) cohorts exhibited papillomas similar to HK1.ra

13 cohorts exhibited papillomas similar to HK1.ras(1205) controls; however, K14.ROCK(er)/HK1.ras(1205)

14 as(1205) controls; however, K14.ROCK(er)/HK1.ras(1205) histotypes comprised a mixed papilloma/well-di

15 By 12 weeks, K14.ROCK(er)/HK1.ras(1205) wdSCCs exhibited increased NF-kappaB and novel

16 expressing epidermal-activated ras(Ha) (HK1.ras(1205)).

17 ber of LVs per bronchiole: 4.75 (BOS), 6.47 (RAS), 4.25 (control), P = 0.97).

18 es that interfere with the palmitoylation of Ras, a high value therapeutic target that is mutated in

19 on with membranes is essential to understand RAS action and to intervene in RAS-driven diseases.

20 erary centrosomes in cancer cells eliminates Ras-activated cells through mitotic catastrophe.

21 etastatic colon cancers and that oncogenic K-RAS activates TGF-beta signaling to promote tumor invasi

22 Ras activation and phosphorylation of ERK1/2 downstream

23 Loss of Hippo switches Ras activation from promoting cellular differentiation t

24 However, RAS activation in hematopoietic cells has immunologic ef

25 own-regulated both c-Met phosphorylation and Ras activation in renal cancer cells.

26 buffer, excitability starts frequently with Ras activation in the back/side of the cell or with F-ac

27 how that mutant-K-Ras (G12D), which leads to Ras activation, cooperates with beta-catenin mutants (S3

28 Notably, increased RAS activity and downstream MAPK signaling was observed

29 well as the co-operativity observed between RAS activity and RAF kinase inhibitors in driving RAF ac

30 orrelated almost perfectly with elevation of Ras activity in primary human samples.

31 ence demonstrating a distinct role for the R-Ras-Akt axis.

32 code a pattern of stimuli, a disease-related Ras allele abolished the spacing effect for plastic chan

33 We show that wild-type RAS amplification increases receptor tyrosine kinase-dep

34 We found that the K-Ras anchor binds selected plasma membrane anionic lipids

35 em leads to short-lived patches of activated Ras and associated F-actin that precede the extension of

36 Here, we show that oncogenic RAS and BRAF induce perinuclear relocalization of severa

37 However, specific combinations of RAS and deletion of amino acid 32 led to significant res

38 MAPK activation depends on Ras and is caused by RasGRP3, which is significantly and

39 were tested retrospectively for NOTCH1/FBXW7/RAS and PTEN alterations.

40 in a negative feedback loop that encompasses RAS and RAF, MEK, and ERK that inhibits SOS via phosphor

41 del system, we have recently shown that both Ras and Rap1 are required for cAMP signaling to ERKs.

42 ned previously, to those of active RasGRP4:H-Ras and RasGRP2:Rap1b complexes.

43 A positive feedback loop involving RAS and SOS, which leads to bistability and allows for s

44 heir effectors that transduce the signals of RAS and that drive and sustain malignant transformation

45 focused on the constitutively active G12V K-Ras and two of its variants, K101E and K101C/E107C, whic

46 The renin-angiotensin system (RAS) and angiotensin AT1 receptors within the brain are

47 f these intrabodies colocalize with H-Ras, K-Ras, and G12V mutants inside the cells, providing new po

48 f both protein kinase A (PKA) and the GTPase Ras, and is induced upon the activation of beta-adrenerg

49 Oncogenic KRas, HRas, and NRas (K-Ras, H-Ras, and N-Ras) differentially populate distinct cancers

50 chanism of transcriptional regulation during Ras- and TGF-beta-induced EMT that involves alterations

51 or axis as counter-regulatory to the classic RAS Ang II/Ang II Type 1 (AT1) receptor axis.

52 Accordingly, treatment with global RAS antagonists attenuates cardiovascular risk and slows

53 and phosphorylation of ERK1/2 downstream of Ras are both greatly increased in Nf123aIN/23aIN mouse b

54 acids found in K-Ras4B (K-Ras) but not in H-Ras are important for permanent K-Ras localization to th

55 Mutated forms of Ras are involved in approximately 30% of human cancers.

56 K- and H-Ras are the most commonly mutated genes in human tumors

57 n et al. (2017) describe ADP-ribosylation of Ras as a strategy to inhibit assembly of neutrophil NADP

58 OX2, which is broadly expressed in oncogenic RAS-associated cancers, we show that despite widespread

59 affinity cyclic nucleotide-binding (CNB) and Ras association domains, but not the disheveled-Egl-10-p

60 ent resistance to pibrentasvir, and HCV with RAS at amino acid 93 had a low level of resistance to th

61 For the remaining NS5A inhibitors tested, RAS at amino acids 28 and 93 led to high levels of resis

62 l of efficacy against variants; viruses with RAS at amino acids 28, 30, or 31 had no apparent resista

63 lation of Ras by directly binding prenylated Ras at the plasma membrane.

64 K-Ras-beta-catenin tumors showed up-regulation of beta-cat

65 ucleus in Deltaras2 RAS2 interacted with the RAS-binding domain of the adenylate cyclase in vitro, an

66 h B-Raf binding to Rap1 independently of its Ras-binding domain.

67 All RAS biology occurs in membranes: a precise understanding

68 as the incidence of somatic mutations of the RAS, BRAF, and EGFR genes and association of cetuximab e

69 e have identified here that the incidence of RAS, BRAF, and EGFR mutations is low in cSCC.

70 in the common synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduction cascade.

71 ds and basic amino acids found in K-Ras4B (K-Ras) but not in H-Ras are important for permanent K-Ras

72 Our findings demonstrate that H-Ras, but not K-Ras, promotes cardiomyocyte hypertrophy b

73 e NgBR promotes the membrane accumulation of Ras by directly binding prenylated Ras at the plasma mem

74 Oncogenic Ras causes proliferation followed by premature senescenc

75 detailed structural information for a CaM-K-Ras complex is still challenging.

76 of the switch and many of the pathways that RAS controls are well known, but the precise mechanisms

77 Oncogenic Ras cooperates with Egfr, which cannot be explained by t

78 In addition, mutant RAS coordinately elevates proteasome subunit expression

79 ctions of PKCdelta also segregate based on K-Ras dependency, as K-Ras-independent cells are more sens

80 ns of differentially essential genes between Ras-dependent and -independent lines uncover synthetic l

81 Our current studies show that K-Ras-dependent cells are refractive to PKCdelta-driven ap

82 utant lung cancer cell lines classified as K-Ras-dependent or -independent for co-dependency on prote

83 r results show that sequence conservation in Ras depends strongly on the biochemical network in which

84 ic KRas, HRas, and NRas (K-Ras, H-Ras, and N-Ras) differentially populate distinct cancers.

85 DC-RAs displayed a mature yet tolerogenic phenotype, expres

86 y and development of clinical candidates for RAS-driven cancers involving mutations in RAS genes or o

87 t there are still no effective therapies for Ras-driven cancers.

88 to understand RAS action and to intervene in RAS-driven diseases.

89 Interestingly, citrate regressed Ras-driven lung tumors.

90 promoting tumor formation and maintenance in Ras-driven tumors.

91 enocopied the histological features of human RAS-driven, poorly differentiated thyroid cancers.

92 Utilizing models of Ras dysregulation as well as inhibitors of the MAPK and

93 ndicated that these miniproteins bind to the Ras effector domain as dimers, and high-resolution cryst

94 nd Ras in an unprecedented mode in which the Ras effector domain is remodeled to expose an extended p

95 otaxin 2, Regucalcin, and Cyclin-D1 and of K-Ras effectors, including phosphorylated extracellular si

96 decreases in beta-catenin targets and some K-Ras effectors, leading to reduced tumor cell proliferati

97 How oncogenic Ras elicits and integrates Egfr and Hedgehog signals to

98 lassic effector molecule of the RAS, several RAS enzymes affect immune homeostasis independently of c

99 a treatment at the developmental stage with Ras-ERK inhibitors.

100 m of epidermal growth factor receptor (EGFR)-Ras-ERK signaling, has identified dynamic features not e

101 Our results demonstrate that the Ras/Erk pathway is decoded by both dynamic filters and l

102 As a central element within the RAS/ERK pathway, the serine/threonine kinase BRAF plays

103 he Wnt, bone morphogenetic protein (BMP), or Ras/ERK pathways, converging on shared nuclear targets t

104 ance by preferentially substituting for EGFR/RAS/ERK signaling rather than ERBB3/PI3K/AKT signaling.

105 ranulocyte macrophage-CSF due to hyperactive RAS/ERK signaling.

106 activation of the renin-angiotensin system (RAS) exacerbates renal and vascular injury.

107 Ras exhibits global sensitivity to mutation when regulat

108 icroscopy in live cells, we show that G12V K-Ras exists as a mixture of monomers, dimers and larger o

109 f KRas4B > > NRas >/= KRas4A > HRas to total Ras expression with KRas4B typically representing 60-99%

110 Appropriate activation of the Ras/extracellular signal-regulated kinase (ERK) protein

111 Rheb is a Ras family GTPase, which binds to and activates mammalia

112 ng context-specific oncogenic phenotypes.The Ras-family small GTPase RAB25 can exert both pro- and an

113 ules are captured from raw cell lysate using Ras-functionalized supported membrane microarrays.

114 ous tumor cells expressing B-Raf(V600E) or K-Ras(G12C/D) Intriguingly, coimmunoprecipitation and in v

115 otein scaffold for preferential binding to K-Ras G12D.

116 We show that mutant-K-Ras (G12D), which leads to Ras activation, cooperates wi

117 data, caveolin-1-null mice overexpressing K-Ras(G12D) display accelerated mortality.

118 Whereas H-Ras(G12V) elicited papillomas and hematopoietic tumors,

119 cited papillomas and hematopoietic tumors, K-Ras(G12V) induced lung tumors and gastric lesions.

120 lin-1 expression inhibits oncogenic K-Ras (K-Ras(G12V))-induced premature senescence in mouse embryon

121 METHODS AND We used H- and K-Ras gene knockout mice and subjected them to pressure ov

122 receptor, a receptor tyrosine kinase) and H-Ras generates strong, synergistic activation of PI3Kalph

123 or RAS-driven cancers involving mutations in RAS genes or otherwise activated RAS proteins.

124 mouse embryonic fibroblasts deficient in all Ras genes.

125 A subset of Ras GTPase genes linked to membrane remodeling were upre

126 Self-assembly of plasma membrane-associated Ras GTPases has major implications to the regulation of

127 Oncogenic KRas, HRas, and NRas (K-Ras, H-Ras, and N-Ras) differentially populate distinct

128 sed with mice expressing epidermal-activated ras(Ha) (HK1.ras(1205)).

129 that ROCK2 activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of

130 mor activity through the inhibition of c-Met-Ras-HO-1 axis; and it can have significant therapeutic p

131 at promotes the expression and activation of Ras homolog family member A (RhoA) and subsequent activa

132 linked to the activation of the small GTPase Ras homolog family member A (RhoA) by the Galpha12/13 pa

133 smission correlates with increased levels of Ras homolog gene family, member A (RhoA), a KCTD13/CUL3

134 Here, we show that Akt activation by a Ras homolog, R-Ras, stabilizes the microtubule cytoskele

135 TORC1 is activated by the small GTPase RHEB (Ras homologue enriched in brain) and inhibited by PRAS40

136 dynamics regulated by Ror2, which influenced Ras Homology Family Member A (RhoA) and Rho-Associated C

137 RAS hotspots in NS5A were found at amino acids 28, 30, 3

138 revealed that these miniprotein dimers bind Ras in an unprecedented mode in which the Ras effector d

139 not impact the time to development of BOS or RAS in lung transplantation (low vs high LVD: 38.5 vs 86

140 his study was to define the role of H- and K-Ras in modulating stress-induced myocardial hypertrophy

141 RASs in NS3 associated with simeprevir or paritaprevir f

142 sis for resistance-associated substitutions (RASs) in HCV genes (nonstructural protein [NS]3, NS5A, N

143 so segregate based on K-Ras dependency, as K-Ras-independent cells are more sensitive to topoisomeras

144 I leads to the development of several rare K-ras-independent forms of PC, with infrequent PDAC.

145 PSCs provide an essential platform for RAS-induced phosphorylation and activation of the prosen

146 ive selection driven by BCL-XL modulation of RAS-induced self-renewal, and during which apoptotic res

147 e an important mechanism driving escape from Ras-induced senescence.

148 t mediate metastatic dissemination of mutant Ras-induced tumors in the developing nervous system.

149 Oncogenic Ras induces the expression of Egfr ligands.

150 erent deacylation rates of single-acylated H-Ras influence differentially its overall exchange betwee

151 Decades of effort to develop direct Ras inhibitors for clinical use have thus far failed, la

152 These reports of direct-acting RAS inhibitors provide valuable insight for further disc

153 yperkalemia, especially when associated with RAS inhibitors.

154 7 significantly reduces the amount of active Ras, inhibits downstream signalling, in particular the l

155 urs in membranes: a precise understanding of RAS' interaction with membranes is essential to understa

156 conclude that TCR/ITK signalling through the Ras/IRF4 pathway is required for functional development

157 ate that continued expression of oncogenic K-RAS is required for the survival of primary and metastat

158 ome (BOS) or restrictive allograft syndrome (RAS) is the major limiting factor of long-term survival

159 However, the contribution of different Ras isoforms has not been investigated.

160 the gene expression profiles of each of the Ras isoforms in a panel of mouse tissues derived from a

161 f caveolin-1 expression inhibits oncogenic K-Ras (K-Ras(G12V))-induced premature senescence in mouse

162 Both of these intrabodies colocalize with H-Ras, K-Ras, and G12V mutants inside the cells, providing

163 f Plexin-D1 with vesicular pools of active R-ras, leading to its inactivation.

164 t not in H-Ras are important for permanent K-Ras localization to the PM.

165 rigenesis by signaling primarily through the Ras-MAPK pathway.

166 lved in signal transduction events involving Ras/MAPK and PI3K/Akt pathways.

167 tigate gastric adenocarcinoma subtypes where RAS/MAPK pathway activation and E-cadherin attenuation a

168 KIT knockdown also increased RAS/MAPK pathway activation in a BRAF(V600E)-mutant huma

169 Ras/MAPK pathway activation is associated with significa

170 f) animals were more invasive and had higher RAS/MAPK pathway activation.

171 ken together, our data suggest that although Ras/MAPK pathway inhibition can increase tumor immunogen

172 Germ-line mutations in components of the Ras/MAPK pathway result in developmental disorders calle

173 nce of multiple inhibitors targeting the RTK/Ras/MAPK pathway.

174 Aberrant activation of RAS/MAPK signaling is a driver of over one third of all

175 cal targets such as Notch1 and SIRT1, and on Ras/MAPK-dependent pathways.

176 emained elusive, prompting a perception that RAS may be undruggable.

177 experiencing renewed excitement that mutant RAS may finally be conquered.

178 text of cancer and illustrates how oncogenic RAS-mediated degradation of FOXOs, via post-translationa

179 chromatin remodeling complex that exhibited Ras-mediated dependence on PRC2 histone methyltransferas

180 new potential tools to monitor and modulate Ras-mediated signaling.

181 ockdown in human breast cancer cells reduces Ras membrane localization, inhibits epidermal growth fac

182 at target the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kinase (MAPK) pathway have

183 Whereas suppressing or enhancing Ras/mitogen-activated protein kinase signaling changed h

184 ptor tyrosine kinase-dependent activation of RAS more potently in colorectal cancer than in melanoma

185 rogenase-A (LDH-A) to tumor formation in a K-Ras murine model of lung carcinoma.

186 ity to eradicate nuclear FOXO4 proteins from RAS-mutant cancer cells.

187 /mitogen-activated protein kinase pathway in RAS-mutant cancers are particularly promising approaches

188 rgistically inhibited the growth of multiple RAS-mutant human cancer cell lines of diverse tissue ori

189 nct molecular features in which mesenchymal, Ras-mutant lung cancer is acutely dependent on TBK1-medi

190 s and membrane trafficking of monoacylated H-Ras mutants to analyze their contributions to H-Ras plas

191 Only 2 RAS mutated samples (6.5%) were identified.

192 l roles in numerous biological processes and Ras mutations are found in many human tumors.

193 Oncogenic RAS mutations are present in 15-30% of thyroid carcinoma

194 Ras mutations associated with intellectual disability ab

195 th these class 3 BRAF mutations also harbour RAS mutations or NF1 deletions.

196 The presence of K-ras mutations was assessed by direct sequencing, locked

197 No evidence of K-ras mutations was observed.

198 oduction and/or oncogene activation, such as RAS, MYC, and c-SRC.

199 Inhibition of Ras nucleotide exchange is a promising new approach but

200 The activation of Ras occurs during basal locomotion and is an essential c

201 xisting resistance-associated substitutions (RAS) on HCV escape from treatment.

202 Our findings demonstrate that Ras oncogene-independent activation of RALB signaling is

203 A few cultures were transformed by ras oncogenes when transfected with DNA from neoplastic

204 lay marked differences in the association of RAS oncogenes with tumor type.

205 Ras-oncogenes were discovered over three decades ago, bu

206 mas in PP;Trp53-deficient mice lacked either Ras or Braf mutations, and hence developed in the absenc

207 cing was lost by suppressing the activity of Ras or mitogen-activated protein kinase, whereas the ove

208 otide exchange factors that are specific for Ras or Rap, and are important regulators of cellular sig

209 y a combination of simulation experiments of Ras overexpression and catalase knockout in conjunction

210 f two RASGAP genes, neurofibromin1 (Nf1) and RAS p21 protein activator (Rasa1).

211 equency and variety of secondary or tertiary Ras pathway activating mutations, though not highly recu

212 uct/DeltaDuct) mice and study the effects of Ras pathway activation on initiation and progression of

213 ith shorter survival than was the absence of RAS pathway mutations (P=0.004), owing to a high risk of

214 did not have TP53 mutations, the presence of RAS pathway mutations was associated with shorter surviv

215 induce perinuclear relocalization of several RAS pathway proteins, including the kinases CK2 and p-ER

216 P2K1 (encoding MEK), a core component of the Ras pathway that is mutated in both RASopathies and canc

217 t tumors most amenable to targeting of the K-Ras pathway, and identify PKCdelta as a potential target

218 rder of childhood caused by mutations in the Ras pathway.

219 posttranscriptional regulation of the early Ras phenotype that is dependent on both oncogenic signal

220 igating the detailed molecular events in the Ras-PI3K interaction has been challenging because it occ

221 tream of the Ras superfamily of GTPases, and Ras-PI3K interaction plays a key role in promoting tumor

222 mutants to analyze their contributions to H-Ras plasma membrane and endomembrane distribution.

223 a surprisingly small number of genes in the Ras processing and MAPK pathways and pinpoint PREX1 as a

224 r findings demonstrate that H-Ras, but not K-Ras, promotes cardiomyocyte hypertrophy both in vivo and

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

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

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

228 tively with the stress elicited by oncogenic Ras protein.

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

230 Ras proteins are highly conserved signaling molecules th

231 Understanding how Ras proteins are regulated is important for elucidating

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

233 Ras proteins play vital roles in numerous biological pro

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

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

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

237 molecule inhibitors that directly target the Ras proteins.

238 utations in RAS genes or otherwise activated RAS proteins.

239 quate subcellular distribution of S-acylated Ras proteins.

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

241 to integrins is mediated by the small GTPase Ras-proximate-1 (Rap1).

242 molecular basis to explain the induction of RAS-RAF association by RAF inhibitors, as well as the co

243 RAF inhibitors also enhance RAS-RAF association.

244 markers, including a signature outperforming RAS/RAF mutations in predicting sensitivity to the EGFR

245 s in members of the receptor tyrosine kinase/Ras/Raf pathway including EGFR and KRAS were not signifi

246 ases that act as downstream effectors of the Ras/Raf/MEK/ERK signaling pathway.

247 tors in breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-

248 In contrast, Rap1GAP-deficient (P489V) and Ras/Rap1GAP-deficient (R371Q) Rasa3 had no effect.

249 a, oncogenic mutations of the proto-oncogene Ras (Ras(V12)) maintain tumorous cells in an 'undead'-li

250 ated with suppression of CXCL8/IL-8-mediated Ras-related C3 botulinum toxin substrate 1 GTPase activi

251 ctivation of Raf kinases by the small GTPase Ras requires two major sets of phosphorylations.

252 nd Oamb can be replaced by its human homolog Ras-responsive element-binding protein 1 (RREB-1).

253 A non-ribosylatable version of Ras restores reactive oxygen species production and resu

254 n II is the classic effector molecule of the RAS, several RAS enzymes affect immune homeostasis indep

255 in factors involved in cytokine receptor and RAS signaling (62.2%), hematopoietic development (29.7%)

256 its epidermal growth factor (EGF)-stimulated Ras signaling and diminishes tumorigenesis of xenografts

257 Statins are believed to inhibit Ras signaling and may also activate the bone morphogenet

258 ndings identify Etv5 as a critical output of Ras signaling in AT2 cells, contributing to both lung ho

259 defined lipid compositions that determine K-Ras signaling output.

260 RB, LYN, NTRK3, PDGFRA, PTK2B, TYK2, and the RAS signaling pathway.

261 Stat and K-Ras signaling pathways were negatively correlated with A

262 increased, as well as attenuated, levels of Ras signaling.

263 , by the PI3K/AKT effector axis of oncogenic RAS signalling.

264 oinformatics analysis detected a prominent K-RAS signature and predicted activation of several import

265 RasGAP (RASA1), a negative regulator of the Ras small GTP-binding protein.

266 in Kinase 1 alpha (CK1alpha) in an oncogenic RAS-specific manner, but whether this mode of regulation

267 Here we report that one of the K-Ras splice variants, K-Ras4a, is subject to lysine fatty

268 show that Akt activation by a Ras homolog, R-Ras, stabilizes the microtubule cytoskeleton in endothel

269 munologic effects that diverge from those of RAS stimulation in the kidney and vasculature.

270 hese findings provide new tools for studying Ras structure and function and present opportunities for

271 n sites provide singular information about H-Ras subcellular distribution that is required for GTPase

272 ass IA PI3Ks are activated downstream of the Ras superfamily of GTPases, and Ras-PI3K interaction pla

273 equate small-molecule-binding pockets on the Ras surface.

274 tion depends on the synergistic induction of Ras target genes.

275 greater appreciation of the complexities of RAS that thwarted past efforts, and armed with new techn

276 f research effort, clinically effective anti-RAS therapies have remained elusive, prompting a percept

277 ted minimal membrane anchor of the GTPase, N-Ras (tN-Ras).

278 Delivery of specific allergen-presenting DC-RAs to half-maximally sensitized mice with ovalbumin or

279 n of ATXN7 mutants cooperated with oncogenic RAS to induce thyroid cell proliferation, pointing to AT

280 ing organ-specific contribution of oncogenic RAS to LCH pathogenesis.

281 KRas4B typically representing 60-99% of all Ras transcripts.

282 In a K-ras transformed cell line we experimentally assessed glu

283 Consequently, Ras-transformed cells override a131-induced growth arres

284 mary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-as

285 ot PtdIns(3,4,5)P3 was sufficient to evoke K-Ras translocation.

286 eling and simulations we further show that K-Ras uses two partially overlapping interfaces to form co

287 apparent sensitivity of glial cells to Pico/Ras(V12) overexpression.

288 cogenic mutations of the proto-oncogene Ras (Ras(V12)) maintain tumorous cells in an 'undead'-like co

289 utophagy at any step of the pathway enhances Ras(V12)-driven epithelial tissue overgrowth via the acc

290 In flies overexpressing mutant Ras(Val12) and S100A4, there was a significant increase

291 we show that Egfr cooperates with oncogenic Ras via Arf6, which functions as a novel regulator of Hh

292 ERK activation downstream of Ras was found to stabilize Etv5 through inactivation of

293 IL-27 (Ebi)(-/-) (ie, IL-27-incompetent) DC-RAs were ineffective in inducing food allergen tolerance

294 iated with resistance to daclatasvir, but no RASs were associated with ledipasvir failure, pointing t

295 In addition, several RASs were specifically associated with failure of simepr

296 lso requires recruitment to membrane-bound H-Ras, which greatly speeds the formation of a stable, mem

297 Among CRYSTAL and FIRE-3 study patients with RAS wt left-sided tumors, FOLFIRI plus cetuximab signifi

298 d FOLFIRI plus bevacizumab); in contrast, in RAS wt patients with poor-prognosis right-sided tumors,

299 In the RAS wt populations of CRYSTAL and FIRE-3, patients with

300 rotein kinase, whereas the overexpression of Ras-WT enhanced it.