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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 e immunological processes leading to BOS and RAS.
6 cover synthetic lethal partners of oncogenic 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                              Surprisingly, H-Ras binding significantly inhibits the specific kinase a
66 ucleus in Deltaras2 RAS2 interacted with the RAS-binding domain of the adenylate cyclase in vitro, an
67 h B-Raf binding to Rap1 independently of its Ras-binding domain.
68                                          All RAS biology occurs in membranes: a precise understanding
69 as the incidence of somatic mutations of the RAS, BRAF, and EGFR genes and association of cetuximab e
70 e have identified here that the incidence of RAS, BRAF, and EGFR mutations is low in cSCC.
71  in the common synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduction cascade.
72 formation is a critical feature of oncogenic RAS/BRAF signaling in cancer cells that controls signal
73 ds and basic amino acids found in K-Ras4B (K-Ras) but not in H-Ras are important for permanent K-Ras
74              Our findings demonstrate that H-Ras, but not K-Ras, promotes cardiomyocyte hypertrophy b
75 e NgBR promotes the membrane accumulation of Ras by directly binding prenylated Ras at the plasma mem
76                                    Oncogenic Ras causes proliferation followed by premature senescenc
77  detailed structural information for a CaM-K-Ras complex is still challenging.
78  of the switch and many of the pathways that RAS controls are well known, but the precise mechanisms
79                                    Oncogenic Ras cooperates with Egfr, which cannot be explained by t
80                          In addition, mutant RAS coordinately elevates proteasome subunit expression
81 ctions of PKCdelta also segregate based on K-Ras dependency, as K-Ras-independent cells are more sens
82 ns of differentially essential genes between Ras-dependent and -independent lines uncover synthetic l
83              Our current studies show that K-Ras-dependent cells are refractive to PKCdelta-driven ap
84 utant lung cancer cell lines classified as K-Ras-dependent or -independent for co-dependency on prote
85 r results show that sequence conservation in Ras depends strongly on the biochemical network in which
86 ic KRas, HRas, and NRas (K-Ras, H-Ras, and N-Ras) differentially populate distinct cancers.
87                                           DC-RAs displayed a mature yet tolerogenic phenotype, expres
88 y and development of clinical candidates for RAS-driven cancers involving mutations in RAS genes or o
89 t there are still no effective therapies for Ras-driven cancers.
90 to understand RAS action and to intervene in RAS-driven diseases.
91             Interestingly, citrate regressed Ras-driven lung tumors.
92 promoting tumor formation and maintenance in Ras-driven tumors.
93 enocopied the histological features of human RAS-driven, poorly differentiated thyroid cancers.
94                          Utilizing models of Ras dysregulation as well as inhibitors of the MAPK and
95 ndicated that these miniproteins bind to the Ras effector domain as dimers, and high-resolution cryst
96 nd Ras in an unprecedented mode in which the Ras effector domain is remodeled to expose an extended p
97 otaxin 2, Regucalcin, and Cyclin-D1 and of K-Ras effectors, including phosphorylated extracellular si
98 decreases in beta-catenin targets and some K-Ras effectors, leading to reduced tumor cell proliferati
99                                How oncogenic Ras elicits and integrates Egfr and Hedgehog signals to
100 lassic effector molecule of the RAS, several RAS enzymes affect immune homeostasis independently of c
101  a treatment at the developmental stage with Ras-ERK inhibitors.
102 m of epidermal growth factor receptor (EGFR)-Ras-ERK signaling, has identified dynamic features not e
103             Our results demonstrate that the Ras/Erk pathway is decoded by both dynamic filters and l
104              As a central element within the RAS/ERK pathway, the serine/threonine kinase BRAF plays
105 he Wnt, bone morphogenetic protein (BMP), or Ras/ERK pathways, converging on shared nuclear targets t
106 ance by preferentially substituting for EGFR/RAS/ERK signaling rather than ERBB3/PI3K/AKT signaling.
107 ranulocyte macrophage-CSF due to hyperactive RAS/ERK signaling.
108  activation of the renin-angiotensin system (RAS) exacerbates renal and vascular injury.
109                                              Ras exhibits global sensitivity to mutation when regulat
110 icroscopy in live cells, we show that G12V K-Ras exists as a mixture of monomers, dimers and larger o
111 f KRas4B > > NRas >/= KRas4A > HRas to total Ras expression with KRas4B typically representing 60-99%
112                Appropriate activation of the Ras/extracellular signal-regulated kinase (ERK) protein
113                                    Rheb is a Ras family GTPase, which binds to and activates mammalia
114 ng context-specific oncogenic phenotypes.The Ras-family small GTPase RAB25 can exert both pro- and an
115 ules are captured from raw cell lysate using Ras-functionalized supported membrane microarrays.
116 ous tumor cells expressing B-Raf(V600E) or K-Ras(G12C/D) Intriguingly, coimmunoprecipitation and in v
117 otein scaffold for preferential binding to K-Ras G12D.
118                        We show that mutant-K-Ras (G12D), which leads to Ras activation, cooperates wi
119  data, caveolin-1-null mice overexpressing K-Ras(G12D) display accelerated mortality.
120                                    Whereas H-Ras(G12V) elicited papillomas and hematopoietic tumors,
121 cited papillomas and hematopoietic tumors, K-Ras(G12V) induced lung tumors and gastric lesions.
122 lin-1 expression inhibits oncogenic K-Ras (K-Ras(G12V))-induced premature senescence in mouse embryon
123                 METHODS AND We used H- and K-Ras gene knockout mice and subjected them to pressure ov
124  receptor, a receptor tyrosine kinase) and H-Ras generates strong, synergistic activation of PI3Kalph
125 or RAS-driven cancers involving mutations in RAS genes or otherwise activated RAS proteins.
126 mouse embryonic fibroblasts deficient in all Ras genes.
127                                  A subset of Ras GTPase genes linked to membrane remodeling were upre
128  Self-assembly of plasma membrane-associated Ras GTPases has major implications to the regulation of
129            Oncogenic KRas, HRas, and NRas (K-Ras, H-Ras, and N-Ras) differentially populate distinct
130 sed with mice expressing epidermal-activated ras(Ha) (HK1.ras(1205)).
131  that ROCK2 activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of
132 mor activity through the inhibition of c-Met-Ras-HO-1 axis; and it can have significant therapeutic p
133 at promotes the expression and activation of Ras homolog family member A (RhoA) and subsequent activa
134 linked to the activation of the small GTPase Ras homolog family member A (RhoA) by the Galpha12/13 pa
135 smission correlates with increased levels of Ras homolog gene family, member A (RhoA), a KCTD13/CUL3
136       Here, we show that Akt activation by a Ras homolog, R-Ras, stabilizes the microtubule cytoskele
137 TORC1 is activated by the small GTPase RHEB (Ras homologue enriched in brain) and inhibited by PRAS40
138 dynamics regulated by Ror2, which influenced Ras Homology Family Member A (RhoA) and Rho-Associated C
139                                              RAS hotspots in NS5A were found at amino acids 28, 30, 3
140  revealed that these miniprotein dimers bind Ras in an unprecedented mode in which the Ras effector d
141 not impact the time to development of BOS or RAS in lung transplantation (low vs high LVD: 38.5 vs 86
142 his study was to define the role of H- and K-Ras in modulating stress-induced myocardial hypertrophy
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  the difference between normal and oncogenic RAS pathway signaling, this study shows that oncogenic R
217 P2K1 (encoding MEK), a core component of the Ras pathway that is mutated in both RASopathies and canc
218 t tumors most amenable to targeting of the K-Ras pathway, and identify PKCdelta as a potential target
219 rder of childhood caused by mutations in the Ras pathway.
220  posttranscriptional regulation of the early Ras phenotype that is dependent on both oncogenic signal
221 igating the detailed molecular events in the Ras-PI3K interaction has been challenging because it occ
222 tream of the Ras superfamily of GTPases, and Ras-PI3K interaction plays a key role in promoting tumor
223  mutants to analyze their contributions to H-Ras plasma membrane and endomembrane distribution.
224  a surprisingly small number of genes in the Ras processing and MAPK pathways and pinpoint PREX1 as a
225 r findings demonstrate that H-Ras, but not K-Ras, promotes cardiomyocyte hypertrophy both in vivo and
226 -, N-, or HRAS genes that encode an abnormal RAS protein locked in a constitutively activated state t
227  expression of ERAS, a constitutively active RAS protein normally expressed only in embryonic stem ce
228 signaling cascade proteins (GO: 0007242) and Ras protein signal transduction (GO: 0007265), and conta
229 tively with the stress elicited by oncogenic Ras protein.
230                                          The Ras proteins are aberrantly activated in a wide range of
231                                              Ras proteins are highly conserved signaling molecules th
232                            Understanding how Ras proteins are regulated is important for elucidating
233 l known, but the precise mechanisms by which RAS proteins function are less clear.
234                                              Ras proteins play vital roles in numerous biological pro
235     Post-translational lipid modification of Ras proteins plays an important role in their recruitmen
236 nds capable of inhibiting the interaction of RAS proteins with their effectors that transduce the sig
237 llular distribution and activity of K- and H-Ras proteins.
238 molecule inhibitors that directly target the Ras proteins.
239 utations in RAS genes or otherwise activated RAS proteins.
240 quate subcellular distribution of S-acylated Ras proteins.
241 gies and well-defined binding pockets on the Ras proteins.
242 to integrins is mediated by the small GTPase Ras-proximate-1 (Rap1).
243  molecular basis to explain the induction of RAS-RAF association by RAF inhibitors, as well as the co
244                  RAF inhibitors also enhance RAS-RAF association.
245 markers, including a signature outperforming RAS/RAF mutations in predicting sensitivity to the EGFR
246 s in members of the receptor tyrosine kinase/Ras/Raf pathway including EGFR and KRAS were not signifi
247 ases that act as downstream effectors of the Ras/Raf/MEK/ERK signaling pathway.
248 tors in breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-
249         The model identifies calcium, actin, Ras, Raf1, PI3K, and JAK as key regulators of cardiac me
250   In contrast, Rap1GAP-deficient (P489V) and Ras/Rap1GAP-deficient (R371Q) Rasa3 had no effect.
251 a, oncogenic mutations of the proto-oncogene Ras (Ras(V12)) maintain tumorous cells in an 'undead'-li
252 ated with suppression of CXCL8/IL-8-mediated Ras-related C3 botulinum toxin substrate 1 GTPase activi
253 ctivation of Raf kinases by the small GTPase Ras requires two major sets of phosphorylations.
254 nd Oamb can be replaced by its human homolog Ras-responsive element-binding protein 1 (RREB-1).
255               A non-ribosylatable version of Ras restores reactive oxygen species production and resu
256 n II is the classic effector molecule of the RAS, several RAS enzymes affect immune homeostasis indep
257 in factors involved in cytokine receptor and RAS signaling (62.2%), hematopoietic development (29.7%)
258 its epidermal growth factor (EGF)-stimulated Ras signaling and diminishes tumorigenesis of xenografts
259              Statins are believed to inhibit Ras signaling and may also activate the bone morphogenet
260 ndings identify Etv5 as a critical output of Ras signaling in AT2 cells, contributing to both lung ho
261  defined lipid compositions that determine K-Ras signaling output.
262 RB, LYN, NTRK3, PDGFRA, PTK2B, TYK2, and the RAS signaling pathway.
263                                   Stat and K-Ras signaling pathways were negatively correlated with A
264  increased, as well as attenuated, levels of Ras signaling.
265 , by the PI3K/AKT effector axis of oncogenic RAS signalling.
266 oinformatics analysis detected a prominent K-RAS signature and predicted activation of several import
267  RasGAP (RASA1), a negative regulator of the Ras small GTP-binding protein.
268 in Kinase 1 alpha (CK1alpha) in an oncogenic RAS-specific manner, but whether this mode of regulation
269 y signaling, this study shows that oncogenic RAS specifically triggers constitutive endocytosis-depen
270             Here we report that one of the K-Ras splice variants, K-Ras4a, is subject to lysine fatty
271 show that Akt activation by a Ras homolog, R-Ras, stabilizes the microtubule cytoskeleton in endothel
272 munologic effects that diverge from those of RAS stimulation in the kidney and vasculature.
273 hese findings provide new tools for studying Ras structure and function and present opportunities for
274 n sites provide singular information about H-Ras subcellular distribution that is required for GTPase
275 ass IA PI3Ks are activated downstream of the Ras superfamily of GTPases, and Ras-PI3K interaction pla
276 equate small-molecule-binding pockets on the Ras surface.
277 tion depends on the synergistic induction of Ras target genes.
278  greater appreciation of the complexities of RAS that thwarted past efforts, and armed with new techn
279 f research effort, clinically effective anti-RAS therapies have remained elusive, prompting a percept
280 ted minimal membrane anchor of the GTPase, N-Ras (tN-Ras).
281  Delivery of specific allergen-presenting DC-RAs to half-maximally sensitized mice with ovalbumin or
282 n of ATXN7 mutants cooperated with oncogenic RAS to induce thyroid cell proliferation, pointing to AT
283 ing organ-specific contribution of oncogenic RAS to LCH pathogenesis.
284  KRas4B typically representing 60-99% of all Ras transcripts.
285                                       In a K-ras transformed cell line we experimentally assessed glu
286                                Consequently, Ras-transformed cells override a131-induced growth arres
287 mary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-as
288 ot PtdIns(3,4,5)P3 was sufficient to evoke K-Ras translocation.
289 eling and simulations we further show that K-Ras uses two partially overlapping interfaces to form co
290  apparent sensitivity of glial cells to Pico/Ras(V12) overexpression.
291 cogenic mutations of the proto-oncogene Ras (Ras(V12)) maintain tumorous cells in an 'undead'-like co
292 utophagy at any step of the pathway enhances Ras(V12)-driven epithelial tissue overgrowth via the acc
293               In flies overexpressing mutant Ras(Val12) and S100A4, there was a significant increase
294  we show that Egfr cooperates with oncogenic Ras via Arf6, which functions as a novel regulator of Hh
295                 ERK activation downstream of Ras was found to stabilize Etv5 through inactivation of
296  IL-27 (Ebi)(-/-) (ie, IL-27-incompetent) DC-RAs were ineffective in inducing food allergen tolerance
297 lso requires recruitment to membrane-bound H-Ras, which greatly speeds the formation of a stable, mem
298 Among CRYSTAL and FIRE-3 study patients with RAS wt left-sided tumors, FOLFIRI plus cetuximab signifi
299 d FOLFIRI plus bevacizumab); in contrast, in RAS wt patients with poor-prognosis right-sided tumors,
300                                       In the RAS wt populations of CRYSTAL and FIRE-3, patients with
301 rotein kinase, whereas the overexpression of Ras-WT enhanced it.

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