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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
18 es that interfere with the palmitoylation of Ras, a high value therapeutic target that is mutated in
21 etastatic colon cancers and that oncogenic K-RAS activates TGF-beta signaling to promote tumor invasi
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
29 well as the co-operativity observed between RAS activity and RAF kinase inhibitors in driving RAF ac
32 code a pattern of stimuli, a disease-related Ras allele abolished the spacing effect for plastic chan
35 em leads to short-lived patches of activated Ras and associated F-actin that precede the extension of
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.
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
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
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
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
66 ucleus in Deltaras2 RAS2 interacted with the RAS-binding domain of the adenylate cyclase in vitro, an
69 as the incidence of somatic mutations of the RAS, BRAF, and EGFR genes and association of cetuximab e
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
75 e NgBR promotes the membrane accumulation of Ras by directly binding prenylated Ras at the plasma mem
78 of the switch and many of the pathways that RAS controls are well known, but the precise mechanisms
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
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
88 y and development of clinical candidates for RAS-driven cancers involving mutations in RAS genes or o
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
100 lassic effector molecule of the RAS, several RAS enzymes affect immune homeostasis independently of c
102 m of epidermal growth factor receptor (EGFR)-Ras-ERK signaling, has identified dynamic features not e
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.
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%
114 ng context-specific oncogenic phenotypes.The Ras-family small GTPase RAB25 can exert both pro- and an
116 ous tumor cells expressing B-Raf(V600E) or K-Ras(G12C/D) Intriguingly, coimmunoprecipitation and in v
122 lin-1 expression inhibits oncogenic K-Ras (K-Ras(G12V))-induced premature senescence in mouse embryon
124 receptor, a receptor tyrosine kinase) and H-Ras generates strong, synergistic activation of PI3Kalph
128 Self-assembly of plasma membrane-associated Ras GTPases has major implications to the regulation of
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
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
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
146 ive selection driven by BCL-XL modulation of RAS-induced self-renewal, and during which apoptotic res
148 t mediate metastatic dissemination of mutant Ras-induced tumors in the developing nervous system.
150 erent deacylation rates of single-acylated H-Ras influence differentially its overall exchange betwee
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
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
167 tigate gastric adenocarcinoma subtypes where RAS/MAPK pathway activation and E-cadherin attenuation a
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
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
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
184 ptor tyrosine kinase-dependent activation of RAS more potently in colorectal cancer than in melanoma
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
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
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
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
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
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
243 molecular basis to explain the induction of RAS-RAF association by RAF inhibitors, as well as the co
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
248 tors in breast cancer, and inhibitors of the RAS/RAF/mitogen-activated protein kinase pathway in RAS-
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
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
260 ndings identify Etv5 as a critical output of Ras signaling in AT2 cells, contributing to both lung ho
266 oinformatics analysis detected a prominent K-RAS signature and predicted activation of several import
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
271 show that Akt activation by a Ras homolog, R-Ras, stabilizes the microtubule cytoskeleton in endothel
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
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
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
287 mary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-as
289 eling and simulations we further show that K-Ras uses two partially overlapping interfaces to form co
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
294 we show that Egfr cooperates with oncogenic Ras via Arf6, which functions as a novel regulator of Hh
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,
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