ライフサイエンスコーパス: Ras

1 ating protein for RAS proto-oncogene GTPase (RAS).

2 components of the renin-angiotensin system (RAS).

3 (-/-)) affects the renin-angiotensin system (RAS).

4 ation and immobilization of most particulate RAs.

5 ent of the counteracting hypotensive axis of RAS.

6 ions with small GTPases, including Rap1A and Ras.

7 ng to membrane-anchored and active GTP-bound RAS.

8 east, and colon cancer driven by oncogenic K-Ras.

9 difies several oncogenic proteins, including RAS.

10 And what about those of K-Ras4B versus N-Ras?

11 RAs(3) where R = Ca, Sr, thus, offers a unique opportuni

12 el of KRas(G12D)-driven PDAC, loss of kappaB-Ras accelerates tumour development and shortens median s

13 Ras activates its effectors at the membrane.

14 In response to Ras-activating cell signaling, SOS autoinhibition is rel

15 Germline Ras-activating mutations have been known to contribute t

16 r tyrosine kinase-mediated and GEF-dependent RAS activation (such as by targeting the scaffolding pho

17 out RAS membrane dynamics and the details of RAS activation of downstream signaling.

18 part to profound metabolic stress induced by RAS activation.

19 Additionally, increasing Ras activity optogenetically after, but not before, acqu

20 the protein, neurofibromin, an inhibitor of Ras activity.

21 is a tractable approach to block oncogenic K-Ras activity.

22 (P < .001), with a low incidence of acquired RAS alterations at the time of progression.

23 , suggesting a disturbed balance between the RAS and kallikrein-kinin systems.

24 istic link between early driver mutations in RAS and KIT and the widespread copy number events by whi

25 s a leucine-rich-repeat (LRR), which binds R-ras and may regulate cdc42.

26 Moreover, we identify the WNT, MAPK/RAS and PI3K pathways as good candidate targets for mole

27 n animal models of HF, central inhibition of RAS and pro-inflammatory cytokines normalizes sympatheti

28 rsisting since, has been competition between Ras and Rap1 for a common target.

29 Small GTPases of the RAS and RHO families are related signaling proteins that

30 e the activation of oncogenic members of the Ras and Rho families of small GTPases through membrane t

31 epend on the combined activities of multiple Ras and Rho family small GTPases, but how their activiti

32 min-based background therapy, specific GLP-1 RAs and SGLT-2 inhibitors have a favorable effect on cer

33 gh Gbetagamma or indirect regulation through RAS and the sufficiency of those inputs is controversial

34 te the structural basis of RAF activation by RAS and to develop inhibitors that can disrupt the KRAS

35 e membrane that impacts its accessibility to RAS and with RBD causing local anionic lipid enrichment

36 the virus and the renin-angiotensin system (RAS) and how this might be affected by RAS inhibitors.

37 domains, mediated association with cdc42, R-ras, and IQGAP1.

38 tions argue that these reintroduced alleles (RAs) are more likely to be tolerated by modern humans th

39 Because the C-terminal Ras association (RA2) domain of PLCepsilon was proposed

40 10alpha proteins is dependent on p85 but not Ras association.

41 ence towards the reno-protective alternative RAS axis.

42 e ceramic pedestals of the FTS, those of the RAS+B did not regularly become biofouled by algae.

43 ere were few effects of light or flow in the RAS+B system, potentially highlighting the importance of

44 Light had a more pronounced effect in the RAS-B system, while flow affected certain coral response

45 r, their individual contribution to baseline RAS balance and whether their activities change in chron

46 Whereas its RAS-binding domain (RBD) contains the main binding inter

47 The Ras-binding domain of the protein kinase c-Raf (c-Raf-RB

48 we show that membrane-localized RBD has its RAS-binding interface mostly inaccessible because of its

49 Here we describe the development of a pan-RAS biologic inhibitor composed of the RAS-RAP1-specific

50 RAS Intracellular delivery of a potent anti-RAS biologic through a receptor-mediated mechanism repre

51 computational RDIs can provide insights into Ras biology and potential clinical applications.

52 None of these parameters were affected by RAS blockade.

53 en speculated that renin-angiotensin system (RAS) blockers may promote COVID-19 by increasing ACE2, w

54 g, SHP2 increases the half-life of activated Ras by blocking recruitment of Ras GTPase-activating pro

55 vocate the active feeding of brine shrimp in RAS by those looking to cultivate P. acuta, and likely o

56 2), but by repressing the nutrient signaling Ras-cAMP-PKA pathway at the level of the protein kinase

57 c migration assay, a population of fluidlike Ras cells invades a population of wild type solidlike ce

58 e affinity with the effector-binding site in Ras compared with WT RBD.

59 n which small changes in orientation control Ras' competence to bind multiple regulator and effector

60 addition to macrophages, lung cells express RAS components; also, some lung cells are able to produc

61 ore, 16S rRNA gene sequencing showed that TA@RAs could increase the diversity of the saliva-derived b

62 model were applied and demonstrated that TA@RAs could prevent secondary dental caries effectively.

63 Loss of R-Ras depalmitoylation caused by APT-1 deficiency constrai

64 rived RDIs faithfully represent a measure of Ras dependency in both cancer cell lines and patient sam

65 l type, with clear distinctions seen between Ras-dependent (1 degrees ) and Notch-dependent (2 degree

66 ble PFAS (T619A) decreases purine synthesis, RAS-dependent cancer cell-colony formation, and tumor gr

67 tentially actionable targets to disrupt this RAS-dependent nutrient acquisition pathway were identifi

68 tinguishes an activation mechanism involving Ras dimerization from another mechanism that does not in

69 are circumstantial evidences supporting the Ras dimerization hypothesis, direct proof of Ras dimeriz

70 It has been hypothesized that Ras dimerization is necessary to create activated Raf di

71 Ras dimerization hypothesis, direct proof of Ras dimerization is still inconclusive.

72 from another mechanism that does not involve Ras dimerization.

73 In addition, UBAP2 regulates RAS downstream signaling and helps maintain RAS in the G

74 In Ras-driven cancer cell models, the peptides have an inhi

75 ic RAS, strategies to target MYC activity in RAS-driven cancers are lacking.

76 GTPase inhibitors and therapeutics targeting Ras-driven cancers.

77 ll GTPase signaling has been shown to combat Ras-driven cancers.

78 osensitizers for the photodynamic therapy of ras-driven cancers.

79 ate the best therapeutic strategies to treat RAS-driven cancers.

80 rs of cell growth and metastasis in numerous Ras-driven cancers.

81 loping PKCe-targeted therapies for oncogenic RAS-driven malignancies.

82 K-Ras-driven tumors can grow and metastasize even in the a

83 safety and efficacy of off-label use of Tpo-RAs during pregnancy, a multicenter observational and re

84 on of Ang II relative to Ang (1-7) is termed RAS dysregulation and leads to cellular signals, which p

85 Severe RAS dysregulation is present in CKD dictated by high chy

86 in one or more radical S-adenosylmethionine (RaS) enzymes, a versatile superfamily known to catalyze

87 olorectal cancer metastatic disease, yet how RAS-ERK signaling regulates colorectal cancer metastasis

88 The RAS-ERK/MAPK (RAS-extracellular signal-regulated kinase/

89 The RAS-ERK1/2 axis controlled expression of the cytokine AN

90 Alterations in the RAS-ERK1/2 pathway are associated with the shortest over

91 The RAS exchange factor RASGRP1 is frequently overexpressed

92 In vivo oncogenic Ras exists in isoform-distinct nanoclusters.

93 s(G12V) expression, but not with wild-type K-Ras expression, and that K-Ras(G12V)-driven MEK/ERK acti

94 The RAS-ERK/MAPK (RAS-extracellular signal-regulated kinase/mitogen-activa

95 pability by combining optogenetic control of Ras/extracellular signal-related kinase (ERK) signaling

96 roteomic analyses suggest that endothelial R-Ras facilitates TNF-dependent transendothelial migration

97 HRAS, NRAS, and KRAS4A/KRAS4B comprise the RAS family of small GTPases that regulate signaling path

98 Prompted by these observations, we chose the RAS family to experimentally demonstrate that the transl

99 that this phenomenon is not exclusive to the RAS family.

100 tic case of this phenomenon is KRAS from the RAS family.

101 e and improvement potentials of a commercial RAS farm of tilapia and Clarias in Sweden.

102 ary findings, temporary off-label use of Tpo-RAs for severe and/or refractory ITP during pregnancy se

103 Traditionally, efforts to disrupt the RAS function have focused on nucleotide exchange inhibit

104 Addressing how SARS-CoV-2 unbalances RAS functionality via ACE2 will help design therapies to

105 ) contains the main binding interface to the RAS G domain, its cysteine-rich domain (CRD) is responsi

106 suppressed the xenograft of MIA PaCa-2, a K-Ras(G12C)-expressing human PDAC line, in athymic nude mi

107 el of non-small cell lung cancer driven by K-Ras G12D and p53 deficiency, G6PD knockout did not block

108 al fibroblasts IMR90E1A when combined with K-Ras(G12V) expression, but not with wild-type K-Ras expre

109 with wild-type K-Ras expression, and that K-Ras(G12V)-driven MEK/ERK activity is necessary for this

110 Oncogenic mutations in RAS genes, like KRAS(G12D) or NRAS(G12D), trap Ras in th

111 Here, we demonstrate that the Ras->Raf->rho kinase (ROCK) pathway in MBn suppresses AR

112 by deregulation of the previously documented Ras GTPase activities.

113 amplified by Rab5A, a small G protein of the Ras GTPase superfamily.

114 Here we show a role for the Ras GTPase, R-Ras, in the functional adaptation of high

115 of activated Ras by blocking recruitment of Ras GTPase-activating protein (RasGAP) to the plasma mem

116 GTPases are directly activated by oncogenic Ras GTPases.

117 Although Ras has been reported to allosterically activate the lip

118 Inhibiting membrane association of RAS has long been considered a rational approach to anti

119 he use of drugs that target this system, the RAS has not been explored fully as a druggable target.

120 r regulatory activity compared to RAs, while RAs have activity levels similar to non-introgressed var

121 Ras homolog enriched in brain, an mTOR activator, rescue

122 ad4) expression in the presence of activated Ras homolog family member A (RhoA) induces precocious po

123 cts with the GTPase-signaling small molecule ras homolog family member A (RhoA).

124 ting in the constitutive activation of RhoA (ras homolog family member A) and impaired flow-induced e

125 ced ERK1/2 phosphorylation and activation of Ras homolog gene family member A.

126 The synaptic Ras homologous (Rho) guanine nucleotide exchange factors

127 ition as a potential therapeutic strategy in RAS-hyperactivated neuroblastomas.

128 h affinity with the effector-binding site of Ras in an active conformation.

129 ainst the most frequently mutated version of RAS in non-small-cell lung cancer, KRAS(G12C), we have t

130 S genes, like KRAS(G12D) or NRAS(G12D), trap Ras in the active state and cause myeloproliferative dis

131 RAS downstream signaling and helps maintain RAS in the GTP-bound form.

132 dependent pathways and upstream signaling of Ras in the ISO-specific context.

133 irst data from clinical trials of autonomous RAS in urology are being published.

134 Here we show a role for the Ras GTPase, R-Ras, in the functional adaptation of high endothelial ve

135 ed activity of the renin-angiotensin system (RAS), including the balanced synthesis of its main effec

136 activation of the renin-angiotensin system (RAS) increases sympathetic drive.

137 p53-mutant protein effectively suppressed K-Ras-induced PDAC development in the absence of robust p5

138 omes and epigenome profiles during oncogenic RAS-induced senescence and validating central findings i

139 These results suggest that RAS-induced senescence represents a cell fate determinat

140 albuminuria and potassium, and when modeling RAS inhibition as a time-dependent exposure using a marg

141 lts were consistent whether patients stopped RAS inhibition at higher or lower eGFR, across prespecif

142 priorities necessary to clarify the role of RAS inhibition in COVID-19 mortality that could be rapid

143 s was insufficient to predict sensitivity to Ras inhibition, suggesting that not all of these tumors

144 tional status according to their response to Ras inhibition.

145 L-KD) in APL cell lines led to activation of Ras, inhibition of Akt/mTOR pathways, and increased expr

146 <30 ml/min per 1.73 m(2), 1553 (15%) stopped RAS inhibitor therapy within 6 months.

147 Of 10,254 prevalent RAS inhibitor users (median age 72 years, 36% female) wi

148 udy identifies avicin G as a new potent anti-Ras inhibitor, and suggests that neutral SMase can be a

149 sk leukemic cells could only be killed using RAS-inhibitor or PTPN11-inhibitor, but not PI3K/JAK-inhi

150 A patients receiving statin, aspirin, and/or RAS inhibitors was comparable to non-OSA individuals.

151 Even 10 years ago, RAS inhibitors were so elusive that RAS was termed 'undr

152 stem (RAS) and how this might be affected by RAS inhibitors.

153 cused on nucleotide exchange inhibitors, GTP-RAS interaction inhibitors, and activators increasing GT

154 strategies that directly disrupt either the RAS interaction with activating guanine nucleotide excha

155 at 615 nm, and subsequent Eu(3+)-GTP-loaded RAS interaction with RAF-RBD-Alexa680 monitored at 730 n

156 im while suppressing expansion of the active Ras interior domain.

157 d conversion of constitutively active mutant Ras into functionally inactive forms may be accessible v

158 models driven by either wild-type or mutant RAS Intracellular delivery of a potent anti-RAS biologic

159 d-type RAS proteins in the context of mutant RAS is increasingly considered to be targetable, with re

160 Now, autonomous RAS is on the horizon and the first data from clinical t

161 ator of intrarenal renin-angiotensin system (RAS), is predominantly presented in podocytes, proximal

162 roliferation pathways are parallel; those of Ras isoforms are redundant.

163 ariations within the hypervariable region of Ras isoforms underlie differential posttranslational mod

164 ce of particular cancer types and particular Ras isoforms within these datasets.

165 ng a mechanism for sustained activity of the RAS ITD protein.

166 The elevated memory produced by Ras knockdown is a result of increased ARM.

167 Similar to Ras, knockdown of Raf enhanced ARM consolidation and imp

168 kappaB-Ras proteins and highlight low kappaB-Ras levels and consequent loss of Ral control as risk fa

169 RAC1 is an integrin-linked, ras-like protein that promotes cell migration.

170 RAP1, a ras-like protein, has an important role in the progressi

171 Downstream of KRAS, depletion of RalB (RAS-like proto-oncogene B) and IkappaB kinase-related TA

172 SHP2 is unique in that it exhibits oncogenic Ras-like transforming activity.

173 which is likely responsible for SHP2/T507K's Ras-like transforming activity.

174 Ral (Ras-like) GTPases are directly activated by oncogenic Ra

175 Ral (Ras-like) GTPases play an important role in the control

176 including those for disorders affecting the RAS-MAPK cell-signaling pathway (known as RASopathies) (

177 ulate signaling from tyrosine kinases to the Ras-MAPK pathway.

178 RASA1, a negative regulator of Ras-MAPK signaling, is essential for the development and

179 MEK, a central component of the Ras/MAPK cascade, is mutated in human tumors and develop

180 sed miR, and its expression was regulated by RAS/MAPK signaling.

181 cal or genetic inhibition of the endothelial RAS-MAPK1 signaling pathway rescued hepatic vascular cav

182 strains reciprocally modulated CD40-induced Ras-mediated signaling through PI-3K and Raf-1.

183 f cell migration and have been implicated in Ras-mediated tumorigenicity.

184 evealing a mechanism whereby a neurofibromin/Ras/MEK pathway regulates a critical CIN developmental m

185 the direct transforming effect via constant RAS/MEK/ERK signaling, an inflammation-related effect of

186 nd inactivation of the SWI/SNF complex in (N)RAS melanomas, and select co-mutation patterns coordinat

187 However, little is known about RAS membrane dynamics and the details of RAS activation

188 ion caused by APT-1 deficiency constrained R-Ras membrane trafficking, as shown by total internal ref

189 This modification corrected R-Ras membrane trafficking, restored fibronectin processin

190 lying mechanism is a gain-of-function of the RAS-mitogen-activated protein kinase signaling pathway.

191 educes the number of the clustered oncogenic Ras molecules, thus suppressing Raf-1 activation and mit

192 nge factor-induced Eu(3+)-GTP association to RAS, monitored at 615 nm, and subsequent Eu(3+)-GTP-load

193 K-Ras must interact primarily with the plasma membrane (PM

194 am lipid metabolism and drive progression of RAS mutant cancers.

195 udy elucidate the molecular mechanism of the Ras mutant-mediated development of Noonan syndrome.

196 e number of new patients each year that have Ras-mutant cancers.

197 c signaling and reducing drug sensitivity of RAS-mutant cells.

198 tivation, where I24N, T50I, V152G, and D153V Ras mutants evade SOS autoinhibition.

199 ldown analyses, we show that Noonan syndrome Ras mutants I24N, T50I, V152G, and D153V deregulate the

200 In contrast, other Noonan syndrome Ras mutants-V14I, T58I, and G60E-populate their active f

201 ategory (hazard ratio [HR] 2.12; P = 0.021), RAS mutation (HR 1.74; P = 0.015), and double mutation (

202 hly aggressive and treatment-refractory, yet RAS mutation itself is insufficient for tumorigenesis, d

203 rived colorectal cancer organoids with known Ras mutational status according to their response to Ras

204 Yet the biological effects of different RAS mutations and the tissue-specific clinical implicati

205 RAS mutations are frequent drivers of multiple different

206 Human cancers with activating RAS mutations are typically highly aggressive and treatm

207 ecently, several methods for detecting blood RAS mutations have been proposed, generally relying on m

208 ying KRas, NRas, and HRas as well as several Ras mutations in lung and colon cancer cell lines on fas

209 RAS mutations in the blood of colorectal cancer (CRC) pa

210 Oncogenic RAS mutations pose substantial challenges for rational d

211 These results revealed that the presence of Ras mutations was insufficient to predict sensitivity to

212 oximately 19% of patients with cancer harbor Ras mutations, equivalent to approximately 3.4 million n

213 Intriguingly, JAK2 and RAS-mutations are mutually exclusive in leukemic sub-clo

214 r size <3 cm (OR 1.97; P = 0.004), wild-type RAS (OR 2.00; P = 0.003), and absence of double mutation

215 ay be accessible via subtle perturbations of Ras' orientational preferences at the membrane surface.

216 in exacerbate DN at least partly by inducing RAS overactivation and hypoxia.

217 Altered R-Ras trafficking, increased R-Ras palmitoylation, and fibronectin retention were found

218 median, 1; range 0 to 6), which involved the RAS pathway (KRAS, NRAS, and PTPN11) in 32% of patients.

219 ing studies have identified frequent somatic Ras pathway alterations across a diverse group of pediat

220 BRAF mutations, any RAS pathway alterations, and co-altered RAS/RAF-TP53 mut

221 observations suggest that DPP3 regulates the RAS pathway and water homeostasis by degrading circulati

222 ore widely available, the high prevalence of Ras pathway mutations in pediatric diseases has begun to

223 ronment, through both targeted inhibition of RAS pathway-dependent tumor growth and liberation of ant

224 Ang (1-7) is the dominant RAS peptide in healthy human kidneys with NEP rather tha

225 e applied driver mutations targeting the RTK/RAS/PI3K and p53 pathways to induce the formation of hig

226 are common and parallel evolution occurs in RAS, PIK3CA, SWI/SNF-complex genes and in immune evasion

227 Therefore, disrupting K-Ras PM interaction is a tractable approach to block onco

228 RAS protein coclustering is mainly mediated by membrane

229 ent advances in therapies that target mutant RAS proteins and discuss the future challenges of these

230 ence for a tumour suppressive role of kappaB-Ras proteins and highlight low kappaB-Ras levels and con

231 RAS proteins concentrate in the plasma membrane via lipi

232 The role of the nonmutated, wild-type RAS proteins in the context of mutant RAS is increasingl

233 ivators increasing GTPase activity of mutant RAS proteins.

234 urofibromin, a GTPase-activating protein for RAS proto-oncogene GTPase (RAS).

235 tin cytoskeleton around signaling patches of Ras, Rac and the phosphoinositide PIP3 in the plasma mem

236 nhanced TGF-beta-mediated conversion through Ras:RAC1 signaling as well as via the activation of MEK/

237 ears much insight into the complexity of the RAS-RAF axis has been obtained and inactivation and sign

238 As a proof of concept, we investigate the Ras-Raf system, a well-characterized cell signaling syst

239 olid tumours and multiple myeloma harbouring RAS-RAF-MEK pathway mutations.

240 The RAS-RAF-MEK-ERK signaling axis is frequently activated i

241 Presence of SOX9, BRAF, and co-altered RAS/RAF-TP53 mutations are promising biomarkers that, wh

242 any RAS pathway alterations, and co-altered RAS/RAF-TP53 mutations were associated with worse surviv

243 Co-altered RAS/RAF-TP53 remained independently associated with wors

244 tant for Alk signaling, including members of Ras/Raf/ERK-, Pi3K-, and STAT-pathways as well as taille

245 Sproutys are negative regulators of the Ras/Raf/MAPK signaling pathway and involved in regulatio

246 The RAS/RAF/MEK/ERK pathway promotes gliogenesis but the kin

247 a pan-RAS biologic inhibitor composed of the RAS-RAP1-specific endopeptidase fused to the protein del

248 Secretion-associated Ras-related GTPase 1 (SAR1) is a small GTPase that is pa

249 The small GTPase Ras-related protein Rab-7a (Rab7a) serves as a key organ

250 o frame-shift mutations in the gene encoding Ras-related protein-38 (RAB38), which regulates the traf

251 We identify RAS-responsive element binding protein 1 (RREB1), a RAS

252 prenylation of multiple small GTPases in the Ras, Rho, and Rab families and inhibits ERK activity, re

253 increased genetic heterogeneity and gain of RAS/RTK pathway mutations.

254 ine phosphatase SHP2, a critical mediator of RAS signal transduction downstream of multiple RTK, repr

255 lung cancer cell proliferation by activating RAS signaling and that CYP24A1 knockdown inhibits tumor

256 Aberrant Ras signaling drives 30% of cancers, and inhibition of t

257 esting that not all of these tumors required Ras signaling for proliferation.

258 at expression of these RBD variants inhibits Ras signaling, reducing cell growth and inducing apoptos

259 (GDC) to simultaneously block both PI3K and RAS signaling, thereby exerting synergistic anti-tumor e

260 This dephosphorylation hyperactivates Ras signaling, which is likely responsible for SHP2/T507

261 iple oncogenic mutations activating PI3K and RAS signaling.

262 Grb2 is an adaptor protein that recruits Ras-specific guanine nucleotide exchange factor, Son of

263 y T4, right colon), biological features (K/N-RAS status), and response to chemotherapy (Response Eval

264 cal role for MYC as an effector of oncogenic RAS, strategies to target MYC activity in RAS-driven can

265 The Ras superfamily of small GTPases are guanine-nucleotide-

266 Oncogenic mutations were identified in the Ras superfamily.

267 ing interest in Rap1 envisages capturing its Ras suppression action by inhibitors.

268 lights questions whose answers could advance RAS-targeting agents as mechanism-driven ways to blunt t

269 epresents a promising approach to developing RAS therapeutics against a broad array of cancers.

270 be a tractable target for developing anti-K-Ras therapeutics.

271 owed that IQGAP1 associated with cdc42 and R-ras; this association required the GAP-related domain (1

272 ith IQGAP1 and co-ordinates with cdc42 and R-ras to control the formation of cell extensions that ena

273 s acinar atrophy but combines with oncogenic Ras to produce pancreatic tumors.

274 RNF43 phosphorylation cooperate with active Ras to promote tumorigenesis by abolishing the inhibitor

275 eritoneal EHD (HR, 2.2; 95% CI, 1.1-4.2) and RAS/TP53 co-mutation (HR, 2.8; 95% CI, 1.1-7.2) were ind

276 without RAS/TP53 co-mutation, patients with RAS/TP53 co-mutation had lower median OS: 39 vs. 51 mont

277 Compared to patients without RAS/TP53 co-mutation, patients with RAS/TP53 co-mutation

278 Altered R-Ras trafficking, increased R-Ras palmitoylation, and fib

279 ponsive element binding protein 1 (RREB1), a RAS transcriptional effector(20,21), as a key partner of

280 SLIT2 also inhibits macropinocytosis in RAS-transformed cancer cells, thereby decreasing their s

281 opinocytosis in mammalian cell growth beyond Ras-transformed tumor cells via sustained mTORC1 activat

282 These lipids slow Ras' translational and orientational diffusion and promo

283 1 receptor (AT1R) axis, a deleterious arm of RAS, unleashing its detrimental effects in diabetes.

284 nhibited while the renin-angiotensin system (RAS) upregulated in the kidney of KS-tg/OVE mice compare

285 TNF induces R-Ras upregulation in endothelial cells via JNK and p38 mi

286 found that short-term induction of oncogenic Ras(V12) activates downstream mitogen-activated protein

287 to phenocopy the PYCR1 knockdown in MCF10A H-RAS(V12) breast cancer cells by inhibiting de novo proli

288 vel ER Ca(2+) regulator that synergizes with Ras(V12) to induce tumor growth via JNK-mediated Hippo s

289 hanics and enhance mitotic rounding, so that Ras(V12)-expressing cells are softer in interphase but s

290 (2020) reveal that oncogenic Ras(V12)-mediated cell rounding and cortical stiffening

291 cellular events occurring over the course of Ras(V12)-transformed cell dissemination.

292 o the physical interactions of this class of RAS variants with its regulatory and effector proteins.

293 Response to Tpo-RAs was achieved in 77% of cases, mostly in combination

294 or the formation of short extensions while R-ras was required for the formation of long extensions.

295 ars ago, RAS inhibitors were so elusive that RAS was termed 'undruggable'.

296 ation of each of these radionuclide analogs (RAs) was shown to be dependent upon their chemical speci

297 As no direct inhibitors of pan-RAS were available, an inhibitor of the protein tyrosine

298 with gene regulatory activity and that these RAs were more tolerated than NDAs.

299 depleted for regulatory activity compared to RAs, while RAs have activity levels similar to non-intro

300 In RAS wild-type patients, a third arm testing perioperativ

301 nd to the scaffold KSR (kinase suppressor of RAS) with various MEK inhibitors, including the clinical