ライフサイエンスコーパス: RAS

1 RAS inhibition could mitigate this effect.

2 RAS mutations are frequent drivers of multiple different

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

4 RAS pathway abnormalities cause developmental disorders

5 RAS protein coclustering is mainly mediated by membrane

6 RAS proteins concentrate in the plasma membrane via lipi

7 RAS-induced de novo cohesin peaks are transcription-depe

8 RAS/TP53 co-mutation is associated with worse OS after c

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

10 ut exogenous biological input (RAS-B), (2) a RAS with "live" rocks and an exogenous food supply (RAS+

11 inhibits growth of tumor cells and acts as a RAS mimetic by binding to Ras binding domains of RAS eff

12 novel tumor suppressor whose loss defines a RAS mutant tumor subset characterized by reprogramming o

13 the H3K27M transcriptome is activation of a RAS/MYC axis, which we find can be targeted therapeutica

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

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

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

17 tant KRAS for the treatment of CRC-activated RAS pathways, offering a new therapeutic genome-editing

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

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

20 roteins in cancer biology, and mutant active RAS is a driver in many types of solid tumors and hemato

21 s an active monomer in the absence of active RAS, however, in many tumors BRAF dimers mediate ERK sig

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

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

24 of activated-NOTCH as compared with the AKT-RAS-driven tumors.

25 n of the phosphatidylinositol 3-kinase/AKT-, RAS/MAPK-, and STAT5-signaling pathways.

26 lusters of genomic risk to reveal co-altered RAS/RAF-TP53 as the highest risk subgroup.

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

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

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

30 ence towards the reno-protective alternative RAS axis.

31 nhanced plasmonic method for detecting ~1 aM RAS single nucleotide variants (SNVs) in the plasma of C

32 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

33 tation, identified in 75 patients (69%), and RAS/TP53 co-mutation was identified in 31 patients (28%)

34 wo non-tagged endogenous proteins, actin and RAS GTPase, involved in complex functional networks sens

35 le detection of both nucleotide exchange and RAS/RAF interaction inhibitors using low nanomolar prote

36 oduced in linked RAS nucleotide exchange and RAS/RAF-RBD interaction assays.

37 and oncogenic regulators, including IGFR and RAS signaling, that significantly contribute to aggressi

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

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

40 iple oncogenic mutations activating PI3K and RAS signaling.

41 pathway play key roles in MYC regulation and RAS-driven tumorigenesis.

42 ve been substantial advances in finding anti-RAS therapeutic strategies.

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

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

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

46 Integration of autonomous RAS can be viewed as a positive aid, but it might also b

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

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

49 h most of the amino acid differences between RAS isoforms lie within the hypervariable region, the ad

50 despite the high amino acid identity between RAS family members, KRAS employs an intriguing different

51 hus, RREB1 provides a molecular link between RAS and TGF-beta pathways for coordinated induction of d

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

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

54 ly mutated in melanoma independently of BRAF/RAS mutations.

55 The RAF kinases activated by RAS GTPases regulate cell growth and division by signal

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

57 None of these parameters were affected by RAS blockade.

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

59 part to profound metabolic stress induced by RAS activation.

60 gulation is driven by comorbidity and not by RAS blockade.

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

62 Here, we characterize RAS in live human and mouse cells using single-molecule-

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

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

65 nd remaining off treatment versus continuing RAS inhibitor therapy.

66 Compared with continuing RAS inhibition, stopping this therapy was associated wit

67 Using the RAS-RBD (CRAF RAS binding domain) interaction as a model system, we sh

68 bolic profiling reveals that REDD1-deficient/RAS mutant cells exhibit enhanced uptake of lysophosphol

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

70 ng proteins inhibit RAS activity and deplete RAS proteins through an autophagosome-lysosome-mediated

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

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

73 pathways could be combined with these direct RAS inhibitors, immune checkpoint inhibitors or T cell-t

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

75 1 and SHP2, but not inhibitors of downstream RAS effector pathways.

76 ribed causal link between LZTR1 dysfunction, RAS-mitogen-activated protein kinase signaling hyperacti

77 rly phase of PanIN formation reliant on EGFR-RAS signaling, and an AGO2-dependent phase wherein the m

78 ce with altered microRNA expression and EGFR/RAS signaling, bypassed by loss of p53.

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

80 ingle-molecule-tracking methods and estimate RAS mobility parameters.

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

82 and even paled; however, once they were fed (RAS-B modified to RAS+B), their pigmentation increased,

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

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

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

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

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

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

89 ue and colleagues (Su et al., 2020) identify RAS-responsive element binding protein 1 (RREB1) as a cr

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

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

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

93 from cell lines representing the extremes in RAS dependency, we identified enriched pathways distingu

94 K) As this disease mutation is also found in RAS GTPases, we assessed GAP-stimulated GTP hydrolysis f

95 controls identifies a critical imbalance in RAS represented by decreased expression of ACE in combin

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

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

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

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

100 vo through activation of the MAPK pathway in RAS-mutant transformed cells.

101 ncoded by PTPN11, plays an essential role in RAS-mitogen-activated protein kinase (MAPK) signaling du

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

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

104 tumors, as are upstream activators including RAS and receptor tyrosine kinases.

105 difies several oncogenic proteins, including RAS.

106 I3K or JAK-signaling, prevented TSLP-induced RAS-GTP boost.

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

108 mbrane-targeted RAS binding proteins inhibit RAS activity and deplete RAS proteins through an autopha

109 em (RAS) without exogenous biological input (RAS-B), (2) a RAS with "live" rocks and an exogenous foo

110 rsibly cleaves and inactivates intracellular RAS at low picomolar concentrations terminating downstre

111 involvement in the regulation of intrarenal RAS thereby control blood pressure, renal injury, and ur

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

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

114 e CRAF at arginine 100, interfering with its RAS/RAF binding potential, and therefore altering extrac

115 h increases in ACE2, renin, angiotensin, key RAS receptors, kinogen and many kallikrein enzymes that

116 Kidney RAS enzyme analysis might lead to novel therapeutic appr

117 in the RAS-mitogen-activated protein kinase (RAS/MAPK) pathway yet show unexplained variability in th

118 dual-parametric method introduced in linked RAS nucleotide exchange and RAS/RAF-RBD interaction assa

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

120 the pathophysiological response of the local RAS within the intestinal epithelium involves mechanisms

121 rge cluster, in which 96% harbored NS5A M28V RAS.

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

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

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

125 one is not sufficient to induce RBD-mediated RAS inhibition.

126 c flux, a process that required RAB24 member RAS oncogene family (RAB24), a small GTPase that facilit

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

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

129 ivators increasing GTPase activity of mutant RAS proteins.

130 Currently, direct inhibition of mutant RAS through allele-specific inhibitors provides the best

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

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

133 genomic properties among subtypes (BRAF, (N)RAS, NF1, triple wild-type (TWT)), subtype-specific pref

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

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

136 inases (RTK) that converges on activation of RAS as a mechanism to limit sensitivity to MEK inhibitio

137 Sevenless (SOS) catalyzes the activation of RAS by converting it from its inactive GDP-bound state t

138 tors of SOS1 that can increase the amount of RAS-GTP in cells.

139 1 receptor (AT1R) axis, a deleterious arm of RAS, unleashing its detrimental effects in diabetes.

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

141 ent of the counteracting hypotensive axis of RAS.

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

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

144 mimetic by binding to Ras binding domains of RAS effectors.

145 f agents that target downstream effectors of RAS signaling has advanced substantially.

146 The spatial expression of RAS enzymes was determined by immunohistochemistry.

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

148 o survey their environment and for growth of RAS-transformed cancer cells.

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

150 Pre-inhibition of RAS or PTPN11, but not of PI3K or JAK-signaling, prevent

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

152 SAFB knockdown decreased GTP loading of RAS, abrogated alternative prenylation, and sensitized R

153 th increased plasma membrane localization of RAS/AGO2.

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

155 teins, as well as simultaneous monitoring of RAS signaling with visible-light biosensors, enabling al

156 the RAC1-GTPase is a key downstream node of RAS and that genetic disruption of the Rac1 allele compl

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

158 NF1 is essential for negative regulation of RAS activity and is altered in about 90% of malignant pe

159 ytosis supports the metabolic requirement of RAS-transformed pancreatic ductal adenocarcinoma cells (

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

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

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

163 ht some important trends in the targeting of RAS proteins in cancer.

164 um involves mechanisms distinct from that of RAS in the lung; however, both lung and gut are impacted

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

166 TGF-beta depends on RAS and mitogen-activated protein kinase (MAPK) pathway

167 se SOS1(cat)-mediated nucleotide exchange on RAS and display cellular action consistent with our prio

168 CKD (eGFR<30 ml/min per 1.73 m(2)) while on RAS inhibitor therapy.

169 The oncogene RAS is one of the most widely studied proteins in cancer

170 Oncogenic RAS mutations are associated with DNA methylation change

171 Oncogenic RAS mutations pose substantial challenges for rational d

172 egies for inhibiting and depleting oncogenic RAS proteins.

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

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

175 orm, position, and substitution of oncogenic RAS mutations are often unique to human cancers.

176 des of effort, broad inhibition of oncogenic RAS using small-molecule approaches has proven to be a m

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

178 molecules that directly target one oncogenic RAS mutant (G12C) undergoing clinical evaluation, there

179 Here, we use Hi-C to show that oncogenic RAS-induced senescence in human diploid fibroblasts is a

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

181 h harbored allelically imbalanced p53 and/or RAS pathway mutations.

182 iven by aberrant receptor tyrosine kinase or RAS signaling.

183 of CRLF2-rearrangements, JAK2-mutations, or RAS-pathway mutations.

184 apies that target RAS-activating pathways or RAS effector pathways could be combined with these direc

185 ree diffusive states distinct from the other RAS isoforms (KRAS4a, NRAS, and HRAS); and although most

186 colocalizes on the cell membrane with other RAS isoforms and a subset of prenylated small GTPase fam

187 Pan-RAS protein degradation, however, affects proliferation

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

189 ed to the VHL E3 ligase is compared to a pan-RAS intracellular single domain antibody (iDAb) fused to

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

191 Cardiovascular disease and pharmacologic RAS inhibition both increase ACE2 levels, which may incr

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

193 We found that SAFB promoted RAS membrane association by controlling FNTA expression.

194 our activity across various cancers with RAF-RAS-MEK pathway mutations, and that this inhibitor is to

195 Subsequent interaction of the RAF1 RAS binding domain with KRAS does not significantly chan

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

197 ysiological findings, we therefore recommend RAS+B systems as a superior means of biopreservating and

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

199 r results provide a mechanism for regulating RAS activity and protein levels, a more detailed underst

200 RNA and whole-exome sequencing revealed RAS-mediated TORC1 activation in a subset of neratinib-r

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

202 ated alternative prenylation, and sensitized RAS-mutant cells to growth inhibition by FTI.

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

204 nvestigational therapeutic approach for some RAS pathway-driven cancers.

205 <30 ml/min per 1.73 m(2), 1553 (15%) stopped RAS inhibitor therapy within 6 months.

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

207 h "live" rocks and an exogenous food supply (RAS+B), and (3) a simple flow-through system (FTS) featu

208 espite advances in robotic-assisted surgery (RAS) in the past two decades, control of the robotic sys

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

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

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

212 The renin-angiotensin system (RAS) has long been appreciated as a major regulator of b

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

214 n whether stopping renin-angiotensin system (RAS) inhibitor therapy in patients with advanced CKD aff

215 ogy related to the renin-angiotensin system (RAS) that may be clinically insightful.

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

217 ive hormone of the renin-angiotensin system (RAS), angiotensin II (Ang II), is involved in several hu

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

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

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

221 to a dysregulated renin-angiotensin system (RAS).

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

223 cum: (1) a recirculating aquaculture system (RAS) without exogenous biological input (RAS-B), (2) a R

224 tured in a recirculating aquaculture system (RAS).

225 In addition to systemic RAS, the pathophysiological response of the local RAS wi

226 and intra-tubular renin angiotensin systems (RAS), which are in turn associated with increased blood

227 ed closed Recirculating Aquaculture Systems (RASs) has overcome many local environmental challenges w

228 Therapies that target RAS-activating pathways or RAS effector pathways could b

229 covered that high-affinity membrane-targeted RAS binding proteins inhibit RAS activity and deplete RA

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

231 The N-terminal RAS-binding domain (RBD) of ELMO (ELMO(RBD)) interacts w

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

233 and p84 regulatory subunits, indicating that RAS binding to p110gamma is insufficient to support GPCR

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

235 ent potential identified, this suggests that RASs may play a more important role in a future, environ

236 The RAS exchange factor RASGRP1 is frequently overexpressed

237 The RAS oncoprotein drives elevated macropinocytosis, a meta

238 The RAS proteins are GTP-dependent switches that regulate si

239 The RAS-binding domain (RBD) and cysteine-rich domain (CRD)

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

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

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

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

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

245 hway, despite inhibition of the HER2 and the RAS-ERK pathways in tumor cells.

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

247 ation, suggesting that mechanisms beyond the RAS pathway play key roles in MYC regulation and RAS-dri

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

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

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

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

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

253 Indeed, in the RAS family and other oncogene families with two or three

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

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

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

257 quently driven by genetic alterations in the RAS-mitogen-activated protein kinase (RAS/MAPK) pathway

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

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

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

261 alysis revealed increased interaction of the RAS ITD with Raf proto-oncogene Ser/Thr kinase (RAF), le

262 r, affects proliferation irrespective of the RAS mutation.

263 The abbreviated description of the RAS suggests that its dysregulation may be at the center

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

265 the multi-month incubation, yet those of the RAS-B grew slowly and even paled; however, once they wer

266 4-targeted tumors revealed inhibition of the RAS-GTPase, Hedgehog, and Notch pathways, along with evi

267 The oncogenic activation of the RAS-MEK pathway suppresses CASZ1 expression in ERMS.

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

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

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

271 ion also often exhibited upregulation of the RAS/MAPK pathway.

272 macological inhibition of PAK6 perturbed the RAS/MAPK pathway and mitochondrial activity, sensitizing

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

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

275 lated to oncogenic ERK signaling through the RAS-SHOC2-PP1 phosphatase complex.

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

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

278 Other approaches related to the RAS pathway might be considered, for example, inhalation

279 Using the RAS-RBD (CRAF RAS binding domain) interaction as a model

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

281 To elucidate the principles underlying this RAS mutation tropism of urethane, we adapted an error-co

282 utations are the most prevalent in the three RAS-family isoforms and involve many different amino-aci

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

284 Careful targeting of the systemic and tissue RAS may optimize clinical outcomes in subjects with diab

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

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

287 ken together, loss of CASZ1 activity, due to RAS-MEK signaling or genetic alteration, impairs ERMS di

288 wever, once they were fed (RAS-B modified to RAS+B), their pigmentation increased, and their oral dis

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

290 tors or T cell-targeting approaches to treat RAS-mutant tumours.

291 ers, and the activation of the intra-tubular RAS even in normotensive young adults.

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

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

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

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

296 amirez et al. elucidated a mechanism whereby RAS controls V-ATPase association with the plasma membra

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

298 T) assay for nucleotide binding studies with RAS and heterotrimeric G proteins.

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

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