ライフサイエンスコーパス: RTK

1 RTK (receptor tyrosine kinase) and p53 signalling were f

2 RTK-integrin cooperation has been assumed to occur at th

3 RTKs are believed to form both homodimers and heterodime

4 ollectively, our results identify an miR-218-RTK-HIF2alpha signaling axis that promotes GBM cell surv

5 All 58 RTKs consist of an extracellular (EC) domain, a transmem

6 GFR, MET/GAB1, and IGF1R/IRS2, implicating a RTK-driven adaptive response associated with dasatinib.

7 of expression or function promotes aberrant RTK signaling and rapid growth of cancer cells.

8 presented here can yield new knowledge about RTK interactions and can further our understanding of si

9 ibit compensatory signaling from accumulated RTKs, which actually enhances cell motility in some cont

10 the compensatory signaling from accumulated RTKs.

11 for dynamic association of ligand-activated RTKs with Galphai, and for noncanonical transactivation

12 BV entry factor that cooperatively activates RTK signalling, which subsequently promotes EBV infectio

13 simple and intuitive mechanism of activating RTKs, K.-I.

14 tif to membranes via association with active RTKs, instead of via chemically induced dimerization, is

15 These results reveal a role for alternate RTKs in maintaining progrowth and survival signaling in

16 Here we identify an RTK of the Eph family, EphA2, to be a cargo of an RCP-re

17 of a classic Gi/Go-coupled receptor into an RTK-like entity, resulting in a noncanonical pathway eve

18 that an integrin influences signalling of an RTK, c-Met, from inside the cell, to promote anchorage-i

19 distinct sensitivities to growth factors and RTK inhibitors.

20 Together, these data suggest that Irf6 and RTK signaling interact in regulating periderm differenti

21 ic interactions between variants in IRF6 and RTK signaling pathway genes in human orofacial clefting

22 These include activation of the MYC and RTK-RAS-PI3K pathways and upregulation of the FOXM1- and

23 ar recognition, i.e., of both G proteins and RTKs, and reveal the workings of a novel platform for ac

24 tify RPTPs in the human genome that serve as RTK phosphatases.

25 e kinase signaling nodes that facilitate AXL-RTK cross-talk, protracted signaling, converging on ERK,

26 ts, promoting synergistic cross-talk between RTKs and integrins.

27 GIV mutant (Arg 1745-->Leu) that cannot bind RTKs impaired all previously demonstrated functions of G

28 o rescue the phenotype in cells lacking both RTKs indicating that Egfr is required for activation of

29 est that treatment strategies targeting both RTKs may be more effective than singly-targeted agents.

30 vel platform for activation of G proteins by RTKs in single living cells.

31 tivity suppressed phosphorylation of certain RTKs, restoring the antitumor effects of sunitinib in mo

32 Functional analysis of the cleavable RTKs indicated that proliferation promoted by overexpres

33 f inhibitors targeting all three coactivated RTKs and MEK1 was needed to inhibit proliferation and in

34 almost ubiquitous; thus tailored combination RTK inhibitor (RTKi) therapy might be required, as we de

35 hey are mutually exclusive from other common RTK variants in lung cancer, that they correspond to ana

36 We demonstrated that, among the common RTKs, PDGFR-alphabeta was specifically phosphorylated in

37 new therapeutic opportunities for correcting RTK signaling output.

38 tyrosine phosphatases (PTPs) counterbalance RTK signaling; however, the functions of receptor PTPs i

39 indings demonstrate that PDGFR is a critical RTK required for the prodestructive phenotype of RA syno

40 aned from computer simulation in deciphering RTK regulatory function.

41 otentially rapid path to clinic demonstrated RTK blockade, inhibition of mitogenic signaling, and pro

42 insights into the mechanisms of deregulated RTK-induced carcinogenesis and provides the basis for th

43 plasma membranes composed of many different RTKs with the potential to interact.

44 Moreover, AZD4547 downregulated RTK, mTOR, and Wnt/beta-catenin signaling pathways in pr

45 uently driven by GAs in the highly druggable RTK/Ras/mitogen-activated protein kinase (MAPK) signalin

46 Although single inhibition of each RTK alone or plus MEK1 inhibitors was ineffective, a com

47 s as a specific cargo adaptor to assist EGFR/RTK anchoring on the trans-Golgi network (TGN) and recyc

48 e of GOLM1, a Golgi-related protein, in EGFR/RTK recycling and metastatic progression of HCC.

49 This elevated RTK signaling also promotes the activation of hypoxia-in

50 provide insight into the mechanisms encoding RTK specificity.

51 xposed cytosolic surface of these endosomes, RTK autophosphorylation selects the downstream signaling

52 dephosphorylation of several tumor-enhancing RTKs, including EGF receptor, ErbB2, hepatocyte growth f

53 uently found that EphB2 and EphA2 of the Eph RTK family were cleaved in their ectodomains by TF/FVIIa

54 These results define Eph RTKs as novel proteolytical targets of TF/FVIIa and prov

55 Furthermore, an ATP-competitive EPHA2 RTK inhibitor, ALW-II-41-27, reduced the number of viabl

56 The EPHA2 RTK is overexpressed in aggressive forms of breast cance

57 turns on GIV-GEF downstream of growth factor RTKs remained unknown.

58 regions of insulin receptor and EGFR family RTKs to reduce their expression.

59 bers of the receptor tyrosine kinase family (RTK) have been shown to be present in the nucleus of cel

60 tic lymphoma kinase (ALK) is one of very few RTKs that remain without a firmly established protein li

61 ibition of stemness, and suppression of FGFR/RTK signaling in ErbB2-overexpressing human breast cance

62 r, accuracy (63% for EGFR [P < .01], 61% for RTK II [P = .01]) than prediction by chance; prediction

63 a set of pathway reactivation essential for RTK-mediated bypass resistance.

64 n together, our results provide evidence for RTK/RAS pathway activation and p53 deficiency as a combi

65 RTK) recycling is of critical importance for RTK signaling and cancer, yet the process is poorly unde

66 here we show a non-cell-autonomous role for RTK-Ras signaling in the delamination of a neuroblast fr

67 tion provides spatiotemporal specificity for RTK degradation and sequesters CRL3(GCL) to prevent it f

68 ous stimuli, we investigated the role of HER RTKs in IR-induced G2/M checkpoint response in breast ca

69 However, RTK heterodimers remain poorly characterized, as compare

70 interaction pattern shared across the human RTK family.

71 The screen covering 45 of the 55 human RTKs identified 12 new as well as all nine previously pu

72 lity to gamma-secretase cleavage among human RTKs.

73 c lipid interactions with all 58 known human RTKs.

74 ional signaling mechanism for numerous human RTKs.

75 cific to EGFR and HER3, show that changes in RTK expression indicative of resistance to PI3K and AKT

76 by mutually exclusive oncogenic mutations in RTK/RAS pathway members KRAS, EGFR, BRAF and ERBB2, and

77 Fusion with lysosomes then results in RTK degradation and downregulation.

78 hat JM-lipid interactions play a key role in RTK structure and function, and more generally in the na

79 le RTK mutation may affect multiple steps in RTK activation.

80 of the involvement of the RPTP subfamily in RTK tyrosyl dephosphorylation has not been established.

81 els between partial and/or biased agonism in RTKs and G-protein-coupled receptors, as well as new the

82 n expansion mutants is enhanced by increased RTK signaling and suppressed by reduced RTK signaling.

83 Our results report a novel mode of integrin-RTK cooperation, which we term 'inside-in signalling'.

84 of RTKs have provided critical insights into RTK structures and functions, lack of a full-length rece

85 isplayed increased receptor tyrosine kinase (RTK) activity and activation of the Src/FAK/signal trans

86 tion of endogenous receptor tyrosine kinase (RTK) activity can modulate cell polarity and establish p

87 interestingly, the receptor tyrosine kinase (RTK) agonist, platelet-derived growth factor-BB (PDGF-BB

88 ne receptor with a receptor tyrosine kinase (RTK) also elicited a signaling response.

89 dation of Torso, a receptor tyrosine kinase (RTK) and major determinant of somatic cell fate.

90 diated through the receptor tyrosine kinase (RTK) and Notch (N) signaling pathways and their combined

91 The receptor tyrosine kinase (RTK) AXL has been intrinsically linked to epithelial-mes

92 The receptor tyrosine kinase (RTK) AXL is induced in response to type I interferons (I

93 c hypotheses about receptor tyrosine kinase (RTK) biology.

94 Resistance to receptor tyrosine kinase (RTK) blockade in breast cancer is often mediated by acti

95 AM10 substrate), a receptor tyrosine kinase (RTK) coreceptor required for cellular migration, and pro

96 reviously that the receptor tyrosine kinase (RTK) EPHA2 is commonly overexpressed in non-small cell l

97 viously orphanized receptor tyrosine kinase (RTK) from A. aegypti encoded by the gene AAEL001915 is a

98 The EPHB4 receptor tyrosine kinase (RTK) has recently emerged as an oncogenic factor in many

99 trastuzumab or the receptor tyrosine kinase (RTK) inhibitor lapatinib significantly improves survival

100 hat sensitivity to receptor tyrosine kinase (RTK) inhibitors can be bypassed by various ligands throu

101 Receptor tyrosine kinase (RTK) inhibitors have advanced colon cancer treatment.

102 The receptor tyrosine kinase (RTK) insulin-like growth factor-1 receptor (IGF1R) is im

103 We report several receptor tyrosine kinase (RTK) ligands increase RhoA-guanosine triphosphate (GTP)

104 MerTK, a receptor tyrosine kinase (RTK) of the TYRO3/AXL/MerTK family, is expressed in myel

105 Receptor tyrosine kinase (RTK) pathways that are implicated in proliferation and t

106 ively regulate the receptor tyrosine kinase (RTK) pathways, especially epithelial growth factor recep

107 Receptor tyrosine kinase (RTK) recycling is of critical importance for RTK signali

108 genes that encode receptor tyrosine kinase (RTK) signaling components, including members of the FGF

109 Deregulated receptor tyrosine kinase (RTK) signaling is frequently associated with tumorigenes

110 (PHLPP) suppresses receptor tyrosine kinase (RTK) signaling output by a previously unidentified epige

111 iple components of receptor tyrosine kinase (RTK) signaling pathways, and miR-218 repression increase

112 nes activating RAS/receptor tyrosine kinase (RTK) signaling pathways.

113 for understanding receptor tyrosine kinase (RTK) signaling specificity.

114 Receptor tyrosine kinase (RTK) signaling through Ras influences many aspects of no

115 between Notch and receptor tyrosine kinase (RTK) signaling.

116 and NRP1-dependent receptor tyrosine kinase (RTK) signalling promotes EBV infection.

117 EphA2 is a receptor tyrosine kinase (RTK) that is sensitive to spatial and mechanical aspects

118 TTH) activates the receptor tyrosine kinase (RTK) Torso to initiate metamorphosis through the release

119 lling integrin and receptor tyrosine kinase (RTK) trafficking, but how RCP influences metastasis in v

120 Axl is a receptor tyrosine kinase (RTK) upregulated in various tumors including cutaneous s

121 nase (JAK/TYK), or Receptor Tyrosine Kinase (RTK)-mediated trans-phosphorylation.

122 e effectiveness of receptor tyrosine kinase (RTK)-targeted therapies.

123 alterations in the receptor tyrosine kinase (RTK)/Ras signaling pathway including alterations in ALK,

124 rs that target the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kinase (MAPK) pathway

125 The receptor-tyrosine kinase (RTK)/Ras/Raf pathway is an essential cascade for mediati

126 activation through receptor tyrosine kinase (RTK)/SRC-family kinase (SFK) signaling or mutant NRAS, w

127 h-factor) or CD44 (receptor-tyrosine-kinase (RTK) co-receptor) to chymotrypsin/trypsin or soluble ADA

128 m other oncogenic receptor tyrosine kinases (RTK) and/or compensatory signals exist that dampen dasat

129 Receptor tyrosine kinases (RTK) are important cell signaling molecules that influen

130 Receptor tyrosine kinases (RTK) are major regulators of key biological processes, i

131 Dysregulation of receptor tyrosine kinases (RTK) contributes to cellular transformation and cancer p

132 expression of the receptor tyrosine kinases (RTK) epidermal growth factor receptor 1 (EGFR) and human

133 DGFRa, and HER1-2 receptor tyrosine kinases (RTK) expressed in a large proportion of human PDAC sampl

134 (PDGFR) family of receptor tyrosine kinases (RTK) has been shown to cooperate with TGF-beta in variou

135 ting mutations in receptor tyrosine kinases (RTKs) and BRAF.

136 ross-talk between receptor tyrosine kinases (RTKs) and heterotrimeric G proteins, two major and disti

137 Receptor tyrosine kinases (RTKs) and integrins cooperate to stimulate cell migratio

138 (ErbB) family of receptor tyrosine kinases (RTKs) and their ligands is common in human cancers.

139 In eukaryotes, receptor tyrosine kinases (RTKs) and trimeric G proteins are two major signaling hu

140 Receptor tyrosine kinases (RTKs) and trimeric G proteins are two such major signali

141 -amplification of receptor tyrosine kinases (RTKs) and/or downstream mitogenic activation is almost u

142 Receptor tyrosine kinases (RTKs) are a class of cell surface receptors that, upon l

143 Receptor tyrosine kinases (RTKs) are cell surface receptors that initiate signal ca

144 sm by which these receptor tyrosine kinases (RTKs) are exported from the endoplasmic reticulum (ER) r

145 genic variants of receptor tyrosine kinases (RTKs) are frequent events during tumorigenesis; however,

146 Receptor tyrosine kinases (RTKs) are increasingly recognized as having the capacity

147 action among the receptor tyrosine kinases (RTKs) because their catalytic activity is induced by ext

148 als propagated by receptor tyrosine kinases (RTKs) can drive cell migration and proliferation, two ce

149 Receptor tyrosine kinases (RTKs) conduct biochemical signals upon dimerization in t

150 g question is how receptor tyrosine kinases (RTKs) determine different cell-fate decisions despite sh

151 (EGF) and insulin receptor tyrosine kinases (RTKs) exemplify how receptor location is coupled to sign

152 ributions of five receptor tyrosine kinases (RTKs) from the ErbB, IGF-1R and Met families in breast c

153 molecules against receptor tyrosine kinases (RTKs) has been shown to be a valuable strategy.

154 Receptor tyrosine kinases (RTKs) have been demonstrated to signal via regulated int

155 eine mutations in receptor tyrosine kinases (RTKs) have been previously proposed to induce constituti

156 ommonly amplified receptor tyrosine kinases (RTKs) in glioblastoma (GBM).

157 ressions of these receptor tyrosine kinases (RTKs) in stable tumor sphere lines, frequently defining

158 l transduction by receptor tyrosine kinases (RTKs) involves complex ligand- and time-dependent change

159 n dimerization of receptor tyrosine kinases (RTKs) is a simple and intuitive mechanism of activating

160 hat activation of receptor tyrosine kinases (RTKs) is an important determinant of this innate drug re

161 The activity of receptor tyrosine kinases (RTKs) is controlled through their lateral association in

162 the HER family of receptor tyrosine kinases (RTKs) often respond well to targeted inhibition.

163 ed Mer and Axl as receptor tyrosine kinases (RTKs) overexpressed in 69% and 93%, respectively, of tum

164 Receptor tyrosine kinases (RTKs) play a critical role in diverse cellular processes

165 Receptor tyrosine kinases (RTKs) play critical roles in physiological and pathologi

166 s have shown that receptor tyrosine kinases (RTKs) play important roles in EBV-associated neoplasia.

167 iated from mutant receptor tyrosine kinases (RTKs) provides critical growth and survival signals in h

168 ar basis by which receptor tyrosine kinases (RTKs) recruit and phosphorylate Src Homology 2 (SH2) dom

169 r carcinoma (Eph) receptor tyrosine kinases (RTKs) regulate a variety of dynamic cellular events, inc

170 chanisms by which receptor tyrosine kinases (RTKs) regulate catalytic activity are diverse and often

171 Members of the receptor tyrosine kinases (RTKs) regulate important cellular functions such as cell

172 (FGFR) family of receptor tyrosine kinases (RTKs) regulates signaling pathways involved in cell prol

173 Ubiquitylation of receptor tyrosine kinases (RTKs) regulates their trafficking and lysosomal degradat

174 Receptor tyrosine kinases (RTKs) signal through shared intracellular pathways yet m

175 Receptor tyrosine kinases (RTKs) such as MET and its downstream target PI3K are ove

176 Receptor tyrosine kinases (RTKs) such as PDGFRalpha (platelet-derived growth factor

177 ified as "orphan" receptor tyrosine kinases (RTKs) with oncogenic potential.

178 vation of various receptor tyrosine kinases (RTKs), although the underlying mechanisms have been larg

179 milies of protein receptor tyrosine kinases (RTKs), Eph receptors are unique in possessing a sterile

180 bition, including receptor tyrosine kinases (RTKs), v-erb-b2 erythroblastic leukemia viral oncogene h

181 As HER receptor tyrosine kinases (RTKs), which have important roles in cell proliferation

182 largest family of receptor tyrosine kinases (RTKs), with fourteen receptors divided into two subfamil

183 The TAM receptor tyrosine kinases (RTKs)-TYRO3, AXL, and MERTK-together with their cognate

184 s is regulated by receptor tyrosine kinases (RTKs).

185 by activation of receptor tyrosine kinases (RTKs).

186 thrin, actin, and receptor tyrosine kinases (RTKs).

187 expressing colon tumors can benefit from KIT RTK inhibitors.

188 tor A4 (EphA4), which belongs to the largest RTK Eph family, was downregulated in primary B cells pos

189 ic and drug discovery studies of full-length RTKs require protein that is both fully functional and f

190 We first used antibodies to localize RTK signals and discovered that phosphorylated ERK1/2 (p

191 Although stimulation of many RTKs leads to activation of trimeric G proteins, the mol

192 Among the many RTKs, vascular endothelial growth factor receptor (VEGFR

193 DNA methylation subgroups (eg, mesenchymal, RTK I "PGFRA," RTK II "classic"), MGMT promoter methylat

194 the liver subtle increases in wild-type Met RTK levels are sufficient for spontaneous tumors in mice

195 For most RTKs, however, it is unknown whether they can exploit th

196 ntrinsic targets that are downstream of most RTKs.

197 eases the abundance and activity of multiple RTK effectors.

198 , to serve as a direct platform for multiple RTKs to activate Galphai proteins.

199 perative and parallel activation of multiple RTKs in GBM and suggest that the development of selectiv

200 gence of a non-receptor tyrosine kinase (non-RTK), ACK1 (also known as activated Cdc42-associated kin

201 iver cells to subtle changes in nononcogenic RTK levels, allowing them to acquire a molecular profile

202 , the cellular vulnerability to nononcogenic RTK fluctuations has not been characterized.

203 6 residue is selective for only GPCR but not RTK agonist-induced nuclear export and proteolytic degra

204 Notably, RTK-MAPK-PI3K pathways, cell cycle and epigenetic regula

205 s innate drug resistance despite blockade of RTK activity in NSCLC cells.

206 Dysregulation of RTK and p53 signalling in hiPSC-derived NPCs (iNPCs) rec

207 ere, we uncovered an unexpected mechanism of RTK trafficking in this process.

208 This mode of RTK degradation does not depend upon receptor activation

209 ure has hindered a comprehensive overview of RTK activation.

210 anced tyrosine phosphorylation in a panel of RTK and their signaling adaptor complexes, including EGF

211 RNA-seq data included negative regulators of RTK/RAF/MAPK signaling along with potential oncogenic ef

212 e a novel means of promoting the activity of RTKs.

213 designated AAEL001915, belongs to a clade of RTKs related to the insulin receptor, which are distingu

214 rotrimeric G protein signaling downstream of RTKs and integrins, thereby serving as a platform for si

215 ufficient for activation of Gi downstream of RTKs, and used them to engineer signaling networks and a

216 of the MAPK pathway along with inhibitors of RTKs, SRC or STAT3 to counteract STAT3-mediated resistan

217 However, details of the involvement of RTKs in EBV-regulated B-cell neoplasia and malignancies

218 ovel mechanism that regulates the loading of RTKs into COPII vesicles.

219 onventional wisdom holds that methylation of RTKs should be restricted to intracellular sites.

220 structural works on the soluble portions of RTKs have provided critical insights into RTK structures

221 Through the spatial positioning of RTKs in target cells for EGF and insulin action, the tem

222 trate that the juxtamembrane (JM) regions of RTKs are critical for inducing clustering of anionic lip

223 new level of complexity in the regulation of RTKs by Cbl through ITSN1 binding with Shp2 and Spry2.

224 The TAM (Tyro3, Axl, Mer) subfamily of RTKs in particular feature in a variety of cancer types

225 es, it is now apparent that the targeting of RTKs with selective inhibitors is only transiently effec

226 nd dysregulated intracellular trafficking of RTKs have been shown to be involved in tumorigenesis.

227 histone code to control the transcription of RTKs.

228 rtails AKT inhibitor-induced upregulation of RTKs in prostate cancer cells.

229 factor that links G proteins to a variety of RTKs, these biosensors provide direct evidence that RTK-

230 However, their effect on RTK dimer stability has never been measured experimental

231 e and other subtleties involved in oncogenic RTK activation and their response to targeted therapies

232 ulating normal ligand-dependent or oncogenic RTK activation via a "zipper-like" mechanism for recepto

233 t signaling downstream of multiple oncogenic RTKs.

234 ability to block sensitivity to the original RTK inhibitor.

235 Other RTKs have been reported to bind, and be regulated by, ov

236 or cancers driven by activated KIT and other RTKs may rely on clear understanding of the dynamic prop

237 they correspond to analogous sites of other RTKs' variations in cancers, and that they are predicted

238 ed to the cell surface, in contrast to other RTKs whose ligands are generally soluble.

239 We propose that the packaging of p-RTKs in endosomes is a general mechanism to ensure the f

240 am pathway activation provided by particular RTKs lead to qualitative differences in the capacity of

241 n subgroups (eg, mesenchymal, RTK I "PGFRA," RTK II "classic"), MGMT promoter methylation status, and

242 Our results highlight potential RTK-driven adaptive-resistant mechanisms upon DDR2 targe

243 The high incidence of activating RAS/RTK signaling mutations may provide a target for a ratio

244 he involvement of tyrosine kinase receptors (RTKs) in TF/FVIIa signaling by antibody array analysis a

245 ack activation of tyrosine kinase receptors (RTKs), AKT, mTOR, and MYC.

246 ased RTK signaling and suppressed by reduced RTK signaling.

247 resistance to Mek inhibition through reduced RTK shedding that can be overcome with rationally direct

248 One long-standing puzzle regarding RTKs centers on how the extracellular domain (ECD), whic

249 rongly suggest that Exp negatively regulates RTK (EGFR, Btl) signaling to ensure proper tube sizes.

250 r KIT is an example of a clinically relevant RTK.

251 ulated through distinct pathways by the same RTK depending on which endosome it is localized to in th

252 on of substrates are carried out by the same RTK monomer in cis and disclose an obligatory role for r

253 sorders and highlight the fact that a single RTK mutation may affect multiple steps in RTK activation

254 The regulatory mechanism of one such RTK, fibroblast growth factor receptor 2 (FGFR2) kinase,

255 s direct inactivation of AKT: By suppressing RTK levels, PHLPP dampens the downstream signaling outpu

256 t on the long-standing questions surrounding RTK/G protein cross-talk, set a novel paradigm, and char

257 s that may circumvent resistance to targeted RTK therapies.

258 he basis for the use of inhibitors targeting RTK-mediated signals for p53 restoration.

259 hese biosensors provide direct evidence that RTK-GIV-Galphai ternary complexes are formed in living c

260 we obtained evidence in transgenic mice that RTK/RAS pathway activation in urothelial cells causes hy

261 We further show that RTK-mediated HIF2alpha regulation is JNK dependent, via

262 The RTK/ERK signaling pathway has been implicated in prostat

263 wed activation not only of Egfr but also the RTK Axl in response to HBEGF stimulation.

264 diction of EGFR amplification status and the RTK II glioblastoma subgroup with a moderate, yet signif

265 that different mechanisms are engaged by the RTK c-Met in two different endosomes to control the acti

266 Some mice were given the RTK inhibitor imatinib after injection of cancer cells;

267 a nonoverlapping pattern of mutations in the RTK-RAS-RAF and phosphoinositide 3-kinase/AKT/mammalian

268 ciation of genetic variants and genes in the RTK/ERK pathway with prostate cancer aggressiveness, and

269 utually exclusive gene set that included the RTK/RAS/RAF pathway genes BRAF, EGFR, KRAS, MET, and NF1

270 Ror1), a surface antigen, is a member of the RTK family of Ror, which plays a crucial role in cancers

271 We investigated the role of the RTK KIT in development of human colon cancer.

272 P and gene-based association analysis of the RTK/ERK pathway with aggressive prostate cancer in a coh

273 In the present study, we focus on the RTK ErbB3 and elucidate the mechanisms regulating its tr

274 Treatment with inhibitors targeting the RTK/MAPK pathway increased reactive oxygen species (ROS)

275 resence of multiple inhibitors targeting the RTK/Ras/MAPK pathway.

276 In this study, we have shown that the RTK human epidermal growth factor receptor 4 (Her4, also

277 We can now combine this with the RTK/N signaling to provide a cell fate specification cod

278 dly transduce extracellular signals from the RTKs to the intracellular effectors, recent data unfold

279 in tyrosine phosphatases that inactivate the RTKs and deliver them by membrane fusion and fission to

280 and determine this phenomenon depends on the RTKs activating the AKT serine/threonine kinase.

281 Therefore, RTKs have emerged as major targets for selective therapy

282 We sought to determine how these RTK signals alter proliferation and migration to accompl

283 Noninvasive PET monitoring of these RTK feedback loops should help to rapidly assess resista

284 portant milestones in the discovery of these RTKs and their ligands and the studies that underscore t

285 Extracellular binding of ligands to these RTKs triggers their concentration into vesicles that bud

286 Third, RTK/N signaling and Lz need only be presented to the cel

287 ligand release and negative feedback through RTK shedding.

288 and EGFR PET probe accumulation correlate to RTK expression change as assessed by Western blot (R(2)

289 th dysregulated signaling pathways linked to RTKs represents a key element in targeted cancer therapi

290 ytosolic effector of activated transmembrane RTKs, wherein it shuttles between the cytosol and the nu

291 s represent one of the most underappreciated RTK families.

292 To investigate the mechanisms underlying RTK specificity in craniofacial development, we performe

293 Targeting various RTKs, Src, FAK and STAT3 with small molecule inhibitors

294 m of resistance is bypass signaling, wherein RTKs not targeted by an inhibitor can direct reactivatio

295 We therefore sought to determine whether RTK activity played a role in invadosome biogenesis.

296 ggest a model for ductal elongation in which RTK-dependent proliferation creates motile cells with hi

297 ted in human cancers, the processes by which RTKs including PDGFRalpha mediate EMT are largely unknow

298 While RTKs are generally known to be activated in response to

299 We show Exp genetically interacts with RTK signaling, the downstream targets of RPTPs.

300 ting the dynamic association of Galphai with RTKs for noncanonical transactivation of G proteins in c