ライフサイエンスコーパス: RTK

1 RTKs are believed to form both homodimers and heterodime

2 RTKs can hydrolyze phosphatidylinositol 4,5-bisphosphate

3 RTKs can translocate to the nucleus via a nuclear locali

4 cell type and reveal the important role of 3 RTKs and their ligands in orchestrating the selective ac

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

6 ging genetic targeting of tdnano, we achieve RTK activation at a specific subcellular location even w

7 mors harboring a broad spectrum of activated RTKs as the oncogenic driver.

8 rm for unbiased identification of activating RTK variants that are enriched under selection pressure

9 tumor growth, as well as an increase in all RTK protein levels at the tumor in vivo on immuno-PET an

10 vation of the MAPK pathway through alternate RTK (RTK-bypass).

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

12 distinct sensitivities to growth factors and RTK inhibitors.

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

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

15 ing in colocalization of these molecules and RTK transactivation by GPCRs and CAMs, giving rise to ex

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

17 ivity of innate immune response pathways and RTK signaling in bone marrow progenitors from mice with

18 upregulating activity of the RTK-RAS-RAF and RTK-PI3K-AKT signaling cascade.

19 or crosstalk between oncogenic signaling and RTK trafficking that controls cancer progression.

20 ility of RTK-targeted immuno-PET to annotate RTK changes in protein expression and inform tumor respo

21 ograft model, we use the (89)Zr-labeled anti-RTK antibodies (immuno-PET) onartuzumab, panitumumab, an

22 ctionability and clinical significance of AR RTK fusions we present all available data demonstrating

23 enefit of concurrent dual blockade of the AR RTK fusion and the original EGFR mutation.

24 However, detailed examination of the AR RTK fusion landscape in non-small-cell lung cancer is la

25 r, RTK interactions are more complicated, as RTKs can interact in the absence of ligand and heterodim

26 opto-RTKs is considered using the available RTK structures.

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

28 aling and provide a mechanistic link between RTK-initiated phosphoinositide microdomains and Arf6 dur

29 be the strengths of the interactions between RTKs and their ligands and between different RTKs.

30 radigm of GEM-facilitated cross-talk between RTKs and G proteins and how that impacts cellular cAMP.

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

32 Because it has been hypothesized that biased RTK ligands induce differential stabilization of RTK dim

33 I3K)beta isoform is uniquely coupled to both RTK and GPCRs.

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

35 ng mechanisms or to manage cancers driven by RTK signaling.

36 f activation of heterotrimeric G proteins by RTKs and chart the key steps that mediate such activatio

37 control activity and to mediate signaling by RTKs that induce neuronal differentiation.

38 e oncogenic mechanisms and output of certain RTK fusion oncoproteins.

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

40 ity assay, we demonstrate how these chimeric RTKs, termed light-controlled human insulin receptor (Li

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

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

43 We show that the common RTK signaling intermediate SOS1 was required for 3D sphe

44 Our results reveal that a conserved RTK signaling pathway regulates baseline mechanical noci

45 ne a potentially general strategy to convert RTKs into photoreceptors.

46 new therapeutic opportunities for correcting RTK signaling output.

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

48 aned from computer simulation in deciphering RTK regulatory function.

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

50 RTKs and their ligands and between different RTKs.

51 that are structurally regulated by different RTKs or cellular perturbations are largely unique, these

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

53 ng that enables the stimulation of different RTKs to oxidize distinct sets of downstream proteins.

54 TKs involves membrane tethering of dimerizer-RTK ICD fusions.

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

56 logical roles of biased signaling downstream RTK and provides a novel "system bias" strategy to incre

57 e conformational changes are unique for each RTK subfamily, limiting cross-activation between unrelat

58 eningioma cells, we showed activation of EPH RTKs, c-KIT, and SFK members independent of mTORC1/2 act

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

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

61 found that ERK signaling faithfully followed RTK dynamics when receptor signaling was modulated in di

62 G1, influences cell fate decisions following RTK activation.

63 e kinases (RTKs) and found a requirement for RTK-like orphan receptor (Ror).

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

65 sis of mutations conferring gain-of-function RTK activity promoting clonal growth.

66 ead to a better understanding of fundamental RTK signaling processes in health and disease.

67 utcome can be modified by activating a given RTK in different ways.

68 However, RTK heterodimers remain poorly characterized, as compare

69 However, RTK interactions are more complicated, as RTKs can inter

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

71 lity to gamma-secretase cleavage among human RTKs.

72 ional signaling mechanism for numerous human RTKs.

73 blastoma (GBM), is attributed to hyperactive RTK/Ras/ERK signaling.

74 in molecularly defined subsets and identify RTK inhibition as a potential therapeutic approach to co

75 + tdnano system recruits two copies of iLID-RTK to tdnano, dimerizing, and activating the RTK.

76 In the absence of light, the iLID-RTK is cytosolic, monomeric, and inactive.

77 -3 (HER3 or ERBB3), a catalytically impaired RTK whose phosphorylation by MET has been described as a

78 s interested in investigating ligand bias in RTK signaling.

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

80 ly blunted and corresponded to a decrease in RTK levels.

81 has demonstrated tumor growth inhibition in RTK-activated cancers in preclinical studies.

82 nal role of the N-terminal fusion partner in RTK fusion oncoproteins is poorly understood.

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

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

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

86 Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation pathways 'paralle

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

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

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

90 Receptor tyrosine kinase (RTK) coexpression facilitates tumor resistance due to re

91 ng mutation of the receptor tyrosine kinase (RTK) ERBB2 In some contexts, notably breast cancer, alte

92 VKRs) constitute a Receptor Tyrosine Kinase (RTK) family only found in invertebrates.

93 rs invariably, and receptor tyrosine kinase (RTK) fusions have emerged as rare but actionable resista

94 riants of a single receptor tyrosine kinase (RTK) gene in a single assay.

95 these unamplified receptor tyrosine kinase (RTK) genes through a large enhancer domain, resulting in

96 Sunitinib, a multi-receptor tyrosine kinase (RTK) inhibitor approved for the management of gastrointe

97 itors, such as the receptor tyrosine kinase (RTK) inhibitor sunitinib, target vascular endothelial gr

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

99 The Met receptor tyrosine kinase (RTK) modulates invasive growth and migration in developm

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

101 ions that activate receptor tyrosine kinase (RTK) signaling frequently occur in bladder cancer.

102 genes involved in receptor tyrosine kinase (RTK) signaling in SMARCA4/A2-deficient cells, including

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

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

105 (EGFR/ERBB1) is a receptor tyrosine kinase (RTK) that forms activated oligomers in response to ligan

106 Trk-A is a receptor tyrosine kinase (RTK) that plays an essential role in the development and

107 RET is a receptor tyrosine kinase (RTK) that plays essential roles in development and has b

108 , poor efficacy of receptor tyrosine kinase (RTK) therapies has been alternatively ascribed to geneti

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

110 ctivated by a dual-receptor tyrosine kinase (RTK)-dependent signaling event, m-SCF/c-Kit and VEGF-A/v

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

112 DDR1 is a receptor tyrosine kinase (RTK).

113 enes downstream of receptor tyrosine kinase (RTK)/Ras/ERK signaling.

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

115 tream of multiple receptor tyrosine kinases (RTK) and is required for full activation of the MAPK pat

116 gements involving receptor tyrosine kinases (RTK) are a clinically relevant oncogenic mechanism in hu

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

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

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

120 L, MER) family of receptor tyrosine kinases (RTK) has been associated with cancer progression, metast

121 overexpression of receptor tyrosine kinases (RTK) such as EGFR, and activating mutations in component

122 ation of upstream receptor tyrosine kinases (RTK) that converges on activation of RAS as a mechanism

123 red downstream of receptor tyrosine kinases (RTK), including the cancer-relevant insulin-like growth

124 sed expression of receptor tyrosine kinases (RTK).

125 All receptor tyrosine kinases (RTKs) activate similar downstream signaling pathways thr

126 ent activation of receptor tyrosine kinases (RTKs) allows for dissecting out the receptor-specific si

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

128 ndidate screen of receptor tyrosine kinases (RTKs) and found a requirement for RTK-like orphan recept

129 chanisms by which receptor tyrosine kinases (RTKs) and heterotrimeric G proteins, two major signaling

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

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

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

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

134 Receptor tyrosine kinases (RTKs) are key regulators of cellular functions in metazo

135 Receptor tyrosine kinases (RTKs) are often overexpressed or mutated in cancers and

136 Receptor tyrosine kinases (RTKs) are single-pass membrane proteins that control vit

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

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

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

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

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

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

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

144 translocation of receptor tyrosine kinases (RTKs) is one way to locally activate signaling cascades

145 g plasma membrane receptor tyrosine kinases (RTKs) lack multiplexing capabilities, limiting detailed

146 dia binds several receptor tyrosine kinases (RTKs) on host cells, including the epidermal growth fact

147 Receptor tyrosine kinases (RTKs) play crucial roles in human health, and their misr

148 Receptor tyrosine kinases (RTKs) play important roles in cell growth, motility, dif

149 r the activity of receptor tyrosine kinases (RTKs) provides an efficient way to reversibly and non-in

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

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

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

153 ligomerization of receptor tyrosine kinases (RTKs) results in their activation through highly specifi

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

155 Receptor tyrosine kinases (RTKs) typically contain multiple autophosphorylation sit

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

157 molecules (CAMs), receptor tyrosine kinases (RTKs), and related signaling molecules were recruited to

158 to activation of receptor tyrosine kinases (RTKs), crucial cell fate decisions depend on the duratio

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

160 ) is regulated by receptor tyrosine kinases (RTKs), G protein-coupled receptors (GPCRs), and small GT

161 Receptor tyrosine kinases (RTKs), including the FGF receptor, are TRIAD1 substrates

162 Receptor tyrosine kinases (RTKs), MET and epidermal growth factor receptor (EGFR),

163 nction studies of receptor tyrosine kinases (RTKs), RPTP activities have been reported to be suppress

164 f plasma membrane receptor tyrosine kinases (RTKs), such as the epidermal growth factor receptor (EGF

165 so identified Met receptor tyrosine kinases (RTKs), which carry a truncated plexin extracellular doma

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

167 f ligand bias for receptor tyrosine kinases (RTKs).

168 ing downstream of receptor tyrosine kinases (RTKs).

169 ich growth factor-receptor tyrosine kinases (RTKs; e.g., EGFR) access and modulate G proteins via a c

170 a low-cost and portable real-time kinematic (RTK) GPS to create DTMs which are highly accurate (<10 c

171 original version of this Article, the label "RTK" in Figure 6a was inadvertently changed to "RTE".

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

173 In addition, a novel type of Met-like RTK with a complete plexin extracellular domain was dete

174 hotrochozoa and Echinodermata (termed Met-LP RTK).

175 egulated platform for GPCR- and CAM-mediated RTK signaling.

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

177 tical strategies for quantifying two or more RTKs at single-level using Qdots, which will help provid

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

179 S signal transduction downstream of multiple RTK, represented an alternate strategy.

180 glioma (HGG) mouse models driven by mutated RTK oncogenes, PDGFRA and NTRK1, analyzing 13,860 protei

181 k, we studied the heterointeractions of nine RTK pairs, epidermal growth factor receptor (EGFR)-EPH r

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

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

184 Nuclear RTKs, including the epidermal growth factor receptor (EG

185 In the nucleus, RTKs regulate gene expression by binding chromatin direc

186 melanogaster, constitutive co-activation of RTK and PI3K signaling in glial progenitor cells recapit

187 ovide insights into the biophysical basis of RTK activation and ligand bias.

188 ractions can contribute to the complexity of RTK signal transduction, and we highlight the utility of

189 In 2015, the detection of RTK fusions as acquired resistance (AR) in two cases was

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

191 of EGFR TKIs demonstrating the emergence of RTK fusions in AR.

192 is highly effective to inhibit the growth of RTK-addicted cell lines and hepatocellular (HCC) cells i

193 We argue that a deeper knowledge of RTK interactome thermodynamics can lead to a better unde

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

195 In the current model of RTK signaling, including that of MET, downstream phospha

196 sine kinases (opto-RTKs) allow regulation of RTK signaling using light.

197 the opto-kinases of choice for regulation of RTK signaling: high activation range, fast and reversibl

198 be similar, underscoring the significance of RTK heterointeractions in signaling.

199 ligands induce differential stabilization of RTK dimers, here, we seek to test this hypothesis for NG

200 However, the understanding of RTK ligand bias is lagging behind the knowledge of GPCR

201 Conclusion: These data show the utility of RTK-targeted immuno-PET to annotate RTK changes in prote

202 common strategy for synthetic activation of RTKs involves membrane tethering of dimerizer-RTK ICD fu

203 highly conserved mechanism of activation of RTKs makes them especially appealing candidates for cont

204 The surface levels and activity of RTKs are governed mainly through clathrin-mediated endoc

205 In turn, oncogenic signaling downstream of RTKs can reciprocally regulate endocytic trafficking by

206 e of GIST upon enhancer-driven expression of RTKs, we hypothesized that the enhancer domains could be

207 nase receptors (VKRs), an atypical family of RTKs found in nature, we have transformed the human insu

208 Trk (tropomyosin receptor kinase) family of RTKs, naturally activated by neurotrophins, with photose

209 Different from most of RTKs, RET requires not only its cognate ligands but also

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

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

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

213 nano) to build light-activatable versions of RTKs.

214 To investigate the effects of competition on RTK signaling, we used a rule-based modeling approach to

215 Crosstalk between the oncogenic RTK hepatocyte growth factor receptor (MET), epidermal g

216 /A2-deficient cells, including the oncogenic RTK HER3.

217 AML, but remission was sustained by ongoing RTK inhibition.

218 ction mechanism of the DrBphP-PCM-based opto-RTKs is considered using the available RTK structures.

219 The resultant Dr-EGFR and Dr-FGFR1 opto-RTKs are rapidly activated with near-infrared and inacti

220 s of neurotrophin receptors resulted in opto-RTKs controlled with light above 650 nm.

221 y controlled receptor tyrosine kinases (opto-RTKs) allow regulation of RTK signaling using light.

222 a versatile scaffold for engineering of opto-RTKs that are reversibly regulated with far-red and near

223 Until recently, the majority of opto-RTKs were activated with blue-green light.

224 sence of spectral crosstalk between the opto-RTKs and green fluorescent protein-based biosensors enab

225 The opto-RTKs efficiently trigger ERK1/2, PI3K/Akt, and PLCgamma

226 on that these ligand-independent optogenetic RTKs will provide useful toolsets for the delineation of

227 ly, a survey of FGFR3-TACC3 fusion and other RTK fusions from a large commercial genomic sequencing c

228 selectively cross-target the IGF1R or other RTK.

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

230 canonical interactions between MET and other RTKs occur during maturation of receptors.

231 feedback loop to up-regulate multiple other RTKs, and confers higher oncogenic potency than the PDGF

232 n addition to HER3, MET phosphorylates other RTKs in the Golgi, suggesting that this mechanism is not

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

234 Simultaneous inhibition of multiple parallel RTKs further enhances EGFR-TKI effectiveness.

235 gnaling can be used to identify and quantify RTK ligand bias.

236 reased genetic heterogeneity and gain of RAS/RTK pathway mutations.

237 ration of several tyrosine kinase receptors (RTKs), consistent with a partial block of their traffick

238 onal suppression of IRS2, leading to reduced RTK levels and activity.

239 In this regard, RTK intracellular domains (ICD) are of interest due to t

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

241 rties of different, clinically relevant ROS1 RTK fusion oncoproteins.

242 n of the MAPK pathway through alternate RTK (RTK-bypass).

243 ability to reversibly light-control several RTK pathways, calcium level, and demonstrated that their

244 ifferent studies and for the failure of some RTK inhibitors to produce the desired therapeutic effect

245 by the generation of EGFR TKIs, the specific RTK fusions and their fusion partners, the founder EGFR

246 ow thermodynamic models can be used to study RTKs and to explain many of the complicated biological e

247 Here, we review the known cross-subfamily RTK heterointeractions and their possible biological imp

248 e mice with an inhibitor of TRIAD1-substrate RTKs terminated emergency granulopoiesis, delayed leukem

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

250 We hypothesized that sustained RTK signaling, because of decreased TRIAD1 activity, imp

251 e RXDX-106 as a selective and potent pan-TAM RTK inhibitor with slow dissociation kinetics and signif

252 In immune cells, TAM RTKs can dampen inflammation in favor of homeostatic wou

253 ibited its effects via direct actions on TAM RTKs expressed on intratumoral macrophages and dendritic

254 Our results argue that RTK activation kinetics play a crucial role in determini

255 Surprisingly, we found that RTK heterodimerization and homodimerization strengths ca

256 There is a growing body of evidence that RTKs from different subfamilies can interact and that th

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

258 TK to tdnano, dimerizing, and activating the RTK.

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

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

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

262 (also known as KDM6A) and activation of the RTK FGFR3, two events that commonly cooccur in muscle in

263 The existence of the RTK interactome could provide an explanation for the irr

264 Finally, we discuss the concept of the RTK interactome: a putative, extensive network of intera

265 contain the C-terminal kinase domain of the RTK joined in cis to various N-terminal, nonkinase fusio

266 Disruption of the RTK-mediated signaling was achieved using MET knockout (

267 6 inhibition by upregulating activity of the RTK-RAS-RAF and RTK-PI3K-AKT signaling cascade.

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

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

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

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

272 have applied driver mutations targeting the RTK/RAS/PI3K and p53 pathways to induce the formation of

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

274 We demonstrated that the RTK PDGF/VEGF receptor (Pvr) and its ligands (Pvfs 2 and

275 xtensive network of interactions between the RTKs.

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

277 rt that FCHSD2 loss impacts recycling of the RTKs, epidermal growth factor receptor (EGFR) and proto-

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

279 which may prevent RPTPs from accessing their RTK substrates.

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

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

282 This RTK interactome can produce unique signaling outputs; ca

283 Thus, RTK and JAK-STAT-driven proliferation pathways are paral

284 Thus, RTK-mediated host invasion by chlamydia upregulated TGF-

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

286 strategies that might overcome resistance to RTK inhibitors in patients with cancer.

287 2 (HER2) are involved in tumor resistance to RTK-targeted therapies.

288 To expand this engineering approach to RTKs of other families, here we combined the DrBpP-PCM w

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

290 unresponsive to TRKA and RET signaling, two RTKs that induce neuronal differentiation, but retained

291 s represent one of the most underappreciated RTK families.

292 we discuss possible mechanisms underpinning RTK ligand bias.

293 limiting cross-activation between unrelated RTKs.

294 ral constraints and phosphorylates unrelated RTKs in numerous cancer cell lines.

295 In vertebrates, RTKs are mostly activated by polypeptides but are not na

296 ve pro-angiogenic growth factors, acting via RTK or G-protein coupled receptors (GPCR), may mediate V

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

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

299 in stem-like glioblastoma cells treated with RTK inhibitors.

300 ma trimers, scaffolds monomeric Galphai with RTKs, and facilitates the phosphorylation on two tyrosin