ライフサイエンスコーパス: receptor tyrosine kinase

1 between the Na,K-ATPase and Src kinase (non-receptor tyrosine kinase).

2 The EGF receptor is a classic receptor tyrosine kinase.

3 ll fate by specifically destroying the Torso Receptor Tyrosine Kinase.

4 f tyrosine-protein kinase receptor UFO (AXL) receptor tyrosine kinase.

5 ernal tandem duplications (ITDs) of the FLT3 receptor tyrosine kinase.

6 ane protein that is associated with the MuSK receptor tyrosine kinase.

7 ires Lrp4, a LDLR family member, and MuSK, a receptor tyrosine kinase.

8 ocalization and function of the ICD of ErbB4 receptor tyrosine kinase.

9 nAmb) that express the autism-associated MET receptor tyrosine kinase.

10 feline sarcoma viral oncogene homolog (KIT) receptor tyrosine kinase.

11 sed by gain-of-function mutations in the Kit receptor tyrosine kinase.

12 ber of predicted genomic targets in multiple receptor tyrosine kinases.

13 R belongs to the well-studied ErbB family of receptor tyrosine kinases.

14 ion by a soluble phosphopeptide derived from receptor tyrosine kinases.

15 nhibition of RAS activation by inhibitors of receptor tyrosine kinases.

16 luding the uptake receptor LRP1 and multiple receptor tyrosine kinases.

17 ion between Brevican (BCAN) and Neurotrophic Receptor Tyrosine Kinase 1 (NTRK1), is a potent oncogeni

18 ree proteins that interact with neurotrophic receptor tyrosine kinase 1, a receptor also known as Trk

19 ceptor, type 3 (ITPR3), and discoidin domain receptor tyrosine kinase 2 (DDR2).

20 GROUND & AIMS: Drugs that inhibit the erb-b2 receptor tyrosine kinase 2 (ERBB2 or HER2) are the stand

21 Agents that inhibit the erb-b2 receptor tyrosine kinase 2 (ERBB2 or HER2), or vascular

22 tes along the cell membrane, and that Erb-b2 receptor tyrosine kinase 2 (Erbb2) function is required

23 In a mouse model of basal ErbB2 receptor tyrosine kinase 2 (ErbB2)-positive breast cance

24 Context ERBB2 (erb-b2 receptor tyrosine kinase 2 or HER2) is currently the onl

25 egulated mRNA expression of discoidin domain receptor tyrosine kinase 2, fibronectin, and alpha-smoot

26 Erb-B2 receptor tyrosine kinase 4 (ErbB4) is a kinase that can

27 er on PV interneurons is regulated by erb-b2 receptor tyrosine kinase 4 (ErbB4), whose function is in

28 tal and pathophysiological roles for the MET receptor tyrosine kinase, a multifunctional receptor tha

29 containing proteins, including specific non-receptor tyrosine kinases-Abl via pY251 and C-terminal S

30 cluding many G protein-coupled receptors and receptor tyrosine kinases, activate phospholipase C (PLC

31 , we have identified SAM domain-carrying non-receptor tyrosine kinase, activated Cdc42-associated tyr

32 llular domain (ICD) in addition to classical receptor tyrosine kinase-activated signaling cascades.

33 ould be caused by aberrant activity of other receptor tyrosine kinases, activating overlapping signal

34 y an upstream event, such as RAS mutation or receptor tyrosine kinase activation.

35 Disappointingly, inhibitors targeting receptor tyrosine kinase activity are not clinically eff

36 Further interrogation of the receptor tyrosine kinase activity in these discordant ce

37 K signaling is not perturbed by altering Pvr receptor tyrosine kinase activity.

38 y through inhibition of protein kinase C and receptor tyrosine kinase activity.

39 ctedly resulted in loss of ERK activation to receptor tyrosine kinase agonists such as epidermal grow

40 racting proteins of the ligand-activated MET receptor tyrosine kinase, an autism risk gene that media

41 cells at the ureteric bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfralpha1; Ret s

42 rn of c-Jun N-terminal kinase (JNK), the Axl receptor tyrosine kinase and extracellular signal-regula

43 Downstream of receptor tyrosine kinase and G protein-coupled receptor

44 of PREX1 negative regulation by PAKs within receptor tyrosine kinase and GPCR-stimulated signaling p

45 involving vascular endothelial growth factor-receptor tyrosine kinase and TGF-beta and Notch pathways

46 nized protein kinase oncogenes, including 30 receptor tyrosine kinases and 154 of their disease-assoc

47 Recent studies show that receptor tyrosine kinases and components of signal trans

48 PI3K enzymes in that it is activated by both receptor tyrosine kinases and G-protein-coupled receptor

49 hat target cancer-related vulnerabilities in receptor tyrosine kinases and intracellular signaling pa

50 TAM (Tyro3-Axl-Mer) receptor tyrosine kinases and Met are implicated in seve

51 intracellular signaling downstream of other receptor tyrosine kinases and restrain basal cell prolif

52 , survival, and oncogenesis are activated by receptor tyrosine kinases and small G-proteins of the Ra

53 lasma membrane promotes activation of Ras by receptor tyrosine kinases and stimulates oncogenic signa

54 The family of Eph receptor tyrosine kinases and their ephrin ligands regul

55 Eph receptor tyrosine kinases and their membrane-tethered ep

56 eins that bind to phosphorylated residues in receptor tyrosine kinases and trigger signaling cascades

57 Recent work has shown that non-receptor tyrosine kinases and tyrosine phosphorylation o

58 m platelet-derived growth factor receptor, a receptor tyrosine kinase) and H-Ras generates strong, sy

59 RTK (receptor tyrosine kinase) and p53 signalling were found

60 ernal tandem duplications (ITDs) in the FLT3 receptor tyrosine kinase are common mutations in AML, co

61 hat introduce or remove cysteine residues in receptor tyrosine kinases are believed to cause patholog

62 The analysis indicates that receptor tyrosine kinases are functionally compartmental

63 Mutant receptor tyrosine kinases are mislocalized in the endopl

64 Here, we identify EphA2 receptor tyrosine kinase as a clinically relevant target

65 e-1, and interleukin-10 by activation of mer receptor tyrosine kinase associated with inhibition of m

66 we observe ligand-induced dimerization of a receptor tyrosine kinase at the cell surface and directl

67 Importantly, we discover that receptor tyrosine kinase AXL is a transcriptional target

68 Activation of the receptor tyrosine kinase Axl is associated with poor out

69 In mice, loss of receptor tyrosine kinases AXL and MERTK reduced efferocy

70 two aptamers that bind to, and inhibit, the receptor tyrosine kinases, Axl and PDGFRbeta.

71 identified PBF as a downstream target of the receptor tyrosine kinase-BRAF signalling pathway, emphas

72 ale exists for antibody targeting of the MET receptor tyrosine kinase, but therapeutic agents that ca

73 Stimulation of receptor tyrosine kinases by neuregulin and insulin-like

74 Caspase-9 phosphorylation by the non-receptor tyrosine kinase c-Abl at Tyr-153 reportedly lea

75 The non-receptor tyrosine kinase c-Abl is activated in response

76 Hyperactivation of the receptor tyrosine kinase c-Met and overexpression of the

77 Here we show that the receptor tyrosine kinase c-Met associates with and phosp

78 The receptor tyrosine kinase c-Met is overexpressed in renal

79 ation small-molecule inhibitor of the orphan receptor tyrosine kinase c-ros oncogene 1 (ROS1), which

80 or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).

81 Its receptor tyrosine kinase, c-Met, is expressed in the coc

82 tivated by many upstream pathways, including receptor tyrosine kinase cascades-signal through multipl

83 Inhibition of these receptor tyrosine kinases consequently attenuated the ac

84 One of these receptor tyrosine kinases could be MET, the receptor for

85 Other active receptor tyrosine kinases could not compensate for reduc

86 The collagen-binding receptor tyrosine kinase DDR1 (discoidin domain receptor

87 Intriguingly, TM4SF1 couples the collagen receptor tyrosine kinase DDR1 to the cortical adaptor sy

88 ace protease inhibitor Spint-1, the collagen receptor tyrosine kinase DDR1, N-Cadherin, CLCP1/DCBLD2,

89 w that wild-type RAS amplification increases receptor tyrosine kinase-dependent activation of RAS mor

90 cause pathologies by stabilizing the active receptor tyrosine kinase dimers.

91 ent of cells with chemical inhibitors of the receptor tyrosine kinase EGFR and the kinase Src abrogat

92 and muscarinic acetylcholine receptor 4, the receptor tyrosine kinases EGFR, HGFR, VEGFR, PDGFR, NGFR

93 y percentage against Epidermal Growth Factor Receptor tyrosine kinase (EGFR-TK), in in-vitro assay.

94 grin alpha3beta1 independently activates two receptor tyrosine kinases, EGFR and Met, in the absence

95 Here, we show that genetic ablation of a receptor tyrosine kinase encoded byTyro3in mice or the f

96 ation and fibrogenesis in vivo by disrupting receptor tyrosine kinase endocytosis and signaling.

97 neural cell adhesion molecule (NCAM) and the receptor tyrosine kinase EphA3 regulate the perisomatic

98 ronal surface and that overexpression of the receptor tyrosine kinase EphB2 can counteract this proce

99 the fibronectin type III (FN3) domain of the receptor tyrosine kinase EphB2.

100 Mule also regulates protein levels of the receptor tyrosine kinase EphB3 by targeting it for prote

101 The receptor tyrosine kinase ephrin type-A receptor 2 (EphA2

102 recurrent amplification of the gene encoding receptor tyrosine kinase epidermal growth factor recepto

103 n and progesterone receptors, along with the receptor tyrosine kinase ERB2 (HER2), that define most m

104 Here we show that neuregulin (NRG) and the receptor tyrosine kinase erbB4 determine critical period

105 model to show that neuregulin (NRG) and the receptor tyrosine kinase erbB4 regulate the timing of th

106 cell-type-specific dependencies for specific receptor tyrosine kinases, even in oncogenic KRAS backgr

107 It signals via a receptor tyrosine kinase expressed on the surface on end

108 ity in erythroid precursor cells ensures Kit receptor tyrosine kinase expression and stem cell factor

109 (TAM) is one of the most recently identified receptor tyrosine kinase families.

110 Members of the receptor tyrosine kinase family (RTK) have been shown to

111 The receptor tyrosine kinase family consisting of Tyro3, Axl

112 ble proteins Rpn10 and Rvs167, and the human receptor tyrosine kinase FGFR1 and cardiac IKS potassium

113 e kinase inhibitor with activity against the receptor tyrosine kinase FLT3, and its approval will hop

114 n-of-function mutations in KRAS, NRAS or the receptor tyrosine kinase FLT3.

115 ling protein, the ubiquitously expressed non-receptor tyrosine kinase focal adhesion kinase.

116 ort the retinal expression pattern of Ret, a receptor tyrosine kinase for the glial derived neurotrop

117 immunoglobulin and EGF homology domains, are receptor tyrosine kinases found primarily in endothelial

118 tional genes, including PIK3CA and MEK1, and receptor tyrosine kinase fusions, were also identified i

119 ive enhancer to interact aberrantly with the receptor tyrosine kinase gene PDGFRA, a prominent glioma

120 Dysregulation of the AXL receptor tyrosine kinase has been associated with many t

121 ALK receptor tyrosine kinase has been shown to be a therapeu

122 us, the reciprocal activation of Axl and Mer receptor tyrosine kinases has a major impact on the outc

123 Members of the Eph family of receptor tyrosine kinases have been implicated in a wide

124 es (SrcFKs), a multi-functional group of non-receptor tyrosine kinases highly expressed in vascular s

125 ndergo amplifications of proto-oncogenes and receptor tyrosine kinases, implicating these events in l

126 ph (erythropoietin-producing hepatocellular) receptor tyrosine kinases in developmental processes, ce

127 re the first to implicate the EphB family of receptor tyrosine kinases in liver fibrosis or in the pa

128 nt study, we examined the role of Fyn, a non-receptor tyrosine kinase, in microglial activation and n

129 growth factor receptor (EGFR)/ErbB family of receptor tyrosine kinases includes oncogenes important i

130 pathway and diminished expression of several receptor tyrosine kinases, including epidermal growth fa

131 ts revealed numerous activating mutations in receptor tyrosine kinases, including KIT.

132 a key regulator of not only GPCRs, but also receptor tyrosine kinases, including the highly cancer r

133 tial for both G-protein-coupled receptor and receptor tyrosine kinase-induced actin cytoskeletal reor

134 kade renders tumor cells more susceptible to receptor tyrosine kinase inhibition in a preclinical gli

135 rug can overcome the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) resistance

136 Imatinib (Gleevec), a non-receptor tyrosine kinase inhibitor (nRTKI), is one of th

137 The epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in combinat

138 The PDGF receptor tyrosine kinase inhibitor imatinib mesylate and

139 ion after first-line epidermal growth factor receptor tyrosine kinase inhibitor therapy, and T790M mu

140 linifanib (ABT-869), a novel multi-targeted receptor tyrosine kinase inhibitor, markedly augments cy

141 treat this aggressive tumor, a multi-target receptor tyrosine kinase inhibitor, sunitinib base, was

142 administration of sunitinib, a multitargeted receptor tyrosine kinase inhibitor.

143 Acquired and intrinsic resistance to receptor tyrosine kinase inhibitors (RTKi) represents a

144 Effects of 4 multitargeted receptor tyrosine kinase inhibitors on regional hemodyna

145 Because receptor tyrosine kinase inhibitors render JHCO3 in the

146 Adjuvant treatment with the VEGF receptor tyrosine kinase inhibitors sorafenib or sunitin

147 VEGF inhibitors, including receptor tyrosine kinase inhibitors, are used as adjunct

148 Epidermal growth factor receptor tyrosine kinase inhibitors, including gefitinib

149 wth factor receptor (EGFR) is a prototypical receptor tyrosine kinase involved in cell growth and pro

150 yl cyclases, phosphodiesterases (PDEs)), and receptor tyrosine kinases involved in growth (Trk), but

151 Expression of the Ret receptor tyrosine kinase is a defining feature of enteri

152 In contrast, the EphB2 receptor tyrosine kinase is enriched deeper within the p

153 nsulin receptor substrate (IRS)-1/2 by IGF-I receptor tyrosine kinase is essential for IGF action.

154 We have demonstrated previously that the Ron receptor tyrosine kinase is expressed on tissue-resident

155 Profiling the tumours revealed that the Axl receptor tyrosine kinase is overexpressed in the unrespo

156 th factor receptor, EGFR/ERBB/HER, family of receptor tyrosine kinases is central to many signaling p

157 The Eph family of receptor tyrosine kinases is implicated in a number of n

158 st growth factor (Fgf) family of ligands and receptor tyrosine kinases is required throughout embryon

159 We show that AXL, a receptor tyrosine kinase, is the primary ZIKV entry cofa

160 phA2, a member of the large family of Ephrin receptor tyrosine kinases, is a functional signaling rec

161 ErbB3, a member of the ErbB family of receptor tyrosine kinases, is a potent activator of phos

162 'belly spots' in mice with mutations in the receptor tyrosine kinase Kit are thought to represent a

163 The receptor tyrosine kinase KIT promotes survival and migra

164 ominantly harbor activating mutations in the receptor tyrosine kinase KIT.

165 rognostic significance of KIT proto-oncogene receptor tyrosine kinase (KIT) and platelet-derived grow

166 ediated both by reduced expression of Axl, a receptor tyrosine kinase known to recognize AC, and of t

167 l Wnt signaling from Frizzled 7 (Fz7) to the receptor tyrosine kinase-like orphan receptor 2 (Ror2).

168 Evolutionarily conserved receptor tyrosine kinase-like orphan receptor-1 and -2 (

169 b, were found to modulate the expression of receptor tyrosine kinase mediators (including AKT1, PIK3

170 nases is experimentally validated, including Receptor Tyrosine Kinases, members of the MAP Kinase cas

171 Here we show that the TAM receptor tyrosine kinases Mer and Axl regulate these mic

172 TAM family receptor tyrosine kinases (Mer and Axl) play an importan

173 Deregulation of the receptor tyrosine kinase mesenchymal epithelial transiti

174 ll entry begins with activation of the human receptor tyrosine kinase MET through the bacterial invas

175 in regulating cell surface expression of the receptor tyrosine kinases MET and EGF receptor.

176 Receptor tyrosine kinases MET and epidermal growth facto

177 include the v6 exon are co-receptors for the receptor tyrosine kinases MET and Vascular Endothelial G

178 MET encodes a receptor tyrosine kinase, MET, which has a pleiotropic r

179 ulation, but is due to inhibition of the Axl receptor tyrosine kinase on tumor cells.

180 ter constitutive activation as well as after receptor tyrosine kinase- or GPCR-mediated activation of

181 sion is via its engagement of the ErbB2/HER2 receptor tyrosine kinase, other mechanisms exist and rem

182 progression in conjunction with inputs from receptor tyrosine kinase pathways.

183 wth factor (PDGF) acts through two conserved receptor tyrosine kinases: PDGFRalpha and PDGFRbeta.

184 tly have acquired oncogenic mutations in the receptor tyrosine kinase/phosphatidylinositol 3-kinase/A

185 Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase physiologically expressed by fe

186 onical signaling mechanisms such as Src (non-receptor tyrosine kinase), PI3K, ERK, or MAPK pathways.

187 way and requires autocrine activation of the receptor tyrosine kinases, platelet-derived and epiderma

188 The EphA2 receptor tyrosine kinase plays key roles in tissue homeo

189 ported previously that Janus kinase 3, a non-receptor tyrosine kinase, plays a crucial role in AJ for

190 on additional kinases, an unbiased screen of receptor tyrosine kinases potentially activated by LMP1

191 Signaling through the Ror2 receptor tyrosine kinase promotes invadopodia formation

192 Lung ADCs lacking receptor tyrosine kinase-Ras-Raf pathway alterations had

193 fic activating alterations in members of the receptor tyrosine kinase/Ras/Raf pathway including EGFR

194 Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase responsible for the development

195 is genetic crosstalk between parkin and the receptor tyrosine kinase RET in two different mouse mode

196 DH) inhibitory interneurons that express the receptor tyrosine kinase Ret neonatally.

197 pressed DUX4 in myoblasts and found that the receptor tyrosine kinase Ret was significantly up-regula

198 GDNF, acting through the receptor tyrosine kinase Ret, regulates the expression o

199 Quite interestingly, the receptor tyrosine kinase (RTK) agonist, platelet-derived

200 imerized a JAK/STAT cytokine receptor with a receptor tyrosine kinase (RTK) also elicited a signaling

201 GC fate by mediating degradation of Torso, a receptor tyrosine kinase (RTK) and major determinant of

202 The receptor tyrosine kinase (RTK) AXL has been intrinsicall

203 The receptor tyrosine kinase (RTK) AXL is induced in respons

204 into exploring mechanistic hypotheses about receptor tyrosine kinase (RTK) biology.

205 report here that CD44 (ADAM10 substrate), a receptor tyrosine kinase (RTK) coreceptor required for c

206 The EPHB4 receptor tyrosine kinase (RTK) has recently emerged as a

207 eting HER2(+) tumors with trastuzumab or the receptor tyrosine kinase (RTK) inhibitor lapatinib signi

208 We report several receptor tyrosine kinase (RTK) ligands increase RhoA-gua

209 Receptor tyrosine kinase (RTK) recycling is of critical

210 Similarly, variants within genes that encode receptor tyrosine kinase (RTK) signaling components, inc

211 Deregulated receptor tyrosine kinase (RTK) signaling is frequently a

212 ies harbor mutations in genes activating RAS/receptor tyrosine kinase (RTK) signaling pathways.

213 gs have broad implications for understanding receptor tyrosine kinase (RTK) signaling specificity.

214 sent a point of cross-talk between Notch and receptor tyrosine kinase (RTK) signaling.

215 haviour in vitro by controlling integrin and receptor tyrosine kinase (RTK) trafficking, but how RCP

216 ace receptors via Janus Kinase (JAK/TYK), or Receptor Tyrosine Kinase (RTK)-mediated trans-phosphoryl

217 Resistance limits the effectiveness of receptor tyrosine kinase (RTK)-targeted therapies.

218 Inhibitors that target the receptor tyrosine kinase (RTK)/Ras/mitogen-activated pro

219 ten mediated by pathway reactivation through receptor tyrosine kinase (RTK)/SRC-family kinase (SFK) s

220 Receptor tyrosine kinases (RTK) are important cell signa

221 Receptor tyrosine kinases (RTK) are major regulators of

222 Dysregulation of receptor tyrosine kinases (RTK) contributes to cellular

223 oops that increase surface expression of the receptor tyrosine kinases (RTK) epidermal growth factor

224 by the activation of AXL, PDGFRa, and HER1-2 receptor tyrosine kinases (RTK) expressed in a large pro

225 wth factor (PDGF) receptor (PDGFR) family of receptor tyrosine kinases (RTK) has been shown to cooper

226 The receptor-tyrosine kinase (RTK)/Ras/Raf pathway is an ess

227 n-1 (NRG1; epidermal-growth-factor) or CD44 (receptor-tyrosine-kinase (RTK) co-receptor) to chymotryp

228 ors, even those with activating mutations in receptor tyrosine kinases (RTKs) and BRAF.

229 Receptor tyrosine kinases (RTKs) and integrins cooperate

230 In eukaryotes, receptor tyrosine kinases (RTKs) and trimeric G proteins

231 Co-amplification of receptor tyrosine kinases (RTKs) and/or downstream mitog

232 tumorigenesis, the mechanism by which these receptor tyrosine kinases (RTKs) are exported from the e

233 c mutations leading to oncogenic variants of receptor tyrosine kinases (RTKs) are frequent events dur

234 Signals propagated by receptor tyrosine kinases (RTKs) can drive cell migratio

235 Receptor tyrosine kinases (RTKs) conduct biochemical sig

236 Epidermal growth factor (EGF) and insulin receptor tyrosine kinases (RTKs) exemplify how receptor

237 to measure the precise distributions of five receptor tyrosine kinases (RTKs) from the ErbB, IGF-1R a

238 , the use of small organic molecules against receptor tyrosine kinases (RTKs) has been shown to be a

239 Receptor tyrosine kinases (RTKs) have been demonstrated

240 Cysteine mutations in receptor tyrosine kinases (RTKs) have been previously pr

241 r (EGFR), one of the most commonly amplified receptor tyrosine kinases (RTKs) in glioblastoma (GBM).

242 o-cell variation in the expressions of these receptor tyrosine kinases (RTKs) in stable tumor sphere

243 Signal transduction by receptor tyrosine kinases (RTKs) involves complex ligand

244 The activity of receptor tyrosine kinases (RTKs) is controlled through t

245 Receptor tyrosine kinases (RTKs) play critical roles in

246 Recently, several studies have shown that receptor tyrosine kinases (RTKs) play important roles in

247 ant cytokine signaling initiated from mutant receptor tyrosine kinases (RTKs) provides critical growt

248 The molecular basis by which receptor tyrosine kinases (RTKs) recruit and phosphoryla

249 oducing human hepatocellular carcinoma (Eph) receptor tyrosine kinases (RTKs) regulate a variety of d

250 The structural mechanisms by which receptor tyrosine kinases (RTKs) regulate catalytic acti

251 Members of the receptor tyrosine kinases (RTKs) regulate important cell

252 last growth factor receptor (FGFR) family of receptor tyrosine kinases (RTKs) regulates signaling pat

253 Receptor tyrosine kinases (RTKs) such as MET and its dow

254 Receptor tyrosine kinases (RTKs) such as PDGFRalpha (pla

255 ine kinase (Ltk) were identified as "orphan" receptor tyrosine kinases (RTKs) with oncogenic potentia

256 Among the 20 subfamilies of protein receptor tyrosine kinases (RTKs), Eph receptors are uniq

257 As HER receptor tyrosine kinases (RTKs), which have important r

258 Eph receptors comprise the largest family of receptor tyrosine kinases (RTKs), with fourteen receptor

259 mary branching morphogenesis is regulated by receptor tyrosine kinases (RTKs).

260 (HSC) function is regulated by activation of receptor tyrosine kinases (RTKs).

261 The human EGF receptor (HER/EGFR) family of receptor tyrosine kinases serves as a key target for can

262 CaM can thereby replace a missing receptor-tyrosine kinase signal to fully activate PI3Kal

263 taining proteins, is a negative regulator of receptor tyrosine kinase signaling and a tumor suppresso

264 Sprouty2 (Spry2) is a modulator of receptor tyrosine kinase signaling and inhibits cell pro

265 hrough either G protein-coupled receptors or receptor tyrosine kinase signaling pathways, suggesting

266 gle cells and correlates that potential with receptor tyrosine kinase signaling.

267 biology including mitochondrial function and receptor tyrosine kinase signaling.

268 monotherapy due to feedback reactivation of receptor tyrosine kinase signaling.

269 focal adhesion kinase/Src proto-oncogene non-receptor tyrosine kinase signaling.

270 nic signalling, small molecule inhibition of receptor tyrosine kinase signalling and alleviation of r

271 phenotype illustrates that subtle changes in receptor tyrosine kinase signalling can have significant

272 BRAF mutants, RAS is typically activated by receptor tyrosine kinase signalling.

273 S-glutathionylation within EGFR and the non-receptor-tyrosine kinase Src.

274 However, we have reported that the non-receptor tyrosine kinase, Src, is activated by Tf to fac

275 tionship between Notch and either of the non-receptor tyrosine kinases Src42A and Src64B to promote h

276 Galectin-4 binding to multiple receptor tyrosine kinases stimulated their autophosphory

277 subsets of Nurr1 target genes including the receptor tyrosine kinase subunit Ret.

278 Receptor tyrosine kinase such as orphan receptor 1 (Ror1

279 rotein tyrosine kinase-7 (PTK7), a member of receptor tyrosine kinase superfamily initially identifie

280 ng full-length and functional ERBB2 and EGFR receptor tyrosine kinases supported by water-soluble apo

281 Ret is a receptor tyrosine kinase that achieves full activity whe

282 Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase that binds and transmits signal

283 Rearranged during transfection (RET), a receptor tyrosine kinase that is activated by the glial

284 broblast growth factor receptor 3 (FGFR3), a receptor tyrosine kinase that negatively regulates growt

285 's tyrosine kinase (Btk) is a Tec family non-receptor tyrosine kinase that plays a critical role in i

286 Eph receptors belong to a subfamily of receptor tyrosine kinases that are activated by membrane

287 rtk) are a family of three homologous type I receptor tyrosine kinases that are implicated in several

288 ctor receptor (EGFR) is a well characterized receptor-tyrosine kinase that functions in development a

289 at SOCS protein over-expression may regulate receptor tyrosine kinases through indirect and direct me

290 The endothelial cell (EC)-specific receptor tyrosine kinases Tie1 and Tie2 are necessary fo

291 epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase (TK) that-once activated upon l

292 predictions of structurally uncharacterized receptor tyrosine kinase TMH oligomers provide a plausib

293 a growth factor that acts through the c-Kit receptor tyrosine kinase to elicit hematopoietic progeni

294 ontrolled by the localized activation of the receptor tyrosine kinase Torso.

295 duce long-term depression, and with the BDNF receptor tyrosine kinase TrkB to elicit long-term potent

296 The BDNF receptor tyrosine kinase, TrkB, underlies nervous system

297 Here, we review the TAM receptor tyrosine kinases-TYRO3, AXL, and MERTK-as an em

298 RO3, a member of the TYRO3-AXL-MER family of receptor tyrosine kinases, was identified as being aberr

299 ha6beta4 integrin is known to associate with receptor tyrosine kinases when engaged in epithelial wou

300 min-2 (Dyn2) is implicated in endocytosis of receptor tyrosine kinases, which contribute to hepatic s