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

1 3D cell migration upon activation of the Met receptor tyrosine kinase.

2 ies and require the function of the dBtk non-receptor tyrosine kinase.

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

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

5 h the insulin receptor (IR), a transmembrane receptor tyrosine kinase.

6 Sprouty 1 (SPRY1) is an antagonist of receptor tyrosine kinases.

7 gand for the immunosuppressive TAM family of receptor tyrosine kinases.

8 omers is required for the activation of ErbB receptor tyrosine kinases.

9 ong the latter receptors are the MER and AXL receptor tyrosine kinases.

10 functions by hormones, internal clocks, and receptor tyrosine kinases.

11 whose tumors harbor fusions in neurotrophic receptor tyrosine kinases.

12 tor of VEGFR1, VEGFR2, and VEGFR3, and other receptor tyrosine kinases.

13 cell adhesion receptors, Wnt receptors, and receptor tyrosine kinases.

14 ylation and selectively activated a panel of receptor tyrosine kinases.

15 complex, involving feedback loops and other receptor tyrosine kinases.

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

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

18 as are upstream activators including RAS and receptor tyrosine kinases.

19 for nerve growth factor (NGF): neurotrophic receptor tyrosine kinase 1 and nerve growth factor recep

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

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

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

23 h/repair/remodeling pathways (ERBB2 [erbb-b2 receptor tyrosine kinase 2], TGFB1 [transforming growth

24 ly, we reveal that PRMT1 methylates Fms-like receptor tyrosine kinase 3 (FLT3) at arginine (R) residu

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

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

27 Eph family receptor tyrosine kinase A2 (EphA2) is a cellular recept

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

29 Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by collagens that can

30 ity of CDK7 is regulated by HER2, and by the receptor tyrosine kinases activated in response to HER2

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

32 d BRAF inhibitor resistance was mediated via receptor tyrosine kinase activation, leading to MAPK sig

33 ely confined to intracellular membranes upon receptor tyrosine kinase activation.

34 ncreases in eNOS phosphorylation, as did the receptor tyrosine kinase agonists insulin and Vascular E

35 the dopamine D2 receptor is regulated by the receptor tyrosine kinase ALK.

36 al hemispheres and harbor alterations in the receptor tyrosine kinases ALK, ROS1, NTRK and MET.

37 previous study found that inhibitors of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK

38 or rearrangements in the genes encoding the receptor tyrosine kinases anaplastic lymphoma kinase (AL

39 growth factor receptor (EGFR) is a prototype receptor tyrosine kinase and an oncoprotein in many soli

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

41 Receptor tyrosine kinase and RAS-mediated BRAF activatio

42 and the resulting complex activates the RET receptor tyrosine kinase and subsequent downstream signa

43 rdinate HH, G protein-coupled receptor, WNT, receptor tyrosine kinase and transforming growth factor-

44 phatase 1B (PTP1B)-an important regulator of receptor tyrosine kinases and a therapeutic target for t

45 vascular development, doppel interacts with receptor tyrosine kinases and activates cytoplasmic sign

46 m of PI 3-kinase, which is regulated by both receptor tyrosine kinases and G protein-coupled receptor

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

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

49 including the EC surface receptor, TEK (TEK receptor tyrosine kinase) and its antagonistic ligand, A

50 omain receptor 2 (DDR2), a collagen-specific receptor tyrosine kinase, and integrin-beta1, are report

51 studies have demonstrated that HER2 and MET receptor tyrosine kinases are co-overexpressed in a subs

52 s of the TAM (Tyro3, Axl, and Mer) family of receptor tyrosine kinases are known for their anti-apopt

53 Mutant receptor tyrosine kinases are mislocalized in the endopl

54 vessel painting strategies, implicated EphA4 receptor tyrosine kinase as a major suppressor of pial c

55 eceptor 2 (EPHA2), an oncogenic cell-surface receptor tyrosine kinase, as a therapeutic target that s

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

57 elevated expression of the resistant-leading receptor tyrosine kinase AXL and immune checkpoint ligan

58 Biochemical assays identify the receptor tyrosine kinase Axl and its intracellular signa

59 Recent data suggest that the receptor tyrosine kinase Axl causes a TGF-beta switch to

60 Notably, the receptor tyrosine kinase AXL displayed a dual regulatory

61 Moreover, ALKBH5 affects mRNA stability of receptor tyrosine kinase AXL in an m(6)A-dependent way.

62 is of glycosylated proteins reveals that the receptor tyrosine kinase AXL is a major effector of ST3G

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

64 The oncogenic receptor tyrosine kinase AXL is overexpressed in cancer

65 p85beta upregulates the protein level of the receptor tyrosine kinase AXL to induce oncogenic signali

66 kpoint molecule-in mregDCs is induced by the receptor tyrosine kinase AXL, while upregulation of inte

67 Using the AXL receptor tyrosine kinase (AXL) as a model glycoprotein w

68 ances Gas6-stimulated phosphorylation of the receptor tyrosine kinase, Axl with an upregulation of Cy

69 v1) increases MLR localization of NTR [e.g., receptor tyrosine kinase B (TrkB)], promotes hippocampal

70 conformations that provide access to the non-receptor tyrosine kinases, BCR-ABL and Src, which phosph

71 e is known about how EGFR, or possibly other receptor tyrosine kinases, becomes activated.

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

73 t tumors had a significantly higher level of receptor tyrosine kinase (c-Kit) mRNA.

74 te growth factor (HGF) to MET proto-oncogene receptor tyrosine kinase (c-Met) autocrine feed-forward

75 e 2 (NELL2), specifically binds to an orphan receptor tyrosine kinase, c-ros oncogene 1 (ROS1), and m

76 Two receptor tyrosine kinases, c-KIT and fms-tyrosine kinase

77 t growth, interaction with activated cognate receptor tyrosine kinases, cellular migration, invasion

78 Many cancers are driven by nonmutated receptor tyrosine kinase coactivation networks that defy

79 We hypothesize that a flexible receptor tyrosine kinase coactivation signaling network

80 domains mediate interactions with activated receptor tyrosine kinase complexes including the CD19 su

81 ER4 is a unique member of the ErbB family of receptor tyrosine kinases concerning its activation of a

82 by somatic KIT mutations that result in KIT receptor tyrosine kinase constitutive activity, which dr

83 hemical analysis, we observed that the EphB1 receptor tyrosine kinase constitutively interacts with c

84 How multiple receptor tyrosine kinases coordinate cell fate determina

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

86 rein we demonstrate that activity of the non-receptor tyrosine kinase dBtk protein is required within

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

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

89 s expression of a differentiation regulatory receptor tyrosine kinase, downregulates the telomerase R

90 (ERK) signaling with the genetic loss of the receptor tyrosine-kinase-driven terminal signaling patte

91 inent proliferative oncogenes, including the receptor tyrosine kinases, EGFR and HER2, and downstream

92 resistance through engagement of alternative receptor tyrosine kinases either through upregulation of

93 Activation of the Met receptor tyrosine kinase, either by its ligand, hepatocy

94 which currently has no known role in normal receptor tyrosine kinase endocytosis, under basal condit

95 a negatively charged phospho-tyrosine on the receptor tyrosine kinase EphB2.

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

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

98 They showed that a receptor tyrosine kinase, ephrin-A receptor 2 (EPHA2), r

99 akly with other members of the Eph family of receptor tyrosine kinases (Ephs), and other A-type Ephs

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

101 idermal growth factor receptor (EGFR)/Erb-B2 receptor tyrosine kinase (ERBB) signaling pathway.

102 sphoproteins associated with insulin, erb-b2 receptor tyrosine kinase (Erbb), and Toll-like receptor

103 volved in protein-protein interactions, with receptor tyrosine kinase ErbB2, and fundamental and clin

104 ate (Sunb-malate) targeting against multiple receptor tyrosine kinases, exerts potent antiangiogenesi

105 d growth factor receptor beta (PDGFRbeta), a receptor tyrosine kinase expressed abundantly in glomeru

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

107 The receptor tyrosine kinase family consisting of Tyro3, Axl

108 The ErbB receptor tyrosine kinase family members EGFR (epidermal

109 EphB4 belongs to receptor tyrosine kinase family that interacts with ephr

110 NRGs signal through the ErbB receptor tyrosine kinase family.

111 conjunction with activating mutation in the receptor tyrosine kinase FLT3.

112 The non-receptor tyrosine kinase focal adhesion kinase (FAK) sti

113 t signalling engaging the MET proto-oncogene receptor tyrosine kinase/focal adhesion kinase (FAK) axi

114 growth factor receptor-beta (PDGFRbeta) is a receptor tyrosine kinase found in cells of mesenchymal o

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

116 f Foxa1 and activated HRAS, and that mutated receptor tyrosine kinases, FOXA1 and/or other downstream

117 rafficking as well as cooperation with other receptor tyrosine kinases further enhance ERBB3's role i

118 Therapeutically targeting receptor tyrosine kinases has proven to be paramount to

119 EPHA5, a receptor tyrosine kinase, has been demonstrated to act a

120 Several signaling pathways, including receptor tyrosine kinases, have been recognized to have

121 Here, we show that the receptor tyrosine kinase HER2 (also known as ErbB-2 or N

122 A phage display screen against EphA2, a receptor tyrosine kinase highly expressed in a number of

123 769Tyr) in the catalytic domain of the ERBB2 receptor tyrosine kinase in a patient with schwannomatos

124 our current understanding of this important receptor tyrosine kinase in normal melanocyte proliferat

125 tyrosine phosphorylation and cooperate with receptor-tyrosine kinases in the regulation of cell sign

126 cells (HRECs) vitreous activates a number of receptor tyrosine kinases including Anexelekto (Axl), wh

127 that mediates signaling induced by multiple receptor tyrosine kinases, including signaling by the ep

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

129 unique interactions between VDAC1 and other receptor tyrosine kinases, indicating a novel role for t

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

131 , irreversible, oral epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that poten

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

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

134 Sunitinib (ST), a multitargeted receptor tyrosine kinase inhibitor, has been demonstrate

135 that the mTOR inhibitor, sirolimus, and the receptor tyrosine kinase inhibitor, nintedanib, could sy

136 to identify previously unknown targets of a receptor tyrosine kinase inhibitor.

137 We aimed to assess the activity of the VEGF receptor tyrosine-kinase inhibitor axitinib plus the ant

138 advanced progressed epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) resistant

139 onders to vascular endothelial growth factor receptor tyrosine kinase inhibitors and may help detect

140 pressive clinical activity of small-molecule receptor tyrosine kinase inhibitors for oncogene-addicte

141 Epidermal growth factor receptor tyrosine kinase inhibitors, including gefitinib

142 he safety profile of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs).

143 VEGFR2 is a highly N-glycosylated receptor tyrosine kinase involved in pro-angiogenic sign

144 RET receptor tyrosine kinase is a driver oncogene in human c

145 BDNF signaling thru TrkB receptor tyrosine kinase is one molecular mechanism prom

146 anisms of resistance, activation of multiple receptor tyrosine kinases is a known critical factor tha

147 Dysregulation of the ErbB family of receptor tyrosine kinases is involved in the progression

148 Bruton's tyrosine kinase (BTK), a non-receptor tyrosine kinase, is a member of the Tec family

149 rized by activating mutations in the related receptor tyrosine kinases KIT and PDGFRA.

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

151 o approved inhibitors of KIT proto-oncogene, receptor tyrosine kinase (KIT), and platelet-derived gro

152 Endocan is known as a receptor tyrosine kinase ligand enhancer in tumorigenesi

153 l adhesion protein integrin-alpha2beta1, the receptor tyrosine kinase ligand ephrin-B1, and the class

154 cells targeting the tumor-associated antigen receptor tyrosine kinase-like orphan receptor 1 (ROR1) i

155 emonstrate that aberrant expression of ROR1 (receptor tyrosine kinase-like orphan receptor 1), seen i

156 A receptor tyrosine kinase, receptor tyrosine kinase-like orphan receptor 2 (ROR2),

157 show that Lrp4 interacts with and activates receptor tyrosine kinase-like orphan receptor 2 (Ror2);

158 s were identified in HSPG2 (perlecan), ROR2 (receptor tyrosine kinase-like orphan receptor 2), and WL

159 growth factor-5a (Wnt5a) is a ligand of the receptor tyrosine kinase-like orphan receptor-1 (ROR1).

160 lanoma and pancreatic cancer cells activates receptor tyrosine kinase-MAPK signalling as part of a fe

161 uanine nucleotide exchange factors (GEFs) or receptor tyrosine kinase-mediated and GEF-dependent RAS

162 uced fatty-liver phenotype was not shared by receptor tyrosine kinase MET, investigated using MET kno

163 signaling cascade requires activation of the receptor tyrosine kinase MET, which is a well known auti

164 ocyte growth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) and Wnt/beta-catenin sign

165 Nuclear receptor tyrosine kinases (nRTKs) are aberrantly upregul

166 Much of what is known about the neurotrophic receptor tyrosine kinase (NTRK) genes in cancer was reve

167 we identified the nerve growth factor (NGF) receptor tyrosine kinase (NTRK1), a molecule not previou

168 to three different classes of drug targets (receptor tyrosine kinases, nuclear hormone receptors, an

169 Insulin receptor-related receptor (IRR) is a receptor tyrosine kinase of the insulin receptor family

170 Anaplastic lymphoma kinase (Alk) is a receptor tyrosine kinase of the insulin receptor super-f

171 viral oncogene homolog B2), ErbB3, and ErbB4 receptor tyrosine kinases on various targets cells.

172 Optically controlled receptor tyrosine kinases (opto-RTKs) allow regulation o

173 nd BRAF fusions to tumors driven by aberrant receptor tyrosine kinase or RAS signaling.

174 The oncofetal antigen receptor tyrosine kinase orphan receptor 1 (ROR1) is exp

175 The proto-oncogene MET receptor tyrosine kinase overcomes these structural cons

176 ase signaling, including TGFbeta and several receptor tyrosine kinase pathways.

177 hanistic target of rapamycin, DNA repair and receptor tyrosine kinase pathways.

178 vo calcium signaling dynamics depend on both receptor tyrosine kinase/phospholipase C gamma and G pro

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

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

181 ER3, the fourth member of the ERBB family of receptor tyrosine kinases, plays in these diseases is po

182 engage a signal transduction cascade through receptor tyrosine kinases, prominently engaging ERK1/2 b

183 nder the control of the endothelial-specific receptor tyrosine kinase promoter Tie2.

184 signal-regulated kinase (ERK) activation via receptor tyrosine kinases promotes tumor proliferation a

185 of pseudokinase domains from the Wnt-binding receptor tyrosine kinases (PTK7, ROR1, ROR2, and RYK), w

186 Many of these encode proteins in receptor tyrosine kinase, RAS, or mitogen-activated prot

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

188 A receptor tyrosine kinase, receptor tyrosine kinase-like

189 downstream of multiple critical tumorigenic receptor tyrosine kinase receptors and oncogenic regulat

190 mulating factor 1 (CSF1) receptor (CSF1R), a receptor tyrosine kinase responsible for survival, proli

191 Activating receptor tyrosine kinase RET (rarranged during transfect

192 r regulatory deficiency in the gene encoding receptor tyrosine kinase (RET).

193 e-derived neurotrophic factor (GDNF) and its receptor tyrosine kinase, Ret, in the regulation of inne

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

195 Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proli

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

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

198 Receptor tyrosine kinase (RTK) coexpression facilitates

199 overexpression or activating mutation of the receptor tyrosine kinase (RTK) ERBB2 In some contexts, n

200 Venus kinase receptors (VKRs) constitute a Receptor Tyrosine Kinase (RTK) family only found in inve

201 ase inhibitors (TKIs) occurs invariably, and receptor tyrosine kinase (RTK) fusions have emerged as r

202 ization of thousands of variants of a single receptor tyrosine kinase (RTK) gene in a single assay.

203 ST relies on expression of these unamplified receptor tyrosine kinase (RTK) genes through a large enh

204 Sunitinib, a multi-receptor tyrosine kinase (RTK) inhibitor approved for th

205 Angiogenesis inhibitors, such as the receptor tyrosine kinase (RTK) inhibitor sunitinib, targ

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

207 The Met receptor tyrosine kinase (RTK) modulates invasive growth

208 matin regulators and mutations that activate receptor tyrosine kinase (RTK) signaling frequently occu

209 downregulated a network of genes involved in receptor tyrosine kinase (RTK) signaling in SMARCA4/A2-d

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

211 mal growth factor receptor (EGFR/ERBB1) is a receptor tyrosine kinase (RTK) that forms activated olig

212 Trk-A is a receptor tyrosine kinase (RTK) that plays an essential r

213 RET is a receptor tyrosine kinase (RTK) that plays essential role

214 In glioblastoma, poor efficacy of receptor tyrosine kinase (RTK) therapies has been altern

215 PP3/4, were subsequently activated by a dual-receptor tyrosine kinase (RTK)-dependent signaling event

216 DDR1 is a receptor tyrosine kinase (RTK).

217 ounteracts activation of genes downstream of receptor tyrosine kinase (RTK)/Ras/ERK signaling.

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

219 at mediates signaling downstream of multiple receptor tyrosine kinases (RTK) and is required for full

220 Chromosomal rearrangements involving receptor tyrosine kinases (RTK) are a clinically relevan

221 Receptor tyrosine kinases (RTK) are important cell signa

222 Receptor tyrosine kinases (RTK) are major regulators of

223 ssion of the TAM (TYRO3, AXL, MER) family of receptor tyrosine kinases (RTK) has been associated with

224 plification, mutation, and overexpression of receptor tyrosine kinases (RTK) such as EGFR, and activa

225 ave identified global activation of upstream receptor tyrosine kinases (RTK) that converges on activa

226 s process is scarcely explored downstream of receptor tyrosine kinases (RTK), including the cancer-re

227 K27M mutation led to increased expression of receptor tyrosine kinases (RTK).

228 All receptor tyrosine kinases (RTKs) activate similar downst

229 Ligand-independent activation of receptor tyrosine kinases (RTKs) allows for dissecting o

230 neration, we performed a candidate screen of receptor tyrosine kinases (RTKs) and found a requirement

231 The molecular mechanisms by which receptor tyrosine kinases (RTKs) and heterotrimeric G pr

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

233 Receptor tyrosine kinases (RTKs) are key regulators of c

234 Receptor tyrosine kinases (RTKs) are often overexpressed

235 Receptor tyrosine kinases (RTKs) are single-pass membran

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

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

238 ntly regulated, and nuclear translocation of receptor tyrosine kinases (RTKs) is one way to locally a

239 technologies for quantifying plasma membrane receptor tyrosine kinases (RTKs) lack multiplexing capab

240 Chlamydia binds several receptor tyrosine kinases (RTKs) on host cells, includin

241 Receptor tyrosine kinases (RTKs) play crucial roles in h

242 Receptor tyrosine kinases (RTKs) play important roles in

243 Optical control over the activity of receptor tyrosine kinases (RTKs) provides an efficient w

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

245 Ligand-dependent oligomerization of receptor tyrosine kinases (RTKs) results in their activa

246 Receptor tyrosine kinases (RTKs) typically contain multi

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

248 ors (GPCRs), cell adhesion molecules (CAMs), receptor tyrosine kinases (RTKs), and related signaling

249 In responses to activation of receptor tyrosine kinases (RTKs), crucial cell fate deci

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

251 ide 3-kinase beta (PI3Kbeta) is regulated by receptor tyrosine kinases (RTKs), G protein-coupled rece

252 Receptor tyrosine kinases (RTKs), including the FGF rece

253 Receptor tyrosine kinases (RTKs), MET and epidermal grow

254 is known from structure-function studies of receptor tyrosine kinases (RTKs), RPTP activities have b

255 Stimulation of plasma membrane receptor tyrosine kinases (RTKs), such as the epidermal

256 Our study also identified Met receptor tyrosine kinases (RTKs), which carry a truncate

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

258 ), there are also reports of ligand bias for receptor tyrosine kinases (RTKs).

259 ltered intracellular signaling downstream of receptor tyrosine kinases (RTKs).

260 signaling has emerged in which growth factor-receptor tyrosine kinases (RTKs; e.g., EGFR) access and

261 Reduced angiopoietin-TIE2 receptor tyrosine kinase signaling in the vasculature le

262 tion, we discovered a conserved VEGF-related receptor tyrosine kinase signaling pathway that regulate

263 involve mRNAs from developmental processes, receptor tyrosine kinase signaling, the proteasome, and

264 mechanism by which mTORC1 regulates upstream receptor tyrosine kinase signaling.

265 l agonists of G protein-coupled receptor and receptor tyrosine kinase signaling.

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

267 signaling works independently of phagocytic receptor/tyrosine kinase signaling to promote phagocytos

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

269 tream signalling mechanisms, such as the non-receptor tyrosine kinase Src or N-methyl-D-aspartate rec

270 e of CD2AP and nephrin that is influenced by receptor tyrosine kinase stimulation.

271 Receptor tyrosine kinase such as orphan receptor 1 (Ror1

272 re caused by activating mutations in the KIT receptor tyrosine kinase, such as the exon 11 KIT V559De

273 of targeted EGFR therapy to encompass other receptor tyrosine kinases, such as HER2, and developing

274 s, including G-protein-coupled receptors and receptor tyrosine kinases, suggests that heterodimerizat

275 y reported loss of function mutations in the receptor tyrosine kinase TEK or its ligand ANGPT1 cause

276 ECAD) and occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial

277 The proto-oncoprotein MET is a receptor tyrosine kinase that plays a key role in cancer

278 The collagen receptor DDR1 is a receptor tyrosine kinase that promotes progression of a

279 lin-like growth factor receptor (IGF1R) is a receptor tyrosine kinase that regulates cell growth and

280 Bruton's tyrosine kinase (BTK) is a non-receptor tyrosine kinase that signals downstream of Fc r

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

282 Janus kinases (JAKs) are non-receptor tyrosine kinases that are essential components

283 Eph receptors are a family of receptor tyrosine kinases that control directional cell

284 se (FAK) and its close relative Pyk2 are non-receptor tyrosine kinases that mediate adhesion signalin

285 wth factor receptor (EGFR)/ERBB subfamily of receptor tyrosine kinases that regulates cellular proces

286 scoidin domain receptors (DDR1 and DDR2) are receptor tyrosine kinases that signal in response to col

287 Receptors (DDRs) constitute a unique set of receptor tyrosine kinases that signal in response to col

288 ce of traits, such as point mutations in key receptor tyrosine kinases, that drive drug resistance.

289 ownstream of G protein-coupled receptors and receptor tyrosine kinases through direct interactions wi

290 in vitro, but also reveal that Axl is one of receptor tyrosine kinases to mediate vitreous-induced an

291 ow that KDM5 activates the expression of the receptor tyrosine kinase torso, which then promotes poly

292 between canine and human gliomas such as the receptor tyrosine kinases, TP53 and cell-cycle pathways,

293 en together, these results identify ALK as a receptor tyrosine kinase transactivated by D2R that prom

294 SE-induced activation of the BDNF receptor tyrosine kinase, TrkB, is one signaling pathway

295 Since GPCRs can transactivate receptor tyrosine kinases, we also examined if D2R stimu

296 along with frequent amplification of the Met receptor tyrosine kinase, which conferred a stem cell ph

297 in that may serve such a function is the MET receptor tyrosine kinase, which is tightly regulated dev

298 The proto-oncogene ROS1 encodes a receptor tyrosine kinase with an unknown physiological r

299 in receptor 1 (DDR1) is a collagen-activated receptor tyrosine kinase with important functions in org

300 /gL complex can also interact with other Eph receptor tyrosine kinases with lower avidity.