ライフサイエンスコーパス: tyrosine kinase

1 on and function of the ICD of ErbB4 receptor tyrosine kinase.

2 F-actin-disassembly enzyme Mical and the Abl tyrosine kinase.

3 t express the autism-associated MET receptor tyrosine kinase.

4 y specifically destroying the Torso Receptor Tyrosine Kinase.

5 lpha1) and signals through activation of RET tyrosine kinase.

6 soluble phosphopeptide derived from receptor tyrosine kinases.

7 of RAS activation by inhibitors of receptor tyrosine kinases.

8 to the well-studied ErbB family of receptor tyrosine kinases.

9 including the PE associated gene fms related tyrosine kinase 1 (FLT1).

10 ins that interact with neurotrophic receptor tyrosine kinase 1, a receptor also known as TrkA that up

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

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

13 Proline-rich tyrosine kinase 2 (PYK2), a redox-sensitive tyrosine kin

14 vel substrate and interactor of proline-rich tyrosine kinase 2 (Pyk2).

15 xis, connecting genetic aberrations in FLT3, tyrosine kinase 2 (TYK2), platelet-derived growth factor

16 Context ERBB2 (erb-b2 receptor tyrosine kinase 2 or HER2) is currently the only biomark

17 Inhibition of proline-rich tyrosine kinase 2 restores insulin-induced and shear str

18 Syk, focal adhesion kinase, and proline-rich tyrosine kinase 2, and in the absence of Dectin-1.

19 ith pan-PIM kinase inhibitor and fms-related tyrosine kinase 3 (FLT3) inhibitor as single agents and

20 Oncogenic addiction to the Fms-like tyrosine kinase 3 (FLT3) is a hallmark of acute myeloid

21 stimulation with stem cell factor, Fms-like tyrosine kinase 3 ligand, interleukin-3, interleukin-6,

22 FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI

23 The clinical benefit of adding FMS-like tyrosine kinase-3 (FLT3)-directed small molecule therapy

24 Phosphorylation of RCP at Ser(435) by Lemur tyrosine kinase-3 (LMTK3) and of EphA2 at Ser(897) by Ak

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

26 athophysiological roles for the MET receptor tyrosine kinase, a multifunctional receptor that mediate

27 any G protein-coupled receptors and receptor tyrosine kinases, activate phospholipase C (PLC) isozyme

28 main (ICD) in addition to classical receptor tyrosine kinase-activated signaling cascades.

29 aused by aberrant activity of other receptor tyrosine kinases, activating overlapping signaling pathw

30 or release, as well as Lyn kinase and spleen tyrosine kinase activation and signaling through mechani

31 MAN2A1-FER had tyrosine kinase activity almost 4-fold higher than that

32 Src tyrosine kinase activity and tyrosine phosphorylation of

33 Cediranib (AZD2171) is a potent inhibitor of tyrosine kinase activity associated with vascular endoth

34 Stringent regulation of tyrosine kinase activity is essential for normal cellula

35 o EGFRvIII, and this binding upregulates the tyrosine kinase activity of EGFRvIII and activates the R

36 Genetic or pharmacologic inhibition of EGFR tyrosine kinase activity or downstream MEK activity atte

37 inhibition of protein kinase C and receptor tyrosine kinase activity.

38 ANCE STATEMENT The Src family of nonreceptor tyrosine kinases acts in signaling pathways that regulat

39 Furthermore, this study reveals key tyrosine kinase and DNA methylation pathways in liposarc

40 un N-terminal kinase (JNK), the Axl receptor tyrosine kinase and extracellular signal-regulated kinas

41 on of SYK and its immediate targets Bruton's tyrosine kinase and phospholipase Cgamma2.

42 otein that is required for activation of SRC tyrosine kinase and simultaneously coordinates the atten

43 brane promotes activation of Ras by receptor tyrosine kinases and stimulates oncogenic signaling by m

44 ntative cancer-relevant serine/threonine and tyrosine kinases and their interplay with chromatin remo

45 t-derived growth factor receptor, a receptor tyrosine kinase) and H-Ras generates strong, synergistic

46 y serve as an early indicator of response to tyrosine kinase (angiogenesis) inhibitors such as pazopa

47 Mutant receptor tyrosine kinases are mislocalized in the endoplasmic ret

48 Here, we identify EphA2 receptor tyrosine kinase as a clinically relevant target for TNBC

49 ve ligand-induced dimerization of a receptor tyrosine kinase at the cell surface and directly measure

50 Importantly, we discover that receptor tyrosine kinase AXL is a transcriptional target of BCL6

51 neurotrophic factor (BDNF) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is n

52 d by expression of the constitutively active tyrosine kinase BCR/Abl.

53 coupling to the adaptor protein TYRO protein-tyrosine kinase-binding protein (TYROBP).

54 d PBF as a downstream target of the receptor tyrosine kinase-BRAF signalling pathway, emphasising a r

55 ely correlated with susceptibility to Bruton tyrosine kinase (BTK) and SYK inhibitors in MCL.

56 Ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor approved for the treatme

57 in, dexamethasone, rituximab, and the Bruton tyrosine kinase (BTK) inhibitor ibrutinib induced freque

58 Ibrutinib, a Bruton's tyrosine kinase (BTK) inhibitor, targets BCR signaling a

59 Bruton tyrosine kinase (Btk) is a central player in multiple si

60 Bruton tyrosine kinase (BTK) is a key enzyme in B-cell developm

61 Recent data suggest that Bruton's tyrosine kinase (BTK) is an emerging therapeutic target

62 (AS-PCR) assays that we developed for Bruton tyrosine kinase (BTK) mutations.

63 Therapy targeting Bruton's tyrosine kinase (BTK) with ibrutinib has transformed the

64 Purpose Therapeutic targeting of Bruton tyrosine kinase (BTK) with ibrutinib in chronic lymphocy

65 Ibrutinib, an oral inhibitor of Bruton's tyrosine kinase (BTK), at a once-daily dose of 420 mg ac

66 The ibrutinib target, Bruton's tyrosine kinase (BTK), is essential for B-cell receptor

67 Hyperactivation of the receptor tyrosine kinase c-Met and overexpression of the cytoprot

68 ll-molecule inhibitor of the orphan receptor tyrosine kinase c-ros oncogene 1 (ROS1), which has a kin

69 oncogene activates the cellular nonreceptor tyrosine kinase c-Src and recruits the Hippo pathway eff

70 The tyrosine kinase, c-Src, participates in mu opioid recept

71 In the mammalian brain the ubiquitous tyrosine kinase, C-Src, undergoes splicing to insert sho

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

73 Other active receptor tyrosine kinases could not compensate for reduced IGF-1R

74 Several spleen tyrosine kinase-coupled C-type lectin receptors (CLRs) h

75 oteins that typically involve genes encoding tyrosine kinases, cytokine receptors, and transcription

76 ase inhibitor Spint-1, the collagen receptor tyrosine kinase DDR1, N-Cadherin, CLCP1/DCBLD2, KIRREL,

77 ld-type RAS amplification increases receptor tyrosine kinase-dependent activation of RAS more potentl

78 itment, is downregulated in TAMs through Mer tyrosine kinase-dependent recognition of apoptotic cance

79 ctive oxygen species, thus preventing spleen tyrosine kinase dephosphorylation and perpetuating MC si

80 tyrosine kinase 2 (PYK2), a redox-sensitive tyrosine kinase, directly phosphorylates and inhibits en

81 type of FLT3 mutation: point mutation in the tyrosine kinase domain (TKD) or internal tandem duplicat

82 at WHSC1L1 mono-methylates lysine 721 in the tyrosine kinase domain of EGFR, and that this methylatio

83 ernal tandem duplication mutations, 23% FLT3-tyrosine kinase domain point mutations, and 2% both type

84 ceptor while retaining the transmembrane and tyrosine kinase domains.

85 also observed following inhibition of other tyrosine kinase-driven cancer cells, including EGFR-muta

86 ies reveal an adaptive feedback mechanism in tyrosine kinase-driven cancers associated with reactivat

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

88 nectin type III (FN3) domain of the receptor tyrosine kinase EphB2.

89 ng of both langerin and the receptor protein tyrosine kinase ephrin A2 was required to inhibit HHV-8

90 The receptor tyrosine kinase ephrin type-A receptor 2 (EphA2) was ide

91 amplification of the gene encoding receptor tyrosine kinase epidermal growth factor receptor (EGFR).

92 gesterone receptors, along with the receptor tyrosine kinase ERB2 (HER2), that define most mammary ca

93 It signals via a receptor tyrosine kinase expressed on the surface on endothelial

94 loss-of function assays show that levels of tyrosine kinase expression in SCPs modify neurofibroma i

95 Spleen tyrosine kinase expression was found in human and murine

96 he association and activation of the protein-tyrosine kinases FAK1/PYK1 that phosphorylated LAT selec

97 one of the most recently identified receptor tyrosine kinase families.

98 The receptor tyrosine kinase family consisting of Tyro3, Axl, and Mer

99 Tie1 and Tie2, members of the tyrosine kinase family with immunoglobulin and EGF homol

100 Surprisingly, one of these genes encodes the tyrosine kinase FES.

101 inhibitor with activity against the receptor tyrosine kinase FLT3, and its approval will hopefully ma

102 bulin and EGF homology domains, are receptor tyrosine kinases found primarily in endothelial cells wi

103 nes, including PIK3CA and MEK1, and receptor tyrosine kinase fusions, were also identified in all 3 s

104 lucidated to date, converging on nonreceptor tyrosine kinase Fyn.

105 ene (MAN2A1) and the last 6 exons in the FER tyrosine kinase gene (FER), called MAN2A1-FER.

106 rm of MerTK (myeloid-epithelial-reproductive tyrosine kinase; ie, soluble MER), a critical biomarker

107 We examined the involvement of Lyn tyrosine kinase in TLR4 signaling of macrophages, distin

108 While the importance of protein tyrosine kinases in orchestrating the tyrosine phosphory

109 The key role of tyrosine kinases in this process is further substantiate

110 gulator of not only GPCRs, but also receptor tyrosine kinases, including the highly cancer relevant i

111 GCB) subtype, which is insensitive to Bruton tyrosine kinase inhibition by ibrutinib, and the activat

112 Spleen tyrosine kinase inhibition directly attenuates airway sm

113 ers tumor cells more susceptible to receptor tyrosine kinase inhibition in a preclinical glioblastoma

114 leukemia (ALL) who progress after failure of tyrosine kinase inhibitor (TKI) -based therapy.

115 n chronic myeloid leukemia (CML) patients on tyrosine kinase inhibitor (TKI) therapy and may promote

116 Although tyrosine kinase inhibitor (TKI) therapy has improved cli

117 ents at diagnosis and following conventional tyrosine kinase inhibitor (TKI) treatment.

118 X-82 is an oral tyrosine kinase inhibitor active against vascular endoth

119 Combined treatment with an EGFR tyrosine kinase inhibitor and Akt inhibitor causes apopt

120 al metastases who had never received an EGFR tyrosine kinase inhibitor and patients with leptomeninge

121 of EGFR, HER2, and HER3 signalling with the tyrosine kinase inhibitor AZD8931 will control growth of

122 CP-196) is a highly selective, potent Bruton tyrosine kinase inhibitor developed to minimise off-targ

123 The epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in combination with

124 The tyrosine kinase inhibitor erlotinib poorly penetrates th

125 and safety with that of the reversible EGFR tyrosine kinase inhibitor gefitinib in the first-line tr

126 the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib relative to placebo

127 er substantiated by the rescue effect of the tyrosine kinase inhibitor genistein, and the more specif

128 The novel Bruton's tyrosine kinase inhibitor ibrutinib has demonstrated hig

129 ting us to combine AZD8835 with the Bruton's tyrosine kinase inhibitor ibrutinib.

130 limumab in combination, and nivolumab plus a tyrosine kinase inhibitor in metastatic renal cell carci

131 Vandetanib is a novel tyrosine kinase inhibitor of VEGFR2, RET, and EGFR, all

132 S metastases who had either never received a tyrosine kinase inhibitor or who had been pretreated wit

133 had progressed after treatment with an EGFR tyrosine kinase inhibitor received AZD3759 at 50 mg, 100

134 The diversity and unpredictability of EGFR tyrosine kinase inhibitor resistance mechanisms presents

135 tually all patients succumb to acquired EGFR tyrosine kinase inhibitor resistance that occurs via div

136 ion is a convergent feature of acquired EGFR tyrosine kinase inhibitor resistance, across a spectrum

137 r developing new treatments to overcome EGFR tyrosine kinase inhibitor resistance.

138 ntagonist in polystyrene microspheres (PE) + tyrosine kinase inhibitor SU5416 (SU) group.

139 nitially respond to treatment with the multi-tyrosine kinase inhibitor sunitinib eventually relapse.

140 -C or VEGFR3 deletion, administration of the tyrosine kinase inhibitor sunitinib, or expression of VE

141 odel of mBC resistance to the antiangiogenic tyrosine kinase inhibitor sunitinib.

142 Erlotinib is an EGFR tyrosine kinase inhibitor that has shown a significant b

143 ls at CML diagnosis on molecular response to tyrosine kinase inhibitor therapy in early chronic-phase

144 first-line epidermal growth factor receptor tyrosine kinase inhibitor therapy, and T790M mutation, o

145 ndings indicated that targeted delivery of a tyrosine kinase inhibitor to tumors can be used in a nov

146 AZD3759 is a novel EGFR tyrosine kinase inhibitor with high capability to penetr

147 HER3 mAb) and erlotinib (EGFR small-molecule tyrosine kinase inhibitor) were marginal.

148 1 year of neratinib, an irreversible pan-HER tyrosine kinase inhibitor, significantly improves 2-year

149 is aggressive tumor, a multi-target receptor tyrosine kinase inhibitor, sunitinib base, was efficient

150 nergistic growth inhibition in multiple EGFR tyrosine kinase inhibitor-resistant non-small-cell lung

151 activity of oral BGJ398, a selective FGFR1-3 tyrosine kinase inhibitor.

152 inhibitor or who had been pretreated with a tyrosine kinase inhibitor.

153 ation of sunitinib, a multitargeted receptor tyrosine kinase inhibitor.

154 tured microglia by PP2, a Src family protein tyrosine kinase inhibitor.

155 ib is a second-generation, irreversible EGFR tyrosine kinase inhibitor.

156 astases who had been pretreated with an EGFR tyrosine kinase inhibitor.

157 despite treatment with ibrutinib, a Bruton's tyrosine kinase inhibitor.

158 ilic blocks and dasatinib (DAS, an oncogenic tyrosine kinases inhibitor) conjugated hydrophobic block

159 Tyrosine-kinase inhibitor (TKI) therapy for human cancer

160 before and after treatment of cells with the tyrosine-kinase inhibitor Gefitinib.

161 leukemia (Ph(+) ALL) undergoing maintenance tyrosine-kinase inhibitor treatment, little is known abo

162 multimodal strategy combining multitargeted tyrosine kinase inhibitors (MTKIs) and microRNA (miRNA)

163 cquired and intrinsic resistance to receptor tyrosine kinase inhibitors (RTKi) represents a major hur

164 also enabled monitoring cell sensitivity to tyrosine kinase inhibitors (TKI) - a common drug used fo

165 The BCR-ABL specific tyrosine kinase inhibitors (TKI) changed the outcome of

166 FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI) have been tested extens

167 h(+) ALL) is currently treated with BCR-ABL1 tyrosine kinase inhibitors (TKI) in combination with che

168 Mutant-selective EGFR tyrosine kinase inhibitors (TKI), such as osimertinib, a

169 tumor cells sensitive to treatment with EGFR tyrosine kinase inhibitors (TKI).

170 as a novel pathway of acquired resistance to tyrosine kinase inhibitors (TKIs) and cytotoxic drugs in

171 and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are treatment options

172 Tyrosine kinase inhibitors (TKIs) are used in the clinic

173 cond- and/or third-generation c-Abl-specific tyrosine kinase inhibitors (TKIs) has substantially exte

174 CML therapy based on tyrosine kinase inhibitors (TKIs) is highly effective in

175 Tyrosine kinase inhibitors (TKIs) of the EGF receptor (E

176 Although tyrosine kinase inhibitors (TKIs) that target the kinase

177 c myeloid leukemia (CP-CML) are treated with tyrosine kinase inhibitors (TKIs).

178 hocytic leukemia/lymphoma 2 (BCL2), and many tyrosine kinase inhibitors (TKIs).

179 SCs that is enriched following therapy with tyrosine kinase inhibitors (TKIs).

180 This led to development of small-molecule tyrosine kinase inhibitors and inhibitors of mammalian t

181 on of skin toxicity in patients treated with tyrosine kinase inhibitors at levels not detectable via

182 argeting the fusion oncoprotein BCR-ABL with tyrosine kinase inhibitors has significantly affected ch

183 summary, we show that PI3Kdelta or Bruton's tyrosine kinase inhibitors increase genomic instability

184 Trials comparing the addition of tyrosine kinase inhibitors to conventional therapy are r

185 Bruton tyrosine kinase inhibitors were active in progressive CL

186 l glioma mouse model, we assessed a panel of tyrosine kinase inhibitors with different selectivity pr

187 VEGF inhibitors, including receptor tyrosine kinase inhibitors, are used as adjunct therapie

188 Deregulation of ZAP-70 using tyrosine kinase inhibitors, gefitinib or ibrutinib, dimi

189 d that RCN2 knockout sensitized HCC cells to tyrosine kinase inhibitors, including erlotinib, lapatin

190 Epidermal growth factor receptor tyrosine kinase inhibitors, including gefitinib, erlotin

191 ion of novel targets for two clinically used tyrosine kinase inhibitors, nilotinib and osimertinib.

192 utic considerations, including new and novel tyrosine kinase inhibitors.

193 ure, with the emergence of clinically useful tyrosine kinase inhibitors.

194 nation of PGE1/misoprostol with conventional tyrosine-kinase inhibitors could provide effective thera

195 ansplantation vs long-term administration of tyrosine-kinase inhibitors) as well as on MRD testing.

196 Anthocyanins exhibited tyrosine kinase inhibitory potential in silico and bioch

197 Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase involved in development and human diseas

198 Bruton tyrosine kinase is a clinically validated target in mant

199 Expression of the Ret receptor tyrosine kinase is a defining feature of enteric neurons

200 -specific N1-Src splice variant of the C-Src tyrosine kinase is conserved through vertebrate evolutio

201 The SYK tyrosine kinase is essential for signaling from the B ce

202 The Tec tyrosine kinase is expressed in many cell types, includi

203 The Janus kinase 3 (JAK3) tyrosine kinase is mutated in 10% to 16% of T-cell acute

204 significance of KIT proto-oncogene receptor tyrosine kinase (KIT) and platelet-derived growth factor

205 lar localization and function of the protein tyrosine kinase Lck depends on the Rab11 effector FIP3 (

206 t reversed inhibitory phosphorylation of the tyrosine kinase Lck on Ser59 (Lck(S59)).

207 aplastic lymphoma kinase (Alk) and leucocyte tyrosine kinase (Ltk) were identified as "orphan" recept

208 The tyrosine kinase mast/stem cell growth factor receptor KI

209 found to modulate the expression of receptor tyrosine kinase mediators (including AKT1, PIK3CA and SO

210 experimentally validated, including Receptor Tyrosine Kinases, members of the MAP Kinase cascade, and

211 Mer tyrosine kinase (Mer) signaling maintains immune toleran

212 the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promot

213 and synapses via the phagocytic receptor Mer tyrosine kinase (MerTK).

214 f these candidates, Jak1 (Janus kinase 1), a tyrosine kinase of the nonreceptor type, confirmed the u

215 Activation of Src-family tyrosine kinases on the Golgi is essential for oncogenic

216 cription 5 (STAT5s) are crucial effectors of tyrosine kinase oncogenes in myeloid leukemias.

217 ia its engagement of the ErbB2/HER2 receptor tyrosine kinase, other mechanisms exist and remain to be

218 The two isoforms of the Bcr-Abl tyrosine kinase, p210 and p190, are associated with diff

219 on in a manner that is dependent on Bruton's tyrosine kinase, p38 MAPK, and TANK-binding kinase 1 (TB

220 monstrated by the individual use of Bruton's tyrosine kinase, p38 MAPK, and TBK1 inhibitors.

221 signaling molecules, phosphorylated Brutons tyrosine kinase (pBtk) and phosphorylated SH2-containing

222 increased levels of phosphorylated Bruton's tyrosine kinase (pBtk), phosphorylated Spleen tyrosine k

223 hHB-EGF expression increased tyrosine kinase phosphorylation of EGFR and the subseque

224 aplastic lymphoma kinase (ALK) is a receptor tyrosine kinase physiologically expressed by fetal neura

225 gnaling mechanisms such as Src (non-receptor tyrosine kinase), PI3K, ERK, or MAPK pathways.

226 eviously that Janus kinase 3, a non-receptor tyrosine kinase, plays a crucial role in AJ formation th

227 via the SFK (Src family kinase)-Syk (spleen tyrosine kinase)-PLCgamma2 (phospholipase Cgamma2) pathw

228 yrosine kinase (pBtk), phosphorylated Spleen tyrosine kinase (pSyk), and nuclear receptor Nur77.

229 discovery that work in concert with protein tyrosine kinases (PTK) in controlling cellular homeostas

230 We show that the tyrosine kinase PTK6 (BRK) is a PTEN substrate.

231 gulated by the counter-activities of protein tyrosine kinases (PTKs) and protein tyrosine phosphatase

232 mitant targeting of EGFR and the nonreceptor tyrosine kinases PYK2/FAK synergistically inhibits the p

233 ating alterations in members of the receptor tyrosine kinase/Ras/Raf pathway including EGFR and KRAS

234 l of CD1c(+) DC activation via regulation of tyrosine kinase receptor AXL, an important inhibitory DC

235 The tyrosine kinase receptor EGFR is expressed in Schwann ce

236 nteracts with the calcium pump PMCA2 and the tyrosine kinase receptor ErbB2/HER2 in normal mammary ep

237 ants of Neuregulin 1 (NRG1) and its neuronal tyrosine kinase receptor ErbB4 are associated with risk

238 Here we found that the tyrosine kinase receptor ErbB4 was required for the norm

239 ession of EPHA2 (Ephrin-receptor Type-A2), a tyrosine kinase receptor that has been shown to be impor

240 telet-derived growth factor receptor-beta, a tyrosine kinase receptor that is required for pericyte c

241 d that, upon irradiation, the membrane-bound tyrosine kinase receptor TIE2 translocates into the nucl

242 growth factor receptor alpha (PDGFRalpha), a tyrosine kinase receptor, is up-regulated in hepatic ste

243 y of growth factors that are ligands for the tyrosine kinase receptor, Tie2.

244 2) and VEGF signalling with soluble Fms-like tyrosine kinase receptor-1 (sFlt1).

245 ion prevalence in the ephrin (EPH) family of tyrosine kinase receptors was 10-fold higher in primary

246 SCF, and imatininib which blocks downstream tyrosine kinase receptors, both inhibited lung fibroblas

247 The ErbB/HER family comprises four distinct tyrosine kinase receptors, EGFR/ErbB1/HER1, ErbB2/HER2,

248 a JAK/STAT cytokine receptor with a receptor tyrosine kinase (RTK) also elicited a signaling response

249 y mediating degradation of Torso, a receptor tyrosine kinase (RTK) and major determinant of somatic c

250 The receptor tyrosine kinase (RTK) AXL has been intrinsically linked

251 We report several receptor tyrosine kinase (RTK) ligands increase RhoA-guanosine tr

252 , variants within genes that encode receptor tyrosine kinase (RTK) signaling components, including me

253 road implications for understanding receptor tyrosine kinase (RTK) signaling specificity.

254 int of cross-talk between Notch and receptor tyrosine kinase (RTK) signaling.

255 n vitro by controlling integrin and receptor tyrosine kinase (RTK) trafficking, but how RCP influence

256 tors via Janus Kinase (JAK/TYK), or Receptor Tyrosine Kinase (RTK)-mediated trans-phosphorylation.

257 Inhibitors that target the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kina

258 Receptor tyrosine kinases (RTK) are important cell signaling mole

259 Receptor tyrosine kinases (RTK) are major regulators of key biolo

260 ns leading to oncogenic variants of receptor tyrosine kinases (RTKs) are frequent events during tumor

261 of small organic molecules against receptor tyrosine kinases (RTKs) has been shown to be a valuable

262 Receptor tyrosine kinases (RTKs) have been demonstrated to signal

263 one of the most commonly amplified receptor tyrosine kinases (RTKs) in glioblastoma (GBM).

264 Signal transduction by receptor tyrosine kinases (RTKs) involves complex ligand- and tim

265 ine signaling initiated from mutant receptor tyrosine kinases (RTKs) provides critical growth and sur

266 The structural mechanisms by which receptor tyrosine kinases (RTKs) regulate catalytic activity are

267 e (Ltk) were identified as "orphan" receptor tyrosine kinases (RTKs) with oncogenic potential.

268 Among the 20 subfamilies of protein receptor tyrosine kinases (RTKs), Eph receptors are unique in pos

269 tors comprise the largest family of receptor tyrosine kinases (RTKs), with fourteen receptors divided

270 otein phosphatase 2A (PP2A), YAP, Src family tyrosine kinases, Shc, phosphatidylinositol 3-kinase (PI

271 Stabilization was independent of tyrosine kinase signaling and the actin cytoskeleton, su

272 The Abl tyrosine kinase signaling network controls cell migratio

273 ses CBL and CBL-B are negative regulators of tyrosine kinase signaling with established roles in the

274 apy due to feedback reactivation of receptor tyrosine kinase signaling.

275 ssible role for regulation of RNA binding by tyrosine kinase signaling.

276 ants, RAS is typically activated by receptor tyrosine kinase signalling.

277 ne, while hepatocyte growth factor-regulated tyrosine kinase substrate as the top negative correlated

278 lation of hepatocyte growth factor-regulated tyrosine kinase substrate, were further confirmed in liv

279 Receptor tyrosine kinase such as orphan receptor 1 (Ror1), a surf

280 t increased expression and activation of the tyrosine kinase Syk in TSC2-deficient cells and pulmonar

281 lived positive signals driven by the protein tyrosine kinase Syk; slow, long-lived negative signals d

282 y-mediated TREM2 stimulation enhanced spleen tyrosine kinase (SYK) activity and uptake of Staphylococ

283 Spleen tyrosine kinase (Syk) is an intracellular nonreceptor ty

284 Here we show that spleen tyrosine kinase (SYK) is upregulated during brown adipoc

285 Spleen tyrosine kinase (Syk) promotes leukocyte recruitment and

286 type lectin receptor that signals via spleen tyrosine kinase (Syk) to induce ROS.

287 or DECTIN1) signaling via spleen-associated tyrosine kinase (SYK), a SYK inhibitor to reduce viscera

288 osinylation and specifically recruits spleen tyrosine kinase (Syk), initiating cellular activation.

289 f early signaling proteins, including spleen tyrosine kinase (Syk), linker for activation of T cells

290 igen receptor (BCR)-proximal effector spleen tyrosine kinase (SYK), which we identified as an HSP90 c

291 fy ACK1 as a novel SLP-76-associated protein-tyrosine kinase that modulates early activation events i

292 receptors belong to a subfamily of receptor tyrosine kinases that are activated by membrane-spanning

293 ponsible factor, we tested several candidate tyrosine kinases that are highly expressed in keratinocy

294 f cell-surface receptors and Abl nonreceptor tyrosine kinases that participate in actin cytoskeleton

295 growth factor receptor (EGFR) is a receptor tyrosine kinase (TK) that-once activated upon ligand bin

296 factor that acts through the c-Kit receptor tyrosine kinase to elicit hematopoietic progenitor expan

297 by the localized activation of the receptor tyrosine kinase Torso.

298 mutations that activate receptor-associated tyrosine kinase, vascular endothelial growth factor, and

299 kinase (Syk) is an intracellular nonreceptor tyrosine kinase, which has been implicated as central im

300 elial growth factor (VEGF) receptors and the tyrosine kinase with IgG and EGF domains-2 (Tie2) recept