ライフサイエンスコーパス: tyrosine kinase

1 ulin receptor (IR), a transmembrane receptor tyrosine kinase.

2 he ectopic expression of NPM-ALK, a chimeric tyrosine kinase.

3 oral, highly selective inhibitor of the HER2 tyrosine kinase.

4 stream activators including RAS and receptor tyrosine kinases.

5 routy 1 (SPRY1) is an antagonist of receptor tyrosine kinases.

6 the immunosuppressive TAM family of receptor tyrosine kinases.

7 e growth factor (NGF): neurotrophic receptor tyrosine kinase 1 and nerve growth factor receptor.

8 endotoxin (ETX) or sFlt-1 (soluble fms-like tyrosine kinase 1), and in a postnatal model due to prol

9 ngiogenic biomarker(7), the soluble fms-like tyrosine kinase 1:placental growth factor (sFLT1:PlGF) r

10 kers, mediated primarily by soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng).

11 y hypertension and elevated soluble Fms-Like Tyrosine Kinase-1 (sFlt-1).

12 dothelial (angiopoetin-1/2, soluble fms-like tyrosine kinase-1, soluble vascular cell adhesion molecu

13 y used standard, the plasma soluble fms-like tyrosine kinase-1/placental growth factor (sFlt-1/PlGF)

14 Tyrosine kinase 2 (TYK2) is a member of the JAK kinase f

15 tors 1 and 2 (IFNAR1, IFNAR2, respectively), tyrosine kinase 2 (Tyk2), Jak1, and STAT2 are assembled

16 that MEOX1 knockdown decreased expression of tyrosine kinase 2 (TYK2), signal transducer and activato

17 P = 2.3 x 10(-8)) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs21090

18 Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene in 13q12.2 are among the m

19 tandem duplication mutation in the FMS-like tyrosine kinase 3 gene (FLT3-ITD) have a poor prognosis,

20 ex vivo programming of DCs with fms-related tyrosine kinase 3 ligand (Flt3-L) was found to enhance t

21 ation of cDC1s by administration of FMS-like tyrosine kinase 3 ligand (Flt3L) and TLR/CD40 agonists a

22 sence of stem cell factor (SCF) and FMS-like tyrosine kinase 3 ligand (FLT3L) give rise to numerous c

23 gene, Ser/Thr kinase (Pim1); and Fms-related tyrosine kinase 4 (Flt4).

24 evated expression of another kinase, protein tyrosine kinase 6 (PTK6), upon treatment with a PAK4 inh

25 Eph family receptor tyrosine kinase A2 (EphA2) is a cellular receptor for KS

26 oidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by collagens that can regulate

27 K7 is regulated by HER2, and by the receptor tyrosine kinases activated in response to HER2 inhibitio

28 We show that tyrosine kinase activation is not the only rate-limiting

29 ned to intracellular membranes upon receptor tyrosine kinase activation.

30 ions illuminate a new connection between the tyrosine kinase activity of EGFR and innate immune funct

31 linked to insulin resistance through reduced tyrosine kinase activity of the insulin receptor; howeve

32 ine D2 receptor is regulated by the receptor tyrosine kinase ALK.

33 we demonstrate a design of a sensor for EGFR tyrosine kinase-an important target in cancer research.

34 study found that inhibitors of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) blocked

35 These ligands activate RET tyrosine kinase and afford trophic signals irrespective

36 ctor receptor (EGFR) is a prototype receptor tyrosine kinase and an oncoprotein in many solid tumors.

37 echanotransduction pathway involving the Abl tyrosine kinase and Canoe/Afadin that stabilizes cell ad

38 cell receptor signaling pathway, like Bruton tyrosine kinase and phosphatidylinositol 3 kinase.

39 resulting complex activates the RET receptor tyrosine kinase and subsequent downstream signals.

40 B (PTP1B)-an important regulator of receptor tyrosine kinases and a therapeutic target for the treatm

41 development, doppel interacts with receptor tyrosine kinases and activates cytoplasmic signaling pat

42 ates how TAM receptors act both as oncogenic tyrosine kinases and as receptors that mediate immune ev

43 ER3 signaling via the activation of multiple tyrosine kinases and transcriptional upregulation.

44 the actin-regulatory proteins c-Abl (Abelson tyrosine kinase) and N-WASP (neuronal Wiskott-Aldrich Sy

45 LK fusion protein is a constitutively-active tyrosine kinase, and plays a major role in tumor pathoge

46 Inhibition of Erk1/2, tyrosine kinase, and/or GSK-3beta was implied to be invo

47 Blocking of matrix metalloproteinases or tyrosine kinases are novel modes of action in the treatm

48 We and others have previously identified LYN tyrosine kinase as a key negative regulator of myeloid c

49 inting strategies, implicated EphA4 receptor tyrosine kinase as a major suppressor of pial collateral

50 Further, we identify the ABL2 tyrosine kinase as an upstream regulator of HSF1 protein

51 Biochemical assays identify the receptor tyrosine kinase Axl and its intracellular signaling effe

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

53 The oncogenic receptor tyrosine kinase AXL is overexpressed in cancer and plays

54 pregulates the protein level of the receptor tyrosine kinase AXL to induce oncogenic signaling in ova

55 lecule-in mregDCs is induced by the receptor tyrosine kinase AXL, while upregulation of interleukin (

56 6-stimulated phosphorylation of the receptor tyrosine kinase, Axl with an upregulation of Cyr61, driv

57 therapeutic target proteins, including MAO, tyrosine kinases, BACE1, steroid receptors, mGlu5 recept

58 In CML, the acquisition of the fusion tyrosine kinase BCR-ABL1 in a haematopoietic stem cell d

59 n about how EGFR, or possibly other receptor tyrosine kinases, becomes activated.

60 ealed butyrate-induced downregulation of the tyrosine kinases BTK, SYK, and LAT, critical transducers

61 Furthermore, LTB(4)-mediated Bruton's tyrosine kinase (BTK) activation is required for inflamm

62 Using Bruton's tyrosine kinase (BTK) as a clinically relevant model sys

63 Therapeutic targeting of Bruton tyrosine kinase (BTK) has dramatically improved survival

64 1R)-associated kinase 4 (IRAK4) and Bruton's tyrosine kinase (BTK) in these pathways.

65 Bruton tyrosine kinase (BTK) inhibition is an effective treatme

66 14 confers relative resistance to the Bruton tyrosine kinase (BTK) inhibitor ibrutinib and promotes a

67 sion during or after the receipt of Bruton's tyrosine kinase (BTK) inhibitor therapy have a poor prog

68 Bruton's tyrosine kinase (BTK) is a major drug target for B-cell

69 Bruton's tyrosine kinase (BTK) is a non-receptor tyrosine kinase

70 Bruton's tyrosine kinase (BTK) is an enzyme thought to be essenti

71 Bruton's tyrosine kinase (BTK) is targeted in the treatment of B-

72 Bruton's tyrosine kinase (BTK), a cytoplasmic tyrosine kinase, pl

73 clude genes that modulate NFKB, BCL2, Bruton tyrosine kinase (BTK), and apoptosis.

74 receptor pathway, and specifically of Bruton tyrosine kinase (BTK), is a leading therapeutic strategy

75 c leukemia (CLL) with inhibitors of Bruton's tyrosine kinase (BTK), such as ibrutinib, is limited by

76 binders, affects the degradation of Bruton's Tyrosine Kinase (BTK), we serendipitously discover that

77 onnexin-conductive pathway involving protein tyrosine kinase, but independent from vesicular transpor

78 effect was reproduced in mice lacking Bruton tyrosine kinase, but not in mice treated with 4 weeks of

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

80 nalysis, we observed that the EphB1 receptor tyrosine kinase constitutively interacts with caveolin-1

81 piratory distress syndrome, soluble fms-like tyrosine kinase decreased more quickly and von Willebran

82 vated in cancers through genomic events like tyrosine kinase domain mutations, juxtamembrane splicing

83 imerization domain and the cytosolic protein tyrosine kinase domain of the insulin receptor was not a

84 ion of a differentiation regulatory receptor tyrosine kinase, downregulates the telomerase RNA compon

85 naling with the genetic loss of the receptor tyrosine-kinase-driven terminal signaling patterning in

86 liferative oncogenes, including the receptor tyrosine kinases, EGFR and HER2, and downstream signalin

87 e through engagement of alternative receptor tyrosine kinases either through upregulation of FGF3 or

88 rrently has no known role in normal receptor tyrosine kinase endocytosis, under basal conditions in m

89 ely charged phospho-tyrosine on the receptor tyrosine kinase EphB2.

90 Reducing levels or function of the tyrosine kinase, ephrin type-A receptor 4 (EphA4), has b

91 ins associated with insulin, erb-b2 receptor tyrosine kinase (Erbb), and Toll-like receptor signaling

92 protein-protein interactions, with receptor tyrosine kinase ErbB2, and fundamental and clinical data

93 -malate) targeting against multiple receptor tyrosine kinases, exerts potent antiangiogenesis.

94 factor receptor beta (PDGFRbeta), a receptor tyrosine kinase expressed abundantly in glomerular mesan

95 The ErbB receptor tyrosine kinase family members EGFR (epidermal growth fa

96 NRGs signal through the ErbB receptor tyrosine kinase family.

97 ng driver mutations in the gene encoding the tyrosine kinase FLT3 occur in both leukemias and are par

98 The overexpression of the protein tyrosine kinase, Focal adhesion kinase (FAK), in endothe

99 ctor receptor-beta (PDGFRbeta) is a receptor tyrosine kinase found in cells of mesenchymal origin suc

100 ant synaptic substrates, among which are the tyrosine kinase Fyn and glutamate receptors.

101 locus in the proximity of the gene encoding tyrosine kinase FYN as the most affected region in neuro

102 sed by constitutively active BCR-ABL1 fusion tyrosine kinase, has served as a paradigm for successful

103 age display screen against EphA2, a receptor tyrosine kinase highly expressed in a number of solid tu

104 n the catalytic domain of the ERBB2 receptor tyrosine kinase in a patient with schwannomatosis-associ

105 osphorylation of the target protein Bruton's tyrosine kinase in cells.

106 e of Nef interactions with host cell protein-tyrosine kinases in the broader context of Nef functions

107 ECs) vitreous activates a number of receptor tyrosine kinases including Anexelekto (Axl), which plays

108 iates signaling induced by multiple receptor tyrosine kinases, including signaling by the epidermal g

109 nteractions between VDAC1 and other receptor tyrosine kinases, indicating a novel role for this famil

110 ate that modeling acquired resistance to MET tyrosine kinase inhibition in a MET-amplified gastric ca

111 sitizes primary ALL cells to chemotherapy or tyrosine kinase inhibition in vitro and in vivo.

112 sible, oral epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that potently and s

113 The irreversible ErbB family tyrosine kinase inhibitor (TKI) afatinib plus the EGFR m

114 The development of the tyrosine kinase inhibitor (TKI) imatinib allows patients

115 an therefore be effectively treated with the tyrosine kinase inhibitor (TKI) imatinib mesylate.

116 wing epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant

117 risk of molecular recurrence after stopping tyrosine kinase inhibitor (TKI) treatment substantially

118 vivo deletion of alpha6 in combination with tyrosine kinase inhibitor (TKI) treatment was more effec

119 identified that exhibited potent activity in tyrosine kinase inhibitor (TKI)-sensitive and TKI-resist

120 y and safety of ripretinib, a switch-control tyrosine kinase inhibitor active against a broad spectru

121 ng both BCRs and TLR-MyD88 by using Bruton's tyrosine kinase inhibitor and histone deacetylase inhibi

122 the dual mTORC1/2 inhibitor AZD2014 and the tyrosine kinase inhibitor dasatinib as monotherapies and

123 s differentiation step with an anti-fibrotic tyrosine kinase inhibitor decreases post-myocardial infa

124 o a subset of EGFR-mutant NSCLC to attenuate tyrosine kinase inhibitor delivery to the tumors by limi

125 ta are available, second-line therapy with a tyrosine kinase inhibitor may be recommended for appropr

126 exed and carboplatin chemotherapy to an oral tyrosine kinase inhibitor may improve outcomes.

127 that treatment with a VEGF receptor (VEGFR) tyrosine kinase inhibitor might be effective in patients

128 The tyrosine kinase inhibitor neratinib is a human epidermal

129 hat differ in their mechanism of action (the tyrosine kinase inhibitor pazopanib in MKN45 gastric car

130 g FLT3 inhibitors, such as the multitargeted tyrosine kinase inhibitor sorafenib, improves outcome af

131 Here we report incorporation of sunitinib, a tyrosine kinase inhibitor that blocks VEGF receptors, in

132 ell lymphoma following prior failed Bruton's tyrosine kinase inhibitor therapy, with an overall respo

133 Ibrutinib is a Bruton tyrosine kinase inhibitor with remarkable efficacy again

134 eks of acalabrutinib, a more specific Bruton tyrosine kinase inhibitor, demonstrating that AF is an o

135 nib, a mutant-specific third-generation EGFR tyrosine kinase inhibitor, is emerging as the preferred

136 ither progressed on imatinib and one or more tyrosine kinase inhibitor, or only received imatinib pre

137 emia burden in mice injected with de novo or tyrosine kinase inhibitor-resistant primary Ph+ ALL cell

138 Importantly, we showed that tyrosine kinase inhibitor-resistant tumors, with EGFRT79

139 ify previously unknown targets of a receptor tyrosine kinase inhibitor.

140 growth factor receptor (EGFR)-directed oral tyrosine kinase inhibitor.

141 -cell acute lymphocytic leukaemia in the pre-tyrosine-kinase inhibitor era.

142 f 2 or less, and received no previous Bruton tyrosine-kinase inhibitor therapy.

143 aluating the potential benefit of first-line tyrosine-kinase inhibitor treatment in patients with ABL

144 calabrutinib is a selective, covalent Bruton tyrosine-kinase inhibitor with activity in chronic lymph

145 treated with regimens that do not contain a tyrosine-kinase inhibitor, despite the use of high-risk

146 Lenvatinib, another tyrosine-kinase inhibitor, was found to be non-inferior

147 Acalabrutinib is a selective, potent Bruton tyrosine-kinase inhibitor.

148 PFS than those without these mutations after tyrosine kinase inhibitors (2.1 vs 3.7 months, p < 0.001

149 long-term follow-up data showing that Bruton tyrosine kinase inhibitors (BTKi's) are effective in chr

150 at COVID-19 diagnosis, most commonly Bruton tyrosine kinase inhibitors (BTKi's; n = 68/90 [76%]).

151 Although new generations of EGFR-tyrosine kinase inhibitors (EGFR-TKI) have been develope

152 profile of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs).

153 s in EGFR are proven therapeutic targets for tyrosine kinase inhibitors (TKI) in lung adenocarcinoma,

154 astatic melanoma using immune checkpoint and tyrosine kinase inhibitors (TKI), the majority of stage

155 n of molecularly targeted therapies, such as tyrosine kinase inhibitors (TKI), with concurrent chemot

156 ey obstacle to the clinical efficacy of EGFR tyrosine kinase inhibitors (TKI).

157 FLT3 receptor, including small-molecule FLT3 tyrosine kinase inhibitors (TKIs) and anti-FLT3 antibodi

158 t with the highly effective CML therapeutics tyrosine kinase inhibitors (TKIs) and interferon-alpha (

159 low response rate of those patients to EGFR tyrosine kinase inhibitors (TKIs) are not well understoo

160 ROS1-directed tyrosine kinase inhibitors (TKIs) are therapeutically ac

161 The development of resistance to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with activati

162 Tyrosine kinase inhibitors (TKIs) induce molecular remis

163 In chronic myeloid leukemia (CML) patients, tyrosine kinase inhibitors (TKIs) may select for drug-re

164 Preclinical data suggest that EGFR tyrosine kinase inhibitors (TKIs) plus MET TKIs are a po

165 vestigating the potential of the addition of tyrosine kinase inhibitors (TKIs) to chemotherapy to imp

166 tcome of most patients with CML treated with tyrosine kinase inhibitors (TKIs), a greater number of c

167 tor (EGFR) mutations spurred the use of EGFR tyrosine kinase inhibitors (TKIs), such as erlotinib, as

168 velop drug resistance when treated with EGFR tyrosine kinase inhibitors (TKIs).

169 -185 levels anticipate their response to ABL tyrosine kinase inhibitors (TKIs).

170 ll lymphoma (ALCL) resistant to ALK-specific tyrosine kinase inhibitors (TKIs).

171 r endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs).

172 vascular endothelial growth factor receptor tyrosine kinase inhibitors and may help detect early evi

173 eral epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors have been developed and appro

174 le in vitro data of treatment with different tyrosine kinase inhibitors of BT-20 triple-negative brea

175 Although tyrosine kinase inhibitors provide an effective treatmen

176 Small-molecule tyrosine kinase inhibitors seem well suited to be tailor

177 ications to atezolizumab and/or bevacizumab, tyrosine kinase inhibitors sorafenib or lenvatinib may b

178 The long-term effectiveness of tyrosine kinase inhibitors such as the EGFR inhibitor (E

179 We identified several tyrosine kinase inhibitors that inhibit CAR T-cell cytot

180 ained release platform for local delivery of tyrosine kinase inhibitors to treat corneal NV.

181 The activity of MET tyrosine kinase inhibitors varies by MET alteration cate

182 in patients with EGFR mutations treated with tyrosine kinase inhibitors, HES1 protein levels increase

183 stinal stromal tumour is highly resistant to tyrosine kinase inhibitors.

184 ween Oct 3, 2000, and Aug 28, 2018, in which tyrosine-kinase inhibitors had not been given as a first

185 combination immune checkpoint inhibitor and tyrosine-kinase inhibitors or VEGF inhibitors for increa

186 of (68)Ga-NeoBOMB1 in patients with advanced tyrosine-kinase inhibitors-treated GIST using PET/CT.

187 lass fusions can be targeted successfully by tyrosine-kinase inhibitors.

188 RET receptor tyrosine kinase is a driver oncogene in human cancer.

189 resistance, activation of multiple receptor tyrosine kinases is a known critical factor that contrib

190 e guidance signaling molecule, Abelson (Abl) tyrosine kinase, is to modulate the organization and spa

191 We further show that the activity of the tyrosine kinase ITK acts as a signaling catalyst that ac

192 eters, TCR signal strength (regulated by the tyrosine kinase ITK) and Ag affinity, play important but

193 d inhibitors of KIT proto-oncogene, receptor tyrosine kinase (KIT), and platelet-derived growth facto

194 way, including LCK proto-oncogene SRC family tyrosine kinase (LCK), LYN proto-oncogene SRC family tyr

195 fused Gene (TFG) fused to the 3' end of RET tyrosine kinase leading to a TFG-RET fusion which transf

196 Endocan is known as a receptor tyrosine kinase ligand enhancer in tumorigenesis, but th

197 n protein integrin-alpha2beta1, the receptor tyrosine kinase ligand ephrin-B1, and the classical cadh

198 geting the tumor-associated antigen receptor tyrosine kinase-like orphan receptor 1 (ROR1) infiltrate

199 A receptor tyrosine kinase, receptor tyrosine kinase-like orphan receptor 2 (ROR2), is normal

200 kinase (LCK), LYN proto-oncogene SRC family tyrosine kinase (LYN), zeta chain of T-cell receptor-ass

201 osine kinase (SYK) and Lck/Yes-related novel tyrosine kinase (LYN).

202 cleotide exchange factors (GEFs) or receptor tyrosine kinase-mediated and GEF-dependent RAS activatio

203 e CYP27B1 In multiple sclerosis lesions, the tyrosine kinase MerTK expressed by myeloid cells regulat

204 d the tyrosine kinases of the TAM family Mer tyrosine kinase (MerTK)/Axl.

205 wth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) and Wnt/beta-catenin signaling pat

206 Pathogenic muscle-specific tyrosine kinase (MuSK)-specific IgG4 autoantibodies in a

207 hat is known about the neurotrophic receptor tyrosine kinase (NTRK) genes in cancer was revealed thro

208 different classes of drug targets (receptor tyrosine kinases, nuclear hormone receptors, and cytopla

209 aplastic lymphoma kinase (Alk) is a receptor tyrosine kinase of the insulin receptor super-family tha

210 ways: the purinergic receptor P2Y12, and the tyrosine kinases of the TAM family Mer tyrosine kinase (

211 usions to tumors driven by aberrant receptor tyrosine kinase or RAS signaling.

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

213 which resulted in the activation of Bruton's tyrosine kinase, phospholipase and phosphoinositide-3-ki

214 The present study demonstrates that the Pyk2 tyrosine kinase phosphorylates E2 at tyrosine 131, inter

215 ruton's tyrosine kinase (BTK), a cytoplasmic tyrosine kinase, plays a central role in immunity and is

216 signal transduction cascade through receptor tyrosine kinases, prominently engaging ERK1/2 but also o

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

218 kinase domains from the Wnt-binding receptor tyrosine kinases (PTK7, ROR1, ROR2, and RYK), which play

219 s study, we demonstrate that the nonreceptor tyrosine kinase Pyk2 phosphorylates tyrosine 131 in the

220 hippocampal neurons using a photoactivatable tyrosine kinase receptor (optoFGFR1).

221 Neurotrophic tyrosine kinase receptor 3 (TrkC) is expressed in podocy

222 The tyrosine kinase receptor EphB4 is frequently overexpress

223 In the cerebral cortex, the tyrosine kinase receptor ErbB4 is critical for the wirin

224 in receptor 2 (DDR2) is a collagen-activated tyrosine kinase receptor shown to be essential for skele

225 A receptor tyrosine kinase, receptor tyrosine kinase-like orphan re

226 ion causes an impaired maturation of several tyrosine kinase receptors (RTKs), consistent with a part

227 am of multiple critical tumorigenic receptor tyrosine kinase receptors and oncogenic regulators, incl

228 heral sensory neurons, where it recruits the tyrosine kinase receptors Ror2 and Ryk to modulate dendr

229 ariety of cell surface G-protein coupled and tyrosine kinase receptors.

230 cycle alterations and activation of upstream tyrosine kinase receptors.

231 its effects on neurons by signalling through tyrosine kinase receptors.

232 Activating receptor tyrosine kinase RET (rarranged during transfection) gene

233 Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation

234 Receptor tyrosine kinase (RTK) coexpression facilitates tumor res

235 ssion or activating mutation of the receptor tyrosine kinase (RTK) ERBB2 In some contexts, notably br

236 ngiogenesis inhibitors, such as the receptor tyrosine kinase (RTK) inhibitor sunitinib, target vascul

237 ulators and mutations that activate receptor tyrosine kinase (RTK) signaling frequently occur in blad

238 h factor receptor (EGFR/ERBB1) is a receptor tyrosine kinase (RTK) that forms activated oligomers in

239 Trk-A is a receptor tyrosine kinase (RTK) that plays an essential role in th

240 In glioblastoma, poor efficacy of receptor tyrosine kinase (RTK) therapies has been alternatively a

241 es signaling downstream of multiple receptor tyrosine kinases (RTK) and is required for full activati

242 ified global activation of upstream receptor tyrosine kinases (RTK) that converges on activation of R

243 is scarcely explored downstream of receptor tyrosine kinases (RTK), including the cancer-relevant in

244 All receptor tyrosine kinases (RTKs) activate similar downstream sign

245 Ligand-independent activation of receptor tyrosine kinases (RTKs) allows for dissecting out the re

246 we performed a candidate screen of receptor tyrosine kinases (RTKs) and found a requirement for RTK-

247 The molecular mechanisms by which receptor tyrosine kinases (RTKs) and heterotrimeric G proteins, t

248 Receptor tyrosine kinases (RTKs) are key regulators of cellular f

249 Receptor tyrosine kinases (RTKs) are often overexpressed or mutat

250 Receptor tyrosine kinases (RTKs) are single-pass membrane protein

251 Chlamydia binds several receptor tyrosine kinases (RTKs) on host cells, including the epi

252 Receptor tyrosine kinases (RTKs) play crucial roles in human heal

253 In responses to activation of receptor tyrosine kinases (RTKs), crucial cell fate decisions dep

254 Receptor tyrosine kinases (RTKs), including the FGF receptor, are

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

256 tracellular signaling downstream of receptor tyrosine kinases (RTKs).

257 are also reports of ligand bias for receptor tyrosine kinases (RTKs).

258 the activation of Src family of cytoplasmic tyrosine kinases (SFKs) and two SFK substrates-CUB-domai

259 or of axon guidance signaling, Abelson (Abl) tyrosine kinase, shows that while Abl weakly modulates t

260 d discovered a central role of a nonreceptor tyrosine kinase, spleen tyrosine kinase (SYK), in mediat

261 Using the tyrosine kinase Src as a model, we demonstrate efficient

262 Here, we demonstrate that the tyrosine kinase Src is activated under DNA damage stress

263 delivery of SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) to the plasma membrane and promote

264 omal recruitment of hepatocyte growth factor tyrosine kinase substrate (HRS), which was necessary for

265 by activating mutations in the KIT receptor tyrosine kinase, such as the exon 11 KIT V559Delta mutat

266 s were obtained with mice lacking the spleen-tyrosine kinase Syk in platelets, an essential component

267 ROS generation and spleen tyrosine kinase (Syk) activation induced by heme were cr

268 or to the upstream kinases spleen-associated tyrosine kinase (SYK) and Lck/Yes-related novel tyrosine

269 ed the implication of FcgammaRIIa and spleen tyrosine kinase (Syk) in DC activation and showed that t

270 t al. find a role for the nonreceptor spleen tyrosine kinase (SYK) in upstream signaling leading to I

271 A depletion of Mincle and its adaptor spleen tyrosine kinase (Syk), and Syk pharmacological inhibitio

272 ole of a nonreceptor tyrosine kinase, spleen tyrosine kinase (SYK), in mediating osteomyelitis.

273 nd validated its use for noninvasive in vivo tyrosine kinase-targeted tumor detection in preclinical

274 occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial nitric o

275 ontains the binding motif for endogenous Src tyrosine kinase that constitutively inhibits I(Kv1.5) Di

276 The expression of Fyn, a tyrosine kinase that phosphorylates hnRNPA2, reduces neu

277 on's tyrosine kinase (BTK) is a non-receptor tyrosine kinase that signals downstream of Fc receptors

278 ly kinases (SFKs) are a group of nonreceptor tyrosine kinases that are characterized by their involve

279 Janus kinases (JAKs) are non-receptor tyrosine kinases that are essential components of the JA

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

281 r receptor (EGFR)/ERBB subfamily of receptor tyrosine kinases that regulates cellular processes inclu

282 s (DDRs) constitute a unique set of receptor tyrosine kinases that signal in response to collagen.

283 its, such as point mutations in key receptor tyrosine kinases, that drive drug resistance.

284 gnaling is proximally mediated by Src family tyrosine kinases, the most abundant being Lyn.

285 of G protein-coupled receptors and receptor tyrosine kinases through direct interactions with small

286 Tyrosine kinase (TK) inhibitor, genistein and phosphatid

287 binds to and activates the transmembrane RET tyrosine kinase to signal through intracellular Akt/Erk

288 but also reveal that Axl is one of receptor tyrosine kinases to mediate vitreous-induced angiogenesi

289 They negatively regulate signaling from tyrosine kinases to the Ras-MAPK pathway.

290 adapter protein Nck (noncatalytic region of tyrosine kinase) to the CD3e subunit of the TCR.

291 anine and human gliomas such as the receptor tyrosine kinases, TP53 and cell-cycle pathways, and IDH1

292 er, these results identify ALK as a receptor tyrosine kinase transactivated by D2R that promotes its

293 endothelial growth factor, soluble fms-like tyrosine kinase, von Willebrand factor, E-selectin, inte

294 Since GPCRs can transactivate receptor tyrosine kinases, we also examined if D2R stimulation ac

295 ay serve such a function is the MET receptor tyrosine kinase, which is tightly regulated developmenta

296 The proto-oncogene ROS1 encodes a receptor tyrosine kinase with an unknown physiological role in hu

297 etin-2, angiopoietin-2/angiopoietin-1 ratio, tyrosine kinase with immunoglobulin-like loop epidermal

298 Endothelial (angiopoietin-1, angiopoietin-2, tyrosine kinase with immunoglobulin-like loop epidermal

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

300 The SRC family tyrosine kinase YES1 is upregulated in rhabdomyosarcoma