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

1 uct encoding a protein that has constitutive tyrosine kinase activity.

2 e ABL SH3 and SH2 domains and stimulates ABL tyrosine kinase activity.

3 knowledge of domains that contain intrinsic tyrosine kinase activity.

4 ibit anticarcinogenic activities and inhibit tyrosine kinase activity.

5 levels of activated c-Abl and inhibited its tyrosine kinase activity.

6 substrate coordination, resulting in reduced tyrosine kinase activity.

7 sforming ability through its upregulated Abl tyrosine kinase activity.

8 adic case of LADD syndrome, leads to reduced tyrosine kinase activity.

9 cadherin expression and up-regulated Bcr-abl tyrosine kinase activity.

10 or ROCE, was recently shown to depend on src tyrosine kinase activity.

11 n previously to cause up-regulation of c-Src tyrosine kinase activity.

12 ining a common intracellular domain that has tyrosine kinase activity.

13 s cerebral artery constriction and increases tyrosine kinase activity.

14 ing the nuclear Abl protein and inhibits its tyrosine kinase activity.

15 phoblasts that are less dependent on Bcr/Abl tyrosine kinase activity.

16 ng is not perturbed by altering Pvr receptor tyrosine kinase activity.

17 e hMSH5 P29S variant overactivates the c-Abl tyrosine kinase activity.

18 e in epidermal growth factor receptor (EGFR) tyrosine kinase activity.

19 e activation by nuclear FGFR1 do not require tyrosine kinase activity.

20 by BCR-ABL possesses an aberrantly regulated tyrosine kinase activity.

21 that F-actin exerts a negative effect on Abl tyrosine kinase activity.

22 eraction is strictly dependent upon receptor tyrosine kinase activity.

23 rophy in gene-targeted mice deficient in Bmx tyrosine kinase activity.

24 ibit epidermal growth factor receptor (EGFR) tyrosine kinase activity.

25 tify novel small molecule inhibitors of Jak2 tyrosine kinase activity.

26 ng in constitutive expression of ALK and ALK tyrosine kinase activity.

27 nduced EGFR autophosphorylation and receptor-tyrosine kinase activity.

28 s abolished by inhibition of NO synthase and tyrosine kinase activity.

29 -beta binding to HER3, and inhibition of HER tyrosine kinase activity.

30 ns result in constitutive activation of FLT3 tyrosine kinase activity.

31 c leukemia through the inhibition of BCR-ABL tyrosine kinase activity.

32 pecific homo- and heterodimers with enhanced tyrosine kinase activity.

33 ), the addition of ligands did not stimulate tyrosine kinase activity.

34 spite the absence of detectable FGF receptor tyrosine kinase activity.

35 urotrophic factor, TrkB, by potentiating its tyrosine kinase activity.

36 Electric stimulation also potentiates TrkB tyrosine kinase activity.

37 focused on ligand-receptor interactions and tyrosine kinase activity.

38 te with the KGFR, which is dependent on KGFR tyrosine kinase activity.

39 ive to chemical inhibition of IGF-1 receptor tyrosine kinase activity.

40 ule inhibitors targeting deregulated protein tyrosine kinase activity.

41 hostin AG1478, a specific inhibitor for EGFR tyrosine kinase activity.

42 nted homology oligomerization domain and Abl tyrosine kinase activity.

43 n of the receptor and result in constitutive tyrosine kinase activity.

44 ads to an increase in intrinsic EGF receptor tyrosine kinase activity.

45 pharmacologic antagonists of c-erbB receptor tyrosine kinase activity.

46 o P210(BCR-ABL) expression was caused by its tyrosine kinase activity.

47 receptor (IR), thereby attenuating receptor tyrosine kinase activity.

48 ng activity of these proteins requires their tyrosine kinase activity.

49 uced by P210(BCR-ABL) are independent of its tyrosine kinase activity.

50 g generally occurs through receptors lacking tyrosine kinase activity.

51 partners results in its constitutive protein tyrosine kinase activity.

52 transduction pathways of deregulated protein tyrosine kinase activity.

53 by a mechanism unrelated to VEGFR1 or VEGFR2 tyrosine kinase activity.

54 ne protein with serine and threonine but not tyrosine kinase activity.

55 (4,5)-bisphosphate wave, and requires spleen tyrosine kinase activity.

56 ed CoCsk and found that it has no measurable tyrosine kinase activity.

57 apoptosis in a manner that is independent of tyrosine kinase activity.

58 ion of survival signals, mostly dependent on tyrosine kinase activity.

59 tes autophagy in a process dependent on RIP2 tyrosine kinase activity.

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

61 ding to the stimulation of its intracellular tyrosine kinase activity.

62 nd STI571 application blocked endogenous Abl tyrosine kinase activity.

63 inib is an orally available inhibitor of MEK tyrosine kinase activity.

64 escence can be used as a surrogate for c-Met tyrosine kinase activity.

65 n homology scans, we find that RIP2 also has tyrosine kinase activity.

66 tyrosine phosphorylation is governed by Src tyrosine kinase activity.

67 ed RACK1/IGF-IR binding and increased IGF-IR tyrosine kinase activity.

68 activates STAT3 in part by upregulating JAK2 tyrosine kinase activity.

69 at requires epidermal growth factor receptor-tyrosine kinase activity.

70 nvolved in the stimulation of the receptor's tyrosine kinase activity.

71 omerization of Abl lead to activation of its tyrosine kinase activity.

72 positive for TrkB, the BDNF receptor with a tyrosine kinase activity.

73 ibitors of phosphatidylinositol 3-kinase and tyrosine kinase activity.

74 ase domain where they dramatically increased tyrosine kinase activities.

75 Given this tyrosine kinase activity, a small-molecule inhibitor scr

76 odeling of Kv4.3 channel and increased c-Src tyrosine kinase activity, a stretch-responsive kinase.

77 e targeting VEGFR-2 or inhibition of VEGFR-2 tyrosine kinase activity abolishes P2Y(2)R-mediated VCAM

78 Similarly, inhibition of EGF receptor (EGFR) tyrosine kinase activity abrogated Ang II-stimulated UB

79 Inhibition of Src tyrosine kinase activity abrogated EGF-stimulated Erk ac

80 er, these data indicate that PDGFR-alpha and tyrosine kinase activity act via a common pathway that i

81 ent A431 cells mediated by EGF required EGFR tyrosine kinase activity, actin polymerization, and dyna

82 n synapse formation, as perturbation of EphB tyrosine kinase activity affects the number of synaptic

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

84 Inhibition of C-SRC tyrosine kinase activity also blocks PGE(2)-induced HIF-

85 enite, and that arsenic's suppression of JAK tyrosine kinase activity also occurred in the interferon

86 Inhibition of tyrosine kinase activity also reproduced the effect and

87 ermal growth factor receptor (EGFR), (b) its tyrosine kinase activity and (c) intact autophosphorylat

88 The Dsk5 mutation causes increased tyrosine kinase activity and a decrease in steady-state

89 Both an inhibitor of EGFR tyrosine kinase activity and a neutralizing anti-EGFR an

90 F/P exhibits constitutive tyrosine kinase activity and activates a number of signa

91 osporine) effectively inhibited ZNF198-FGFR1 tyrosine kinase activity and activation of downstream ef

92 se chimeric proteins have constitutive FGFR1 tyrosine kinase activity and are believed to deregulate

93 ene to YTS1 inhibited HGF dose-dependent Met tyrosine kinase activity and cell motility, due to forma

94 ts occurs via a mechanism involving enhanced tyrosine kinase activity and channel endocytosis.

95 /abl, and (1-210) bcr/abl exhibited elevated tyrosine kinase activity and conferred factor-independen

96 protein contains constitutively elevated Met tyrosine kinase activity and constitutes an ideal model

97 ional intermediate possessing intramolecular tyrosine kinase activity and displaying different sensit

98 gfRbeta fusion protein exhibits constitutive tyrosine kinase activity and influences cellular prolife

99 ffectively the drugs inhibit Bcr-Abl protein tyrosine kinase activity and inhibit tumor growth.

100 emonstrate in vitro that ROP16 has intrinsic tyrosine kinase activity and is capable of directly phos

101 This function depends on Ack tyrosine kinase activity and is required cell autonomous

102 This up-regulation required BCR-ABL tyrosine kinase activity and led to IL-3Rbetac/beta chai

103 The opposing actions of tyrosine kinase activity and PKC activity raise the poss

104 2 in unstimulated B cells independent of Lyn tyrosine kinase activity and prevent autoimmune disease

105 role of the 3'-sugar hydroxyl group on trkA tyrosine kinase activity and selectivity.

106 indicate that arsenic directly inhibits JAK tyrosine kinase activity and suggest that this direct in

107 The finding that RIP2 has tyrosine kinase activity and the finding that gefitinib

108 n that this event is dependent on Src family tyrosine kinase activity and the subsequent activation o

109 er these conditions by a mechanism involving tyrosine kinase activity and the urokinase plasminogen a

110 earrangements showed constitutively elevated tyrosine kinase activity and transforming potential that

111 Increased protein tyrosine kinase activity and tyrosine phosphorylation ha

112 Src tyrosine kinase activity and tyrosine phosphorylation of

113 eptors in eukaryotic cells contain intrinsic tyrosine kinase activity and use inter- and intra-molecu

114 with Cbl in osteoclasts was decreased by Src tyrosine kinase activity and we found that destabilizati

115 HIF-1alpha and VEGF expression required TrkB tyrosine kinase activity and were completely blocked by

116 as attenuated by direct inhibition of VEGFR2 tyrosine kinase activity and/or shRNA-mediated knockdown

117 -secretase processing of EphB2 receptor, has tyrosine kinase activity, and directly phosphorylates th

118 JAK2V617F has constitutive tyrosine kinase activity, and is able to transform hemat

119 imulate RhoA activation independently of its tyrosine kinase activity, and mutations within the RhoGE

120 or kinase has recently been shown to possess tyrosine kinase activity, and preventing autophosphoryla

121 hypertonic exposure increased total cellular tyrosine kinase activity approximately 20-fold.

122 P1L1/PDGFRalpha, F/P) and dysregulated c-kit tyrosine kinase activity are associated with systemic ma

123 Inhibitors of EGFR tyrosine kinase activity are being evaluated clinically

124 wth factor receptor (EGFR) and its increased tyrosine kinase activity are implicated in colorectal ca

125 Changes in tyrosine kinase activity are implicated in numerous huma

126 OS and the molecular mechanisms that control tyrosine kinase activity are incompletely understood.

127 sappointingly, inhibitors targeting receptor tyrosine kinase activity are not clinically effective an

128 hose mediated through enhanced c-Src protein tyrosine kinase activity arising from Cas/c-Src interact

129 PDGFRbeta phosphorylation required receptor tyrosine kinase activity, as does PDGFRbeta ubiquitinati

130 ith Met and thereby inhibits HGF-induced Met tyrosine kinase activity, as well as integrin to Met cro

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

132 or HIF-1alpha in a manner that relies on RON tyrosine kinase activity, binding to the c-JUN promoter

133 s with AG1478, a selective inhibitor of EGFR tyrosine kinase activity, blocked the reinitiation of DN

134 However, although inhibition of receptor tyrosine kinase activity blocks EGF-induced nuclear loca

135 dation in a manner that does not require its tyrosine kinase activity both under normal growth condit

136 ese drugs may involve not only inhibition of tyrosine kinase activity but also a dynamic restructurin

137 d binding domains and intracellular receptor tyrosine kinase activity but retains the native amino ac

138 n the context of the FLT3-ITD did not affect tyrosine kinase activity, but abrogated STAT5 activation

139 e 2 pathways of Candida killing required Syk tyrosine kinase activity, but dectin-1 was dispensable f

140 Blocking Src tyrosine kinase activity, but not EGF receptor or JAK fa

141 r pedestal formation in the absence of other tyrosine kinase activity, but they are not necessary.

142 point mutation in EGFR that reduces receptor tyrosine kinase activity by >90%, were studied.

143 Inhibition of protein tyrosine kinase activity by genistein, but not G-protein

144 In addition, inhibition of IGF-IR tyrosine kinase activity by I-OMe-AG538 increased sensit

145 results indicate that inhibition of BCR/ABL tyrosine kinase activity by imatinib mesylate does not e

146 We show that WSTF has intrinsic tyrosine kinase activity by means of a domain that share

147 recordings, we found that inhibition of SFK tyrosine kinase activity by PP2 (4-amino-5-(4-chlorophen

148 Dysregulated tyrosine kinase activity by the Fip1-like1 (FIP1L1)-plat

149 In vitro, the inhibition of c-Kit tyrosine kinase activity by the small molecule tyrosine

150 Interestingly, the tyrosine kinase activity can be measured using the devel

151 ermining whether inhibitors of COX-2 or EGFR tyrosine kinase activity can reduce the risk of tobacco

152 monstrates that inhibition of PDGFB receptor tyrosine kinase activity can significantly impact viabil

153 tosis (BIRC5), and chemokine-related protein tyrosine kinase activity (CCL4).

154 domain (D5) of the ectodomain, rendering KIT tyrosine kinase activity constitutively activated.

155 othelial cells through a TIE2 (receptor with tyrosine kinase activity containing IgG-like loops and e

156 an inhibit this activity suggest that RIP2's tyrosine kinase activity could be targeted specifically

157 Inhibition of EGFR tyrosine kinase activity decreased the generation of ost

158 do not flux calcium nor demonstrate proximal tyrosine kinase activity, deficiencies likely to underli

159 While targeted inhibitors of tyrosine kinase activity demonstrate dramatic efficacy i

160 hibition of epidermal growth factor receptor tyrosine kinase activity did not alter uPA expression.

161 ted IR tyrosine phosphorylation and receptor tyrosine kinase activity did not significantly improve p

162 oward WASP (directed at Ser-242), as well as tyrosine kinase activity directed at Tyr-256.

163 have previously reported the enhancement of tyrosine kinase activities during Salmonella serovar Typ

164 sent study, we have investigated the role of tyrosine kinase activity during early retinal developmen

165 were used to determine the possible role of tyrosine kinase activity during retinal development in v

166 Inhibition of Src tyrosine kinase activity eliminated oxidative stress-ind

167 -MN) synapses, and enhancement of endogenous tyrosine kinase activity facilitates the induction of LT

168 formation and transmembrane receptor protein tyrosine kinase activity gene sets with the modulation o

169 g: (i) the levels of receptor expression and tyrosine kinase activity go up by >50-fold; and (ii) the

170 hibitors of epidermal growth factor receptor tyrosine kinase activity have shown that these targeted

171 of SU11274 as an effective inhibitor of Met tyrosine kinase activity illustrates the potential of ta

172 te cancer demonstrated the enrichment of Src tyrosine kinase activity in approximately 90% of patient

173 was employed as a fluorescent sensor of Abl tyrosine kinase activity in HeLa cell extracts, exhibiti

174 These compounds potently inhibit the RIPK2 tyrosine kinase activity in in vitro biochemical assays

175 ls overexpressing a mutant AATYK that lacked tyrosine kinase activity in low concentrations of KCl.

176 e we present the first large-scale survey of tyrosine kinase activity in lung cancer.

177 AP treatment resulted in an increase in TrkA tyrosine kinase activity in PC12 cells and TrkB activity

178 In vitro, EGFR mutants demonstrated enhanced tyrosine kinase activity in response to epidermal growth

179 FLT3-ITD receptors exhibit constitutive tyrosine kinase activity in the absence of FLT3 ligand (

180 ot bind to the receptor and did not activate tyrosine kinase activity in the presence of an anti-IGF-

181 Further interrogation of the receptor tyrosine kinase activity in these discordant cell lines

182 ating human epidermal growth factor receptor tyrosine kinase activity in vitro and are unable to resc

183 The 50% inhibition of the PDGFRbeta tyrosine kinase activity in vitro by BMS-354825 was obse

184 nsulin receptor (IR) autophosphorylation and tyrosine kinase activity in vitro, in intact cells, and

185 ane domains is important for stabilizing the tyrosine kinase activity in vitro.

186 68-induced inhibition of angiogenic receptor tyrosine kinase activity in vivo is associated with rapi

187 quantitative and dynamic monitoring of EGFR tyrosine kinase activity in xenograft.

188 ppress p185(HER2) oncoprotein expression and tyrosine-kinase activity in breast and ovarian HER2 over

189 that the mutant EPHB4 proteins are devoid of tyrosine kinase activity, indicating that loss of EPHB4

190 Therapeutic inhibition of tyrosine kinase activity induces a retraction of these p

191 Bcr-Abl tyrosine kinase activity initiates a number of intracell

192 ic small-molecule inhibitors of the receptor tyrosine kinase activity (Iressa or Tarceva) has shown c

193 Increased protein-tyrosine kinase activity is a prognostic indicator of de

194 uggested that a predicted constitutive STATc tyrosine kinase activity is counterbalanced in vivo by t

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

196 Taken together, these results suggest that tyrosine kinase activity is essential for regulating neu

197 Thus, increased BCR/ABL oncogenic tyrosine kinase activity is essential for suppression of

198 Bcr-Abl tyrosine kinase activity is essential for the pathogenes

199 Tyrosine kinase activity is essential to lipopolysacchar

200 Receptor tyrosine kinase activity is known to occur in the absenc

201 These findings demonstrate that RIP2 tyrosine kinase activity is not only required for NOD2-d

202 on, raising the question of whether enhanced tyrosine kinase activity is observed in prostate cancer

203 Total tyrosine kinase activity is often elevated in both cytos

204 Tyrosine kinase activity is required for serotonin-induc

205 Since tyrosine kinase activity is stimulated by ligand-induced

206 also called FGFR2-IIIb), which has intrinsic tyrosine kinase activity, is expressed specifically on e

207 ental cells, and by the inhibition of IGF-IR tyrosine kinase activity leading to decreased HER-2 phos

208 Deregulation of c-Met receptor tyrosine kinase activity leads to tumorigenesis and meta

209 Gene sequencing and tyrosine kinase activity measurements demonstrated that

210 and residues, including those necessary for tyrosine kinase activity, mediate the Wnt5a signal.

211 athrin, suggest that the binding and protein tyrosine kinase activities of ACK2 coordinate changes in

212 skeletal and membrane proteins, inhibits the tyrosine kinase activities of both Arg and c-Abl in vitr

213 is study, we showed that E4-ORF1 hijacks the tyrosine kinase activities of cellular epidermal growth

214 We also demonstrate that the tyrosine kinase activities of FGFR2 LADD mutants express

215 Nilotinib inhibits the tyrosine kinase activity of ABL1/BCR-ABL1 and KIT, plate

216 e inhibitor of ALK, we demonstrated that the tyrosine kinase activity of ALK regulates the serine-9 p

217 Constitutive tyrosine kinase activity of Bcr-Abl promotes proliferati

218 A) or aspartate (3D) results in an increased tyrosine kinase activity of c-Abl 3D, and a slight reduc

219 These mutations activate the tyrosine kinase activity of c-KIT and induce constitutiv

220 stone H2A and is mediated by the unsuspected tyrosine kinase activity of casein kinase 2 (CK2).

221 unction on chromatin and is dependent on the tyrosine kinase activity of EGF receptor (EGFR) in the n

222 rovided potent biochemical inhibitors of the tyrosine kinase activity of EGFR, as well as inhibition

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

224 We found that the tyrosine kinase activity of EphBs was required for axon

225 abrogate GA-induced ErbB-2 degradation, the tyrosine kinase activity of ErbB-2 is not disrupted.

226 bility of PSD-95 in the manner that requires tyrosine kinase activity of ErbB4.

227 Targeting the mutation by inhibiting the tyrosine kinase activity of FLT3 is cytotoxic to cell li

228 th types of mutations appear to activate the tyrosine kinase activity of FLT3.

229 We describe here the tyrosine kinase activity of human biliverdin reductase (

230 The tyrosine kinase activity of insulin-like growth factor I

231 -Bbeta is involved in the enhancement of the tyrosine kinase activity of Jak2 following ligand/recept

232 Importantly, the tyrosine kinase activity of NPM-ALK, as assessed by an i

233 otein in COS-1 and Rat-1 cells activated the tyrosine kinase activity of p145 ABL and induced both mo

234 esistance coincides with reactivation of the tyrosine kinase activity of the BCR-ABL fusion oncoprote

235 The deregulated tyrosine kinase activity of the BCR-ABL fusion protein h

236 yeloid leukemia (CML) is due to the abnormal tyrosine kinase activity of the Bcr-Abl oncoprotein.

237 The tyrosine kinase activity of the complex varies with the

238 nduction of TACC3 by EGF is dependent on the tyrosine kinase activity of the EGF receptor (EGFR).

239 ont-rear polarity and chemotaxis require the tyrosine kinase activity of the EGF receptor and are med

240 PD153035, a specific inhibitor of tyrosine kinase activity of the EGF receptor, completely

241 tive disorder that results from dysregulated tyrosine kinase activity of the fusion oncoprotein BCR-A

242 ed as potent and selective inhibitors of the tyrosine kinase activity of the growth factor receptors

243 FSH via PKA acts to sensitize IRS1 to the tyrosine kinase activity of the IGF-1R by activating pro

244 sulin receptor substrate-1 without affecting tyrosine kinase activity of the IGF-IR itself.

245 me Site 1 peptides were able to activate the tyrosine kinase activity of the insulin receptor and act

246 F mutant of p210 Bcr-Abl does not affect the tyrosine kinase activity of the molecule, nor the abilit

247 in forming tetramers, thereby activating the tyrosine kinase activity of the normally silent c-Abl pr

248 This process is dependent on the tyrosine kinase activity of the oncoproteins and is medi

249 zation of EGFR by these ligands involves the tyrosine kinase activity of the receptor itself and c-Sr

250 n receptor and subsequently potentiating the tyrosine kinase activity of the receptor.

251 mechanism is operative independently of the tyrosine kinase activity of the receptor.

252 inase domains, leading to stimulation of the tyrosine kinase activity of the receptor.

253 were generated, which potently inhibited the tyrosine kinase activity of the vascular endothelial gro

254 SU6668 inhibits the tyrosine kinase activity of three angiogenic receptors V

255 ed as potent and selective inhibitors of the tyrosine kinase activity of VEGFR-2 (fetal liver kinase

256 eatment with erlotinib, an inhibitor of EGFR tyrosine kinase activity, on the progression of diabetic

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

258 R) signaling in CLL cells independent of its tyrosine kinase activity or its ability to interact with

259 Inhibition of Src protein-tyrosine kinase activity or mutation of Src phosphorylat

260 Inhibition of Bcr-Abl tyrosine kinase activity or signaling proteins activated

261 The pY peptides inform tyrosine kinase activity, p85 IP informs the activating

262 Studies previously demonstrated that tyrosine kinase activity plays a central role in the con

263 have suggested that constitutively activated tyrosine kinase activity plays an important role for in

264 In addition, general inhibition of receptor tyrosine kinase activity produced a profound global decr

265 tion with anti-phosphotyrosine revealed that tyrosine kinase activity recovered from light-adapted RO

266 that shows elevated and constitutive protein tyrosine kinase activity relative to the normal c-abl ty

267 tures with SU5402, an inhibitor FGF receptor tyrosine kinase activity, rendered FGFs ineffective in i

268 se mechanisms by which inhibition of BCR-ABL tyrosine kinase activity results in generation of antile

269 Receptors with tyrosine kinase activity (RTKs) control tissue growth an

270 been restricted to receptors with intrinsic tyrosine kinase activity such as c-kit and FLT3.

271 horylation results from an intrinsic TbetaRI tyrosine kinase activity that complements its well-defin

272 te (Gleevec, STI-571) is an inhibitor of ABL tyrosine kinase activity that has been remarkably effect

273 signaling modality, independent of receptor tyrosine kinase activity, that couples ErbB4 to decrease

274 veal a function of ErbB4, independent of its tyrosine kinase activity, that modulates postsynaptic in

275 Despite retaining normal levels of tyrosine kinase activity, the RhoGEF mutant of p210 Bcr-

276 actor receptor (EGFR) by down-regulating its tyrosine kinase activity, thereby blocking the growth of

277 RPTP-kappa directly counters intrinsic EGFR tyrosine kinase activity, thereby maintaining EGFR in an

278 described in NSCLC) elevate EGF-independent tyrosine kinase activity, thus providing new insight int

279 Abl SH2 protein reduced the activated c-Abl tyrosine kinase activity to near normal levels and rever

280 addition, the ability of agents that affect tyrosine kinase activity to regulate GAT1 serine phospho

281 pathogen that suppresses Src family protein tyrosine kinase activity to subvert phagocytic signaling

282 or of receptor internalization by recruiting tyrosine kinase activity to the cell surface to phosphor

283 rized by failure to flux calcium or activate tyrosine kinase activity upon contact with cognate tumor

284 n the cell surface and were able to initiate tyrosine kinase activity upon exposure to TPO.

285 able label-free method for detecting protein tyrosine kinase activity using a tyrosinase-based ampero

286 LRP1-deficient fibroblasts, basal PDGFRbeta tyrosine kinase activity was derepressed, and PDGF-BB-in

287 using less than 5 muL of sample, and Abelson tyrosine kinase activity was detectable in samples conta

288 insulin failed to block ADDL binding when IR tyrosine kinase activity was inhibited; in fact, a signi

289 H2O2-induced increase in EGFR tyrosine kinase activity was not observed with the C797S

290 ify pharmacologic agents that inhibit RIP2's tyrosine kinase activity was performed.

291 1 cells, that an incremental increase of Syk tyrosine kinase activity was required and sufficient to

292 We report that most of the amyloid-induced tyrosine kinase activity was stimulated after activation

293 asmic domain antibodies, required Src family tyrosine kinase activity, was independent of inositol tr

294 let-induced epidermal growth factor receptor tyrosine kinase activity, whereas n-acetyl cysteine did

295 The decrease requires tyrosine kinase activity, whereas the subsequent recover

296 tion, and negatively regulated by Src-family tyrosine kinase activity, which restricts the dissociati

297 le, robust, nonradioactive assays of protein tyrosine kinase activity with applications for clinical

298 eonine kinase, BIK1 is shown here to possess tyrosine kinase activity with mass spectrometry, immunob

299 Inhibition of ErbB-4 tyrosine kinase activity with pan-ErbB tyrosine kinase i

300 involves signaling receptors with intrinsic tyrosine kinase activity, yet the underlying molecular m