ライフサイエンスコーパス: PTK

1 PTK can also be used to effectively treat recurrent eros

2 PTK can successfully treat a variety of conditions of th

3 PTK has been shown to regulate the ROMK channel.

4 PTK improved central corneal clarity, alleviated symptom

5 PTK is a minimally invasive procedure that is often succ

6 PTK/ZK infusion did not reduce VEGFR or AKT phosphorylat

7 PTKs in the Csk family, Csk and Chk, are rare exceptions

8 mutations affecting the kinase domains of 19 PTKs and subsequently evaluated the entire coding region

9 oding regions of the genes encoding these 19 PTKs for somatic mutations in 79 melanoma samples.

10 PTK787/ZK 222584 (PTK/ZK) is an oral angiogenesis inhibitor targeting all

11 PTK787/ZK 222584 (PTK/ZK), an orally active inhibitor of vascular endothel

12 PTK787/ZK 222584 (PTK/ZK; vatalanib), an orally active, multitargeted angi

13 We report that the ZAP-70 PTK contains predominately phosphoserine in normal T lym

14 ne residue is conserved only in 8 of the >90 PTKs in the human kinome, including 3 of the 10 Src fami

15 Bath application of lavendustin A, a PTK inhibitor that is structurally unrelated to genistei

16 affected in the presence of herbimycin A, a PTK inhibitor, and was larger in rats that were on a K-d

17 use of this cysteine residue, whereas Csk, a PTK that lacks a cysteine residue at the corresponding p

18 C-terminal Src kinase (Csk) is a PTK that specifically phosphorylates Src family kinases

19 nels by stimulating PTK expression and via a PTK-independent mechanism.

20 eloid leukemia (CML) fusion protein Bcr-Abl, PTKs can promote cancer onset and progression.

21 inase substrate confirmed that the activated PTK could be detected only in flagella isolated from adh

22 horylation by these constitutively activated PTKs.

23 in the expression of Pyk2, an Src-activating PTK.

24 diamond burr polishing, 7 of 7 (100%) after PTK, and 4 of 4 (100%) after epithelial debridement.

25 iamond burr polishing, and 28.6% (2/7) after PTK.

26 mond burr polishing and 28.6% (2 eyes) after PTK.

27 inhibiting development of corneal haze after PTK in rabbits.

28 es (28%) at a mean of 36 and 50 months after PTK, respectively.

29 es (18%) at a mean of 32 and 47 months after PTK, respectively.

30 een correlated to the surgical outcome after PTK.

31 d groups (P <or= 0.05) at 3 to 4 weeks after PTK.

32 All PTKs contain a highly conserved catalytic kinase domain,

33 tion is well recognized; in fact, nearly all PTKs require phosphorylation of tyrosine residues in the

34 Underlying their tight regulation, all PTKs contain multiple regulatory domains in addition to

35 ture structural feature of most, if not all, PTKs.

36 sense mutations in the most commonly altered PTK gene, ERBB4, and found that they resulted in increas

37 Although PTKs have a well-established role in regulating breast c

38 combining gemcitabine with both PKI 166 and PTK 787.

39 nt on transglutaminase, phospholipase C, and PTK, all of which are also required for internalization

40 The discoidin domain and PTK core of DDR-2 were essential for signal transmission

41 r-dependent protein-protein interactions and PTK-mediated signal transduction.

42 l activity through PKC-, NADPH oxidase-, and PTK-dependent pathways under conditions of dietary potas

43 tive management, diamond burr polishing, and PTK, respectively.

44 nhibitors aristolochic acid, quinacrine, and PTK.

45 -docking site has not been determined on any PTK.

46 ion for PTK is still bullous keratopathy, as PTK can be successfully used while waiting for penetrati

47 tudies suggest that VEGFR inhibitors such as PTK/ZK may negatively influence cognition.

48 and dose of angiogenesis inhibitors, such as PTK/ZK, for further clinical development.

49 ysis indicates that PTPs are as important as PTKs in regulating the immune system.

50 ases (PTKs) offers a strategy for augmenting PTK actions.

51 gy and offer a novel approach for augmenting PTK function.

52 hibition with several commercially available PTK inhibitors and a collection of pyridopyrimidine Src/

53 pression of ROMK1 channels, because blocking PTK with herbimycin A abolished the inhibitory effect of

54 Here we show that activation of both PTK and MAPK is involved in the enhancement of HIV-1 inf

55 stigate the regulation of focal adhesions by PTK activity, we examined the effect of lavendustin A on

56 easier to suppress NMDA-elicited feeding by PTK inhibitors, food deprivation readily drives PTK acti

57 ate specificity is thought to be mediated by PTK-substrate docking interactions and recognition of th

58 Ca(2+) current is not directly regulated by PTK activity and that the inhibitory effect of genistein

59 peripheral supramolecular activation cluster PTK: protein tyrosine kinase Signal transduction: bioche

60 than as a simple "off-switch" to counteract PTK activity.

61 which is not treated very well with current PTK techniques, may be addressed better with newer appro

62 n NMDA-R signaling mechanisms, we determined PTK involvement in LHA mechanisms underlying both types

63 ese data indicate that kinases from distinct PTK families are likely responsible for LAT phosphorylat

64 inhibitors, food deprivation readily drives PTK activity in vivo.

65 amilies, we found that the expanding of each PTK family was likely caused by gene or genome duplicati

66 or the fidelity of signal transduction, each PTK phosphorylates only one or a few proteins on specifi

67 Within each PTK gene family, members exhibit functional divergence i

68 actor receptor protein tyrosine kinase (EGFR-PTK) signaling negatively affects transduction by AAV2 v

69 actor receptor-protein-tyrosine kinase (EGFR-PTK), which also restored E1beta protein levels to those

70 s cells contained a high basal level of EGFR-PTK activity that correlated with the high level of ubiq

71 We have also observed that EGFR-PTK can phosphorylate AAV2 capsids at tyrosine residues.

72 ost-translational modification in which EGFR-PTK-mediated tyrosine phosphorylation of the E1beta prot

73 s dependent upon focal adhesion kinase (FAK) PTK, Src PTK and p130Cas adapter protein expression.

74 Two SRC family PTK (SFK)-selective inhibitors, PP2 and SU6656, blocked

75 OMK channels, it is possible that Src family PTK may modulate the effects of SGK1 on WNK4.

76 protein tyrosine kinases (PTKs), Src family PTK, focal adhesion kinase, Rho GTPase Rac1, and neural

77 turn interacts with and activates Src family PTK, thus reducing ROMK activity.

78 The absence of cortical Src-family PTK activity continued until the blastocyst stage when s

79 hocytes, CD19 regulation of other Src family PTKs also influences B cell function and the development

80 that inhibition of NR2B-NMDARs or Src family PTKs in the DMS, but not in the DLS, significantly decre

81 of interactions between CD19 and Src family PTKs in vivo, B cell function was examined in mice defic

82 novel role of Bam32 in connecting Src family PTKs to BCR internalization by an actin-dependent mechan

83 hat Bam32 functions downstream of Src family PTKs to regulate BCR internalization.

84 ther the SH3-dependent binding of Src family PTKs to Shaker family Kvs mediates modulatory events tha

85 macrophages demonstrated that the Src family PTKs were required for this tyrosine phosphorylation act

86 sidues that are phosphorylated by Src family PTKs, enabling the ITAM to recruit activated Syk family

87 These data suggest that while Src-family PTKs are not required for fertilization-induced calcium

88 t the pronuclear stage, activated Src-family PTKs became concentrated around the pronuclei in close a

89 e Fyn construct demonstrated that Src-family PTKs play an essential role in completion of meiosis II

90 of the Src-family PTKs, Lyn, and Src-family PTKs upstream signaling molecules of the p38MAPK pathway

91 ctive, non-phosphorylated form of Src-family PTKs was used to detect these activated kinases by immun

92 antibody to the activated form of Src-family PTKs was used to localize activated Src, Fyn or Yes.

93 Inhibition of the Src-family PTKs, Lyn, and Src-family PTKs upstream signaling molecu

94 chanism of negative regulation of Tec family PTKs is poorly understood.

95 gellar adhesion to activation of a flagellar PTK and cAMP generation during fertilization in Chlamydo

96 s showed that adhesion activated a flagellar PTK that phosphorylated a 105-kDa flagellar protein.

97 et of SH2-containing effectors available for PTK signaling and will facilitate the systems-level anal

98 loping world, the most common indication for PTK is still bullous keratopathy, as PTK can be successf

99 Despite the high levels of Fyn-PTK expression during early OPC differentiation, Fyn def

100 Here we show that Fyn-PTK is significantly up-regulated in early OPC different

101 The latter result may reflect greater PTK recruitment by neurotransmitter receptors, distinct

102 diamond burr polishing, 7 of 166 (4.2%) had PTK, and 4 of 166 (2.4%) had epithelial debridement alon

103 ith the scatterometer suggest that identical PTK treatments indeed result in distinct low- and high-l

104 ecurrent corneal erosion syndrome identified PTK as the most effective treatment.

105 between the % of baseline Ki and increase in PTK/ZK oral dose and plasma levels (P =.01 for oral dose

106 unctional constraint) is a common pattern in PTK gene family evolution.

107 tigen receptor (TCR) signal transduction, in PTKs have been shown.

108 is study tests the hypothesis that increased PTK activity mediates the increased vascular reactivity

109 ing by two novel tyrosine kinase inhibitors, PTK 787 and PKI 166, respectively, can inhibit angiogene

110 tracellular ligand binding and intracellular PTK domains are known, that of the approximately 225-ami

111 excimer laser phototherapeutic keratectomy (PTK) and the specific techniques to best treat each of t

112 Excimer laser phototherapeutic keratectomy (PTK) is an important tool in the management of superfici

113 Phototherapeutic keratectomy (PTK) may be employed in cases wherein visually significa

114 (GCD) prior to phototherapeutic keratectomy (PTK), also calculated the mutation rate of subjects with

115 excimer laser phototherapeutic keratectomy (PTK), and epithelial debridement alone.

116 on the use of phototherapeutic keratectomy (PTK).

117 1 microM) activate a phosphotyrosine kinase (PTK)-dependent pathway.

118 the balance between protein tyrosine kinase (PTK) activation and protein tyrosine phosphatase (PTP) i

119 ent in part through protein-tyrosine kinase (PTK) activation.

120 ecreases Src family protein tyrosine kinase (PTK) activity an inhibitor of ROMK channels, it is possi

121 been suggested that protein tyrosine kinase (PTK) activity can directly regulate cardiac L-type Ca(2+

122 GFR), the intrinsic protein tyrosine kinase (PTK) activity of one receptor monomer is activated, and

123 e have identified a protein-tyrosine kinase (PTK) activity that is stimulated by flagellar adhesion.

124 the contribution of protein tyrosine kinase (PTK) and mitogen-activated protein (MAPK) activation to

125 nction to integrate protein tyrosine kinase (PTK) and phosphatidylinositol 3-kinase (PI3K) signaling

126 Increased levels of protein tyrosine kinase (PTK) are mechanistically associated with increased contr

127 70,000 Mr (ZAP-70) protein tyrosine kinase (PTK) by the CD4/8 coreceptor associated Lck PTK.

128 ltaDS-DDR-2) or the protein tyrosine kinase (PTK) core (DeltaPTK-DDR-2), DDR-2 containing a substitut

129 imulates Src family protein tyrosine kinase (PTK) expression via a superoxide-dependent signaling.

130 ontribution of this protein tyrosine kinase (PTK) family to cell signaling.

131 iquitous Src family protein tyrosine kinase (PTK) Fyn is not activated by these E5 constructs, nor ar

132 nal analysis of the protein tyrosine kinase (PTK) gene family in cutaneous metastatic melanoma.

133 were blocked by the protein tyrosine kinase (PTK) inhibitor genistein, by the MAP kinase kinase (MEK)

134 The protein tyrosine kinase (PTK) inhibitors lavendustin A and genistein were used to

135 bryos with chemical protein tyrosine kinase (PTK) inhibitors such as 4-amino-5-(4-chlorophenyl)-7-(t-

136 Cancer-associated protein tyrosine kinase (PTK) mutations usually are gain-of-function (GOF) mutati

137 nt role in cellular protein tyrosine kinase (PTK) signaling pathways.

138 cancer by promoting protein-tyrosine kinase (PTK) signaling.

139 The protein tyrosine kinase (PTK) supergene family is the key mediator in cellular si

140 lates an Src family protein-tyrosine kinase (PTK) via PKC-NADPH oxidase.

141 Fyn protein-tyrosine kinase (PTK), a member of the Src-PTK family, is essential for m

142 encodes a putative protein tyrosine kinase (PTK), and the second, epsA, encodes a putative polysacch

143 ires the Src family protein tyrosine kinase (PTK), Fyn.

144 family cytoplasmic protein tyrosine kinase (PTK), is required to couple the activated T-cell antigen

145 minal kinase (JNK), protein tyrosine kinase (PTK), phosphatidylinositol 3-kinase (PI3K), protein kina

146 in kinase C (PKC)-, protein tyrosine kinase (PTK)-, and nitric oxide (NO)-mediated pathways were foun

147 monstrated that the protein tyrosine kinase (PTK)-dependent signal transduction pathway is an importa

148 g ROMK1 channels by protein-tyrosine kinase (PTK).

149 to an inhibition of protein tyrosine kinase (PTK).

150 kinase A (PKA), and protein tyrosine kinase (PTK).

151 ), and genistein (a protein tyrosine kinase [PTK] inhibitor).

152 phosphorylated by protein tyrosine kinases (PTK) and binds to the adaptors Gads and Grb2, as well as

153 Protein tyrosine kinases (PTK) are key enzymes of mammalian signal transduction.

154 rk in concert with protein tyrosine kinases (PTK) in controlling cellular homeostasis.

155 in tyrosine phosphatases (PTPs) and kinases (PTKs), is important in signaling pathways underlying tum

156 -terminal sites by protein tyrosine kinases (PTKs) and C-type protein kinases (PKCs).

157 ghtly regulated by protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs), and has

158 nter-activities of protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs).

159 rdinated action of protein-tyrosine kinases (PTKs) and protein-tyrosine phosphatases (PTPs), is a fun

160 rowth factors, and protein tyrosine kinases (PTKs) and regulates the transcription of many genes.

161 ave identified the protein-tyrosine kinases (PTKs) and their substrates required for LPS-induced prot

162 wn to inhibit both protein-tyrosine kinases (PTKs) and tubulin polymerization.

163 not clear whether protein tyrosine kinases (PTKs) are also directly regulated by reduction/oxidation

164 Protein-tyrosine kinases (PTKs) are important regulators of intracellular signal-t

165 Protein tyrosine kinases (PTKs) are important regulators of mammalian cell functio

166 APK, provided that protein tyrosine kinases (PTKs) are inhibited.

167 ow that Src-family protein tyrosine kinases (PTKs) bind to heteromultimeric Shaker-family voltage-gat

168 itor of Src family protein tyrosine kinases (PTKs) blocked both BCR-induced tyrosine phosphorylation

169 Regulation of protein tyrosine kinases (PTKs) by tyrosine phosphorylation is well recognized; in

170 Abnormal protein tyrosine kinases (PTKs) cause many human leukemias.

171 vity of Src-family protein tyrosine kinases (PTKs) during zygotic development in the mouse.

172 active Src family protein tyrosine kinases (PTKs) in these eukaryotic cells.

173 he TCR of a set of protein tyrosine kinases (PTKs) is an early event in this process.

174 ents by Src family protein tyrosine kinases (PTKs) is considered a canonical example of this type of

175 ) counterbalancing protein-tyrosine kinases (PTKs) offers a strategy for augmenting PTK actions.

176 Because protein-tyrosine kinases (PTKs) participate in NMDA-R signaling mechanisms, we det

177 Protein tyrosine kinases (PTKs) play an important role in T cell development and a

178 t the functions of protein-tyrosine kinases (PTKs) than about protein-tyrosine phosphatases (PTPs).

179 inase C (PKC), Src protein tyrosine kinases (PTKs), and nuclear factor-kappaB (NF-kappaB) but not by

180 roteins, including protein tyrosine kinases (PTKs), in a phosphorylation-dependent manner.

181 nositol-3'-kinase, protein tyrosine kinases (PTKs), Src family PTK, focal adhesion kinase, Rho GTPase

182 phosphorylation by protein tyrosine kinases (PTKs), such as c-Abl, is critical to cellular homeostasi

183 The Tec family of protein-tyrosine kinases (PTKs), that includes Tec, Itk, Btk, Bmx, and Txk, plays

184 ogenic nonreceptor protein-tyrosine kinases (PTKs), v-Src and v-Yes, was dramatically reduced in nona

185 over the activity of split-tyrosine kinases (PTKs).

186 the activities of protein-tyrosine kinases (PTKs).

187 million-year-old (Ma) Philip Tobias Korongo (PTK) site at Olduvai Gorge (Tanzania).

188 he eye is a good candidate for excimer laser PTK.

189 (PTK) by the CD4/8 coreceptor associated Lck PTK.

190 e signaling pathway required by leukemogenic PTKs may improve the treatment of primary and relapsed C

191 d in Lyn-deficient mice, suggesting that Lyn PTK has a unique function not compensated for by other S

192 have not been previously associated with Lyn PTK signaling.

193 er conducting phylogenetic analysis on major PTK gene families, we found that the expanding of each P

194 ng massed training in the Morris water maze, PTK/ZK impaired spatial memory retention tested 48 h lat

195 Here we report a novel PTK activity and inhibition screening method using hydro

196 Oral administration of PTK/ZK decreased xenograft head and neck tumor microvess

197 uestioned if post-training administration of PTK/ZK influences hippocampus-dependent memory.

198 emcitabine alone, or with the combination of PTK 787, PKI 166, and gemcitabine produced 69, 50, and 9

199 The maximum-tolerated oral dose of PTK/ZK is 750 mg orally bid.

200 help to define a biologically active dose of PTK/ZK.

201 groups of mice began receiving oral doses of PTK 787 and PKI 166 three times weekly.

202 rly important for the synergistic effects of PTK inhibitor/rapamycin combinations.

203 The pharmacodynamic effects of PTK/ZK were evaluated by assessing changes in contrast-e

204 2+) channel activity is due to inhibition of PTK activity.

205 LHA injections of PTK inhibitors significantly suppressed feeding elicited

206 tients need to understand the limitations of PTK for proper informed consent.

207 t studies confirm the beneficial outcomes of PTK in a variety of anterior corneal disorder: anterior

208 Suppression of PTK by herbimycin A significantly attenuated the inhibit

209 creases the ligand-independent activation of PTKs and induces protein-tyrosine phosphatase (PTP) inac

210 TPs do not always antagonize the activity of PTKs in regulating tyrosine phosphorylation, but can als

211 illustrate how the combinatorial effects of PTKs and PTPs may be integrated to regulate signaling, w

212 In contrast, the phosphorylation of PTKs on serine and threonine residues has not been studi

213 mediating the effect of superoxide anions on PTK expression and ROMK (Kir 1.1) channel activity.

214 combining gemcitabine with either PKI 166 or PTK 787 were similar to those produced by combining gemc

215 m that does not involve estrogen receptor or PTK.

216 Doses of oral PTK/ZK ranged from 50 to 2000 mg once daily.

217 structure-function studies of Csk and other PTKs.

218 erapy for CML has inspired interest in other PTKs as targets for cancer drug discovery.

219 idue in domain-domain communication in other PTKs, was found to be important for maintaining the acti

220 understanding substrate specificity in other PTKs.

221 ses, and essential for the activity of other PTKs so far tested, is not important for Csk activity.

222 associated with mutant and/or overexpressed PTKs.

223 ase inhibitor to rapamycin or rapamycin plus PTK inhibitor further increases efficacy.

224 Cataract extraction, LASIK, PRK, PTK, and various combination procedures have been shown

225 ocal adhesion kinase and endogenous receptor PTKs for insulin, epidermal growth factor, basic fibrobl

226 family receptors and growth factor receptor PTKs in general.

227 small-molecule inhibitor of VEGF receptors (PTK/ZK) on the initial stages of head and neck tumor ang

228 ired subsequent treatment with either repeat PTK or with more invasive surgery such as lamellar or pe

229 kinase activity, to be critical for the Ros-PTK-induced anchorage-independent growth.

230 Both TRAF and SF-PTK signal transductions induced by STP-A were required

231 and Src family protein tyrosine kinases (SF-PTKs) in a genetically and functionally separable manner

232 the other hand, interaction of STP-A with SF-PTKs through its SH2 binding motif effectively elicited

233 Given the activating role that some PTKs play in initiating growth factor-mediated cellular

234 dox regulation conserved in certain specific PTKs.

235 e-dependent manner, and prior broad spectrum PTK inhibition was protective.

236 trol over the activity of user defined split-PTKs and split-PTPs.

237 c PC upregulates cardiac COX-2 via PKC-, Src PTK-, and NF-kappaB-dependent signaling pathways, wherea

238 nt upon focal adhesion kinase (FAK) PTK, Src PTK and p130Cas adapter protein expression.

239 e shown to be phosphorylated by purified Src PTK in vitro.

240 does not transform NIH3T3 cells in which Src PTK activity is maintained at a basal level by means of

241 arked increases in apparent activity for Src PTKs and in the expression of Pyk2, an Src-activating PT

242 Inhibition of the Src PTKs, MAPK, and NF-kappaB activities by Rituximab or by

243 and MBP mRNA was negatively regulated by Src-PTK-dependent phosphorylation of QKI.

244 Therefore, developmental regulation of Src-PTK-dependent tyrosine phosphorylation of QKI suggests a

245 n-tyrosine kinase (PTK), a member of the Src-PTK family, is essential for myelin development in the c

246 the Src family protein tyrosine kinases (Src-PTKs) during CNS myelination.

247 A low-K intake stimulates PTK activity, which leads to increase in phosphorylation

248 MAPK inhibit the SK channels by stimulating PTK expression and via a PTK-independent mechanism.

249 lial ablation, followed by a 100-mum stromal PTK.

250 In this phase I dose-escalating study, PTK/ZK was administered bid to exploit the theoretical a

251 BCR-dependent activation of the SYK PTK initiates downstream signaling events and amplifies

252 9 eyes) underwent epithelial removal using t-PTK (group 1) and 18 patients (19 eyes) underwent mechan

253 Epithelial removal using t-PTK during CXL results in better visual and refractive o

254 TEL) transcription factor to the C-terminal PTK (protein-tyrosine kinase) domain of the neurotrophin

255 ent of THP-1 cells with inhibitors of TGase, PTK, and PLC.

256 Pharmacokinetic data confirmed that PTK/ZK exposure increased with increasing dose up to 500

257 Analysis of these data demonstrates that PTK/ZK blocks downstream targets of VEGF signaling in en

258 E-MRI and pharmacokinetic data indicate that PTK/ZK >/= 1,000 mg total daily dose is the biologically

259 These data show that PTK and MAPK activation by the presence of O(-)(2) contr

260 ling in endothelial cells, and suggests that PTK/ZK may inhibit the angiogenic switch in head and nec

261 d deprivation feeding (24%), suggesting that PTKs may be less critical for signals underlying this fe

262 r protein kinesin-II, failed to activate the PTK at elevated temperatures.

263 ype in dibutyryl cAMP failed to activate the PTK.

264 ch impairment was partially prevented by the PTK inhibitor, genistein, the MAPK (ERK isoform) inhibit

265 f EN leads to constitutive activation of the PTK domain and constitutive signaling of the Ras-MAPK an

266 n the N-terminal and C-terminal lobes of the PTK domain that allows the short CT domain sequence teth

267 ble both the trans-stilbene structure of the PTK inhibitor piceatannol and the cis-stilbene structure

268 Application of the PTK inhibitors blocked focal adhesion assembly in these

269 s was reversed by cumulative addition of the PTK inhibitors genistein (1-30 microM) and tyrphostin 47

270 Our results indicate that stimulation of the PTK is a very early event during fertilization.

271 Instead, activation of the PTK signaling pathway is dependent on the expression of

272 Activation of the PTK was blocked when gametes underwent flagellar adhesio

273 o a large extent on the observation that the PTK inhibitor genistein can inhibit the cardiac L-type C

274 domain sequence tethering P-site-992 to the PTK core to reach the catalytic site.

275 rect oxidative inactivation specific for the PTKs in the Src and fibroblast growth factor receptor (F

276 has resulted in prolonged activation of the PTKs and, therefore, has been implicated in inflammatory

277 The cell surface expression levels of the PTKs are regulated by Cbl-mediated ubiquitination, inter

278 nd Fyn activity suggests activation of these PTKs is solely responsible for the phenotype observed in

279 ews some of the critical substrates of these PTKs, the adapter proteins that, following phosphorylati

280 This PTK signaling pathway can be activated independently of

281 g the specificity of signals induced by this PTK, rather than as a simple "off-switch" to counteract

282 ZAP70, one of those PTKs, is a 70-kDa tyrosine phosphoprotein and associates

283 and anterior stromal lesions respond best to PTK.

284 However, resistance to PTK inhibitors is a major emerging problem that may limi

285 mm-diameter, 150-microm-deep transepithelial PTK, performed with a clinical 193-nm ArF excimer laser

286 OCT-guided transepithelial PTK using a dual ablation excimer laser profile can prov

287 wman layer who had undergone transepithelial PTK according to a novel protocol were reviewed.

288 ter phototherapeutic keratectomy treatments (PTK) in 32 pigmented rabbits.

289 creased neurite outgrowth, and augmented Trk PTK-mediated responses to nerve growth factor (NGF), a p

290 s with granular corneal dystrophy undergoing PTK, in an effort to prevent iatrogenic ectasia.

291 All patients underwent PTK for decreased vision, symptoms of recurrent erosions

292 mprised patients with no graft who underwent PTK (22 eyes of 15 patients), and group 2 comprised pati

293 and group 2 comprised patients who underwent PTK over a previous full-thickness graft (18 eyes of 14

294 In vitro, PTK/ZK blocked head and neck tumor cell (OSCC3 or UM-SCC

295 and ORR were not statistically improved with PTK/ZK (P > .05).

296 ntial marker of hypoxia, PFS was longer with PTK/ZK versus placebo (7.7 v 5.8 months, respectively; H

297 3; P = .118); median OS was 21.4 months with PTK/ZK versus 20.5 months with placebo (HR, 1.08; 95% CI

298 an PFS by central review was 7.7 months with PTK/ZK versus 7.6 months with placebo (hazard ratio [HR]

299 Treatment with PTK 787 and PKI 166, with gemcitabine alone, or with the

300 PTK787/ZK222584 (PTK/ZK) is a reported inhibitor of VEGFR signaling that