ライフサイエンスコーパス: TK

1 TK activity increased 3 logs in hTK1 TGs, but no cardiac

2 am/1203/04 (VN; clade 1) and A/Turkey/15/06 (TK; clade 2.2) influenza viruses containing the H274Y ne

3 etic and functional variability of the HSV-1 TK gene pool in paired trigeminal ganglia (TG) of 5 immu

4 rpes simplex virus 1 thymidine kinase (HSV-1 TK).

5 stitutions (ie, nonsynonymous changes) in 14 TK genes, including TYK2, which had the largest number o

6 adjustments yielded single diastereomers 14 (TK-666) and 46, showing a broad antibacterial spectrum a

7 by fusing the mitochondria DNA depleted 143B TK- rho0 cells from an aggressive osteosarcoma cell line

8 different oncogenic characteristics of 143B TK(-) cell including cell proliferation, viability under

9 put resequencing of the kinase domains of 26 TK genes (11 receptor TK; 15 cytoplasmic TK) expressed i

10 reveals the first atomic structure of both a TK and a PK with a bilobal structure.

11 rcially available products, pyrophosphate, a TK cofactor analog and d-arabinose-5-phosphate, a substr

12 ly selected genetically stable variants of A/TK/OR/71-delNS1[1-124] (H7N3) that differed only in the

13 losely related variants of influenza virus A/TK/OR/71 that differed primarily in the size of the NS1

14 , Vav3 activation only partly depends on ABL TK activity, and Vav3 deficiency collaborates with tyros

15 However, this mutation does not abolish TK activity, which is important for pathogenicity.

16 kably, this appeared to be sufficient active TK to support a low level of reactivation from latently

17 First-generation Ad-TK failed to elicit tumor regression in this model.

18 results pave the way for implementing HC-Ad-TK-mediated gene therapy as a powerful adjuvant for trea

19 and downstream process development of HC-Ad-TK/TetOn-Flt3L for a future phase I clinical trial for G

20 The bicistronic HC-Ad-TK/TetOn-Flt3L was delivered into intracranial gliomas i

21 ytotoxic/immune-stimulatory gene therapy (Ad-TK and Ad-Flt3L) elicits tumor regression and immunologi

22 different cell lines (renal adenocarcinoma (TK-10), breast adenocarcinoma (MCF-7) and melanoma (UACC

23 T and TUNEL assays elucidated that pEpo-AFPL-TK transfected cells showed significant increasing of de

24 The pEpo-AFPL-TK was transfected into hepatoma cell lines in the prese

25 hat the P/Q Ca2+ channel antagonist agatoxin TK (250 nm) abolished GABA release from PV+ basket cells

26 he brain revealed arborizations of AstA- and TK-positive neurons in primary sensory processing center

27 ofluorescence staining against AstA, AT, and TK in the brain revealed arborizations of AstA- and TK-p

28 enzyme genes Gss and Ggt in GC-2 cells, and TK, SMS and Glna in TM-4 cells reinforced these findings

29 satory effect on the fitness of VN-H274Y and TK-H274Y viruses.

30 enin were the major flavonoids in the KT and TK cultivars.

31 ls and hepatocytes from wildtype (TK+/+) and TK-/- mice were studied.

32 f four suicide genes including TK (TK007 and TK(SR39) mutants), yeast cytosine deaminase:uracil phosp

33 ved in dNTP synthesis (i.e., RNR2, TYMS, and TK-1).

34 Additional studies with another TK inhibitor, PLX647 (targeting c-Kit and c-Fms) or an a

35 in Abeta burden or APP processing in APPPS1;TK mice.

36 rying APPPS1 mice crossed to TK mice (APPPS1;TK).

37 ung cancer, suicide gene therapy with LV-ARE-TK/GCV was effective compared with LV-PGK-TK/GCV in redu

38 s method was shown to be useful for assaying TK activity in a broad range of biochemically relevant s

39 WHO-defined group of eosinophilia-associated TK fusion-driven neoplasms.

40 hia coli (TKec) using commercially available TK substrates, namely d-fructose-6-phosphate a physiolog

41 H/GCE biosensor was optimized using the best TK donor substrates, namely l-erythrulose and d-fructose

42 for nucleoside analog development, T. brucei TK was less discriminative against purines than human TK

43 T. brucei TK was primarily monomeric but can be considered a two-d

44 H274Y virus were milder than those caused by TK-WT virus, and all animals survived.

45 thymidine kinase (TK), but not the cellular TK.

46 In CEM/TK(-) cell cultures the difference in antiviral potency

47 activity in CEM/0 and strong activity in CEM/TK(-) cell cultures.

48 Control and chimeric TK-NOG mice with humanized livers were treated orally wi

49 liver toxicity could be detected in chimeric TK-NOG mice with humanized livers.

50 ity could be readily detected using chimeric TK-NOG mice with humanized livers, even when the mice we

51 After a first wave of circulating TK+ cells, the majority of T cells supporting long-term

52 This comprehensive TK transcriptomic reference, and large set of SNPs inclu

53 e course and variable sensitivity to current TK inhibitors, and in most cases, long-term disease-free

54 The expression of cyclic TK (cTK) in healthy cells leads to inactive product, whe

55 26 TK genes (11 receptor TK; 15 cytoplasmic TK) expressed in most AML patients using genomic DNA fro

56 entricular zone (SVZ) and hippocampus of DCX-TK transgenic mice, but not wild-type mice, were specifi

57 GCV treatment of Dcx-TK transgenic, but not WT, mice also increased infarct s

58 inase under control of the DCX promoter (DCX-TK transgenic mice).

59 vere in GCV- compared to vehicle-treated DCX-TK transgenic mice at first 8 weeks, after depletion of

60 wild-type or Ron tyrosine kinase deficient (TK(-/-); Mst1r(-/-)) hosts.

61 r in silico analysis of known cancer-derived TK fusions revealed that most breakpoints occur within a

62 s using either in vitro or in silico derived TK parameters and can be thought of as an important step

63 heless, G8 and G9 mutants express detectable TK activity and can reactivate from latency in mice, a p

64 of the Ron tyrosine kinase signaling domain (TK-/-) was undertaken to determine the influence of Ron

65 is urgent need to characterize dysregulated TK signaling axes in patients with ALL and identify acti

66 V-PK), the EBV-encoded thymidine kinase (EBV-TK), or both is controversial.

67 the Epstein-Barr virus thymidine kinase (EBV-TK).

68 Thus, EBV-PK but not EBV-TK mediates ACV and GCV susceptibilities.

69 ning stop codons in either the EBV-PK or EBV-TK open reading frame and selected for stable 293T clone

70 tumors that constitutively expressed the EBV-TK.

71 Gefitinib and erlotinib are EGFR TK inhibitors (EGFR TKIs) and have antitumor activity in

72 ER2 induces a more potent activation of EGFR TK than does EGFR homodimerization.

73 ith dramatic and sustained responses to EGFR TK inhibitors (TKIs) has allowed the design of trials to

74 not show covalent binding to cell-free EGFR-TK in a fluorescence assay, while it underwent selective

75 ing to show how small molecules inhibit EGFR-TK activity and will aid development of EGFR-TK mutant t

76 heir acrylamide analogues in inhibiting EGFR-TK (TK = tyrosine kinase) autophosphorylation in A549 lu

77 Growth Factor Receptor tyrosine kinase (EGFR-TK), in in-vitro assay.

78 Erlotinib) into the ATP binding site of EGFR-TK domain (PDB ID:1M17) to elucidate vital structural re

79 echanisms by which proper regulation of EGFR-TK is lost in disease.

80 TK activity and will aid development of EGFR-TK mutant targeted therapies.

81 e expected to affect the development of EGFR-TK targeted small molecule kinase inhibitors.

82 nisms of activation for L858R and other EGFR-TK mutations, and compare these distinct activating mech

83 re crystal structures published for the EGFR-TK domain than for any other TK.

84 ing and treatment of malignancies where EGFR-TK is improperly activated.

85 pared to strains expressing insoluble EphB2 (TK domain) or ketosteroid isomerase (KSI).

86 shifting can explain this ability to express TK.

87 , Fc gammaRI colocalized with the Src family TK Hck in F-actin-rich structures, which was enhanced in

88 ure, and peritoneal macrophage isolated from TK-/- mice exhibited blunted production of monocyte chem

89 Neutrophils isolated from TK-/- mice exhibited decreased spontaneous oxidative bur

90 ontrast, patients with FGFR1 and JAK2 fusion TK genes exhibit a more aggressive course and variable s

91 ystems such as thymidine kinase/ganciclovir (TK/GCV), yeast cytosine deaminase/5-fluorocytosine (yCD/

92 ssing the HSV thymidine kinase suicide gene (TK+ cells).

93 we also demonstrate that one of these genes, TK, encodes an enzyme that is capable of activating know

94 ne the roles that these somatic and germline TK gene variants play in AML pathogenesis.

95 geted therapies in tumors that do not harbor TK sensitizing mutations in order to identify markers ca

96 f herpes simplex virus thymidine kinase (HSV TK).

97 cation of ACV can successfully modify an HSV-TK-dependent antiviral drug into an anti-tumor drug.

98 reporter genes (hNET-CD4(+) T cells and HSV-TK-CD8(+) T cells) in the same animal using three-dimens

99 In this setting, ARE-HSV-TK was more effective than a vector in which HSV-TK expr

100 attributed to non-glial toxicity in Gfap(HSV-TK) mice and epithelial-cell expression of GFAP.

101 t, administration of ganciclovir to Gfap(HSV-TK) mice eliminated fewer glia but caused considerable n

102 eliminated glia with ganciclovir in Gfap(HSV-TK) mice.

103 e herpes simplex virus thymidine kinase (HSV-TK) "suicide gene," we demonstrate Smad4-responsive regu

104 , herpes simplex virus thymidine kinase (HSV-TK) gene was introduced for cancer cell killing.

105 d herpes simplex virus-thymidine kinase (HSV-TK) promoter was strongly repressed in the human, but no

106 herpes simplex virus 1 thymidine kinase (HSV-TK).

107 g herpes simplex virus thymidine kinase (HSV-TK/GCV) under the regulation of antioxidant response ele

108 e of injury with ganciclovir in a nestin-HSV-TK transgenic model, we eliminated injury-induced neurog

109 monstrate Smad4-responsive regulation of HSV-TK expression and consequent altered susceptibility to t

110 vector system, a robust differential of HSV-TK expression and GCV toxicity was attained depending on

111 fficient in killing cells independent of HSV-TK.

112 We conclude that ARE-regulated HSV-TK/GCV therapy offers a promising approach for suicide c

113 as more effective than a vector in which HSV-TK expression was driven by a constitutively active prom

114 The differential activity of the HSV1 TK gene and WPRE sequences was detected both in vitro an

115 rapeutic transgenes, i.e., constitutive HSV1-TK and inducible Flt3L genes.

116 simplex virus type 1 thymidine kinase (HSV1-TK) and inducible Tet-mediated expression of Flt3L withi

117 erpes simplex virus 1-thymidine kinase (HSV1-TK) PET reporter whose kinase activity is specifically s

118 ontrast, herpes virus thymidine kinase (HSV1-TK) readily activates ACV.

119 simplex virus type-1 thymidine kinase (HSV1-TK).

120 its feasibility for in vivo imaging of HSV1-TK.

121 es was monitored by microPET imaging of HSV1-TK/GFP expression with [(18)F]FEAU and by a more sensiti

122 ely accumulated in cells expressing the HSV1-TK protein and there was negligible uptake in control ce

123 idine kinase (dCK), which is related to HSV1-TK and phosphorylates deoxyguanosine, does not accept ac

124 e now show that KSHV-TK, in contrast to HSV1-TK, associates with the actin cytoskeleton and induces e

125 In comparison to ACV binding to HSV1-TK, in dCK, the nucleoside base adopts a different orien

126 osides have the potential to be in vivo HSV1-TK PET reporter probes over a dynamic range of reporter

127 lation of resident microglia in CD11b-HSVTK (TK) mice is followed by a rapid repopulation of the brai

128 stematically for fusions within the 90 human TKs; it should detect 92% of known TK fusions.

129 the feasibility of this approach to identify TK fusions across multiple human cancers in a high-throu

130 Unlike other type II TKs, the Trypanosoma brucei enzyme (TbTK) is a tandem pr

131 In TK(-/-) hosts, prostate cancer cell growth was significa

132 tly reduced as compared with tumor growth in TK(+/+) hosts.

133 Hepatocyte protection in TK-/- mice was observed despite paradoxically elevated s

134 Prostate tumors in TK(-/-) hosts exhibited an increase in tumor cell apopto

135 ress a panel of four suicide genes including TK (TK007 and TK(SR39) mutants), yeast cytosine deaminas

136 Interestingly, TK-/- TRAMP+ mice show a significant decrease in prostat

137 We show that isolated TK-/- Kupffer cells produce increased levels of TNF-alph

138 ay inhibitors to perturb ABL1, FLT3, and JAK TK signaling in four xenografted patient samples.

139 own somatic mutations in FLT3, KIT, and JAK2 TK genes at the expected frequencies and found 4 novel s

140 Treatment with the JAK2 TK inhibitor TG101209 attenuated JAK2V617F autophosphory

141 impact was found for FCR, thymidine kinase (TK) >/=10 U/L, unmutated IGHV, 11q deletion, 17p deletio

142 was established using the thymidine kinase (TK) 1(+) wild-type, murine L929 cell line and its TK1(-)

143 ive method for quantifying thymidine kinase (TK) activity that is compatible with both purine and pyr

144 roduce dTMP, one involving thymidine kinase (TK) and the second via thymidylate synthase-dihydrofolat

145 The thymidine kinase (TK) encoded by Epstein-Barr virus (EBV) differs not only

146 Paradoxically, the thymidine kinase (TK) encoded by Kaposi sarcoma-associated herpesvirus (KS

147 s simplex virus (HSV) gene thymidine kinase (TK) gene lead to acyclovir (ACV) resistance.

148 n frequency as detected by thymidine kinase (TK) gene mutation assay.

149 implex virus type 1 (HSV1) thymidine kinase (TK) gene sequences (1,131 bp) fused to the 3' end of lac

150 enes [herpes simplex virus-thymidine kinase (TK) gene] when the adoptively transferred MSC developed

151 erpes simplex virus type 1-thymidine kinase (TK) induce tumor regression and long-term survival in an

152 Thymidine kinase (TK) is a key enzyme in the pyrimidine salvage pathway wh

153 nicity was assessed at the thymidine kinase (TK) locus, CYP1A activity was determined by ethoxyresoru

154 with herpes simplex virus thymidine kinase (TK) PET reporter gene.

155 in genes where two or four thymidine kinase (TK) sequences are fused into a single open reading frame

156 press herpes simplex virus thymidine kinase (TK) under control of the promoter for doublecortin (Dcx)

157 gher levels of ICP0, ICP4, thymidine kinase (TK), and PD-1 ligand 1 (PD-L1) transcripts than those in

158 de kinase B subunit (RRB), thymidine kinase (TK), and UL9-like origin binding protein (OBP) proteins

159 hosphorylated by the viral thymidine kinase (TK), but not the cellular TK.

160 ge, such as those encoding thymidine kinase (TK), cytidylate kinase, and purine nucleotide phosphoryl

161 ring) in the gene encoding thymidine kinase (TK).

162 owth factor receptor (EGFR) tyrosine kinase (TK) domain in lung cancers.

163 eletion of the Ron receptor tyrosine kinase (TK) domain in mice leads to marked hepatocyte protection

164 ned by the presence of EGFR tyrosine kinase (TK) domain mutations.

165 GFR TKIs are present in the tyrosine kinase (TK) domain of the EGFR gene.

166 Tyrosine kinase (TK) fusions are attractive drug targets in cancers.

167 Activating mutations in tyrosine kinase (TK) genes (eg, FLT3 and KIT) are found in more than 30%

168 ated by dysregulated fusion tyrosine kinase (TK) genes is recognized by the World Health Organization

169 velopment of small-molecule tyrosine kinase (TK) inhibitors offers increasing opportunities for the t

170 The Ron receptor tyrosine kinase (TK) is overexpressed in many cancers, including prostate

171 The mutant JAK2V617F tyrosine kinase (TK) is present in the majority of patients with BCR-ABL-

172 BCR-ABL is a causative tyrosine kinase (TK) of chronic myelogenous leukemia (CML).

173 a targeted ablation of the tyrosine kinase (TK) signaling domain of Ron (TK-/-).

174 oliferation, migration, and tyrosine kinase (TK) signaling in breast cancer cells.

175 ceptor (EGFR) is a receptor tyrosine kinase (TK) that-once activated upon ligand binding-leads to rec

176 MAP kinase-dependent, EGFR tyrosine kinase (TK)-independent EGFR internalization induced by ultravio

177 Kit, Met and EphA3 cytokine/tyrosine-kinase (TK) receptors were down regulated.

178 esentative early promoter (thymidine kinase [TK]).

179 le inhibitors of oncogenic tyrosine kinases (TK) has led to well-tolerated, targeted therapies for a

180 f upstream acting receptor tyrosine kinases (TK).

181 general, the activation of tyrosine kinases (TKs) can be antagonized by the action of protein-tyrosin

182 Activating mutations in tyrosine kinases (TKs) drive pediatric high-risk acute lymphoblastic leuke

183 rine-threonine kinases and tyrosine kinases (TKs) on Ca(2+) influx mediated by VOCCs in OPCs.

184 are cell surface receptor tyrosine kinases (TKs) that transduce growth signals through dimerization

185 ytosis is known to require tyrosine kinases (TKs).

186 90 human TKs; it should detect 92% of known TK fusions.

187 Two additional baboons underwent GalT-KO TK transplantation after treatment with LoCD2.

188 o animals and the other two received GalT-KO TK transplants.

189 Kao-Tangkwa (KT), Kao-Numpueng (KN), Ta-Koi (TK), and Tubtim Siam (TS) were evaluated.

190 te that by acting as a tyrosine kinase, KSHV-TK modulates signalling and cell morphology.

191 Auto-phosphorylation of KSHV-TK also induces a loss of FAK and paxillin from focal ad

192 nes 65, 85 and 120 in the N-terminus of KSHV-TK.

193 In the absence of FAK or paxillin, KSHV-TK has no effect on focal adhesion integrity or cell mor

194 We now show that KSHV-TK, in contrast to HSV1-TK, associates with the actin cy

195 The interaction of Crk with KSHV-TK leads to tyrosine phoshorylation of this cellular ada

196 tatus >/=1, beta2-microglobulin >/=3.5 mg/L, TK >/=10 U/L, unmutated IGHV, 17p deletion, and TP53(mut

197 e accounted for by low levels of full-length TK polypeptide produced by net -1 frameshifting during t

198 y 0.1% of the wild-type level of full-length TK, considerably lower than estimated previously.

199 t greatly decreased the level of full-length TK, indicating that frameshifting is strongly stimulated

200 The integrated cellular-level TK/TD model presented here provides significant insight

201 Contrary to minor variants, major TK variants were shared between paired TG.

202 e with relatively low affinity for mammalian TK enzymes, resulting in improved detection sensitivity.

203 from routine CT chest examinations (64 MDCT TK LIGHT SPEED GE Medical System) performed in 202 adult

204 uring routine chest CT examinations (64 MDCT TK LIGHT SPEED GE Medical System) performed using three

205 We measured TK activity by plaque autoradiography and expression of

206 re discussed and compared to other known Met TK inhibitors.

207 To identify selective Met TK inhibitors, we used a high-throughput virtual screen

208 Moreover, TK-/- TRAMP+ prostate tumors exhibited decreased tumor v

209 tant, consistent with previous results, much TK expression could be ascribed to reversion.

210 tope-tagged versions of wild-type and mutant TKs.

211 arker-assisted selection for the breeding of TK.

212 eport the expression and characterization of TK from C. parvum.

213 However, further development of TK models is required for polar, ionizable, and easily b

214 A significant decrease in the expression of TK receptors, the phosphorylation of mediators of ERK1/2

215 f engineered MSC with selective induction of TK in concert with GCV resulted in a toxic tumor-specifi

216 of IL-7 was observed after each infusion of TK+ cells, anticipating the appearance of newly generate

217 assay suggested that extremely low levels of TK are generated by this virus.

218 Thus, remarkably low levels of TK are sufficient for reactivation from latency in mice.

219 d approximately 0.01% of wild-type levels of TK polypeptide.

220 mocyclers enhances the temporal precision of TK assays.

221 DGF response as a model to probe the role of TK receptors (TKr) on OPC Ca(2+) uptake, we found that T

222 H274Y clones increased consistently, that of TK-H274Y virus decreased.

223 ction, followed by the oxidative trapping of TK intermediate alpha,beta-dihydroxyethylthiamine diphos

224 r, and that the smallest functioning unit of TK comprises the PP- and Pyr-domains, whose evolutionary

225 in Drosophila, this age-related variation of TK is suggestive of a modulatory role in locomotion beha

226 cases PTPs can potentiate the activation of TKs.

227 They suggest that dynamic engagement of TKs and the cytoskeleton enables macrophages to serve as

228 caused by JAK2 V617F, whereas both oncogenic TKs activate common downstream molecules at the level of

229 ast partly, explain why respective oncogenic TKs cause different disease phenotypes.

230 ed for the EGFR-TK domain than for any other TK.

231 oups have speculated that mutations in other TK genes may be present in the remaining 70%.

232 Unlike other TKs, CpTK is a stable trimer in the presence and absence

233 RE-TK/GCV was effective compared with LV-PGK-TK/GCV in reducing tumor size.

234 nt the first study to quantitatively profile TK activity in xenografted patient biopsies of high-risk

235 For the biosensor design purpose, TK from Escherichia coli (TKec) was immobilized in Mg2Al

236 phylogenetic-related minor ACV(S) and ACV(R) TK variants.

237 e kinase domains of 26 TK genes (11 receptor TK; 15 cytoplasmic TK) expressed in most AML patients us

238 heir irreversible inhibition of the receptor TK domain.

239 ectly inhibit EGFR or other related receptor TKs in a cell-free system.

240 nsertion, previously shown to greatly reduce TK expression, and from the other, a previously unidenti

241 permits biologically and clinically relevant TK synthesis, and may occur more generally.

242 isease signs caused by oseltamivir-resistant TK-H274Y virus were milder than those caused by TK-WT vi

243 To investigate how this mutant retains TK activity, we engineered and analyzed viruses expressi

244 Ron TK-/- mice had a significant decrease in survival time c

245 yrosine kinase (TK) signaling domain of Ron (TK-/-).

246 6 SNPs were different in high and low rubber TK genotypes.

247 We found that the mutant's TK activity can be accounted for by low levels of full-l

248 icated that unidentified tyrosine kinase(s) (TKs) phosphorylated 2B7 in SYF(-/-).

249 Taraxacum kok-saghyz (TK) is a potential alternative crop for natural rubber (

250 th mice that are deficient in Ron signaling (TK-/-).

251 on level than the truncated mutant HSV1-sr39 TK (ttk) as the third reporter component of this improve

252 ry this mutation did not generate sufficient TK activity for detection by plaque autoradiography, whi

253 short neuropeptide F (sNPF), and tachykinin (TK) as potential candidates.

254 d analyzed viruses expressing epitope-tagged TK.

255 ted GOM and PBM measurements using a Tekran (TK) KCl-coated denuder and quartz regenerable particulat

256 r artificially dark-kept ants, we found that TK distribution changed markedly in the central complex

257 In addition, we observed that TK-/- hepatocytes were more resistant to cell death comp

258 Our data clearly suggest that TKs exert an activating influence on VOCC function in OP

259 in subsets of mesothelioma, suggesting that TKs might represent therapeutic targets in this highly l

260 The TK gene product in combination with the prodrug ganciclo

261 resistance was associated with CN-LOH at the TK locus.

262 uced DNA damage is simulated by coupling the TK/TD formulation with a model describing the multistep

263 ion of KD(app) for thiamine diphosphate, the TK cofactor and the inhibition action of two commerciall

264 erated levels of cytokines produced from the TK-/- Kupffer cells are detrimental to wildtype hepatocy

265 The discovery that mutations in the TK domain are associated with dramatic and sustained res

266 ggerated cytokine production observed in the TK-/- mice in vivo through the use of purified cultured

267 t of the Pax3(neo) allele, as removal of the TK-neo(R) cassette completely relieves the hypomorphic e

268 n is not fixed but varies depending upon the TK(s) that carry out its required phosphorylation.

269 creation of the floxed allele, in which the TK-neo(R) cassette is present between exons 5 and 6.

270 In contrast, in 293T cells infected with the TK mutant virus, viral replication remained sensitive to

271 This TK/TD framework that uses arsenic as an example can be f

272 men) in a GalT-KO pig-to-baboon thymokidney (TK) model.

273 acrylamide analogues in inhibiting EGFR-TK (TK = tyrosine kinase) autophosphorylation in A549 lung c

274 f TNF-alpha and select cytokines compared to TK+/+ cells following LPS stimulation.

275 ere more resistant to cell death compared to TK+/+ hepatocytes, suggesting that Ron functions in both

276 lls in Abeta-carrying APPPS1 mice crossed to TK mice (APPPS1;TK).

277 decreased tumor vascularization relative to TK+/+ TRAMP+ prostate tumors, which correlated with redu

278 Target binding was sensitive to TK inhibitors, profoundly inhibited following depletion

279 fficient nucleoside kinase, when compared to TKs from related herpesviruses.

280 K), pharmacodynamic (PD), and toxicokinetic (TK) studies are used to evaluate a potential drug candid

281 orated in a three-compartment toxicokinetic (TK) model to first predict Cmax for in vivo corroboratio

282 y is to develop a mechanistic toxicokinetic (TK) and toxicodynamic (TD) model for the synergistic mix

283 llular-level semi-mechanistic toxicokinetic (TK) model of arsenic in human hepatocytes with a cellula

284 entrations, we compared three toxicokinetic (TK) models with each other and with literature data of m

285 ble loops of Escherichia coli transketolase (TK).

286 yrophosphate (ThDP)-dependent transketolase (TK)-catalyzed reaction, followed by the oxidative trappi

287 mechanism and specificity of transketolase (TK) has been minor, and that the smallest functioning un

288 show that conditioned media from LPS-treated TK-/- Kupffer cells was more toxic to hepatocytes than c

289 gene duplication, as are all known trematode TKs.

290 i enzyme (TbTK) is a tandem protein with two TK homolog domains of which only the C-terminal one is a

291 was estimated to express 0.09% of wild-type TK activity via a ribosomal frameshift 24 nucleotides up

292 found to be more thermostable than wild-type TK.

293 xpression of frameshifted and unframeshifted TK polypeptides using a very sensitive immunoprecipitati

294 aused by 2B7 phosphorylation by unidentified TK(s).

295 development of T cells, occurring only upon TK+ -cell engraftment.

296 ric detection of L-erythrulose released upon TK-catalyzed reaction.

297 of the drug-kinase complexes using a VEGFR2 TK construct inclusive of the important juxtamembrane do

298 the engineered oncolytic vaccinia virus VVWR-TK(-)RR(-)-Fcu1 can induce immunogenic cell death and ge

299 e is no systematic method to determine which TK signaling cascades activate PI3K in certain cancers,

300 Kupffer cells and hepatocytes from wildtype (TK+/+) and TK-/- mice were studied.

301 and CYP1A1 mRNA levels were correlated with TK MF, supporting involvement of the CYP1A family in mut