ライフサイエンスコーパス: TK

1 TK-1 protein expression was significantly higher in HCC

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 ation with thymidine kinase-deficient HSV-1 (TK(del)) completely abolished reactivation of wild-type

6 U targets, such as TYMS, thymidine kinase 1 (TK-1) and thymidine phosphorylase (TYMP).

7 idylate synthase (TYMS), thymidine kinase 1 (TK-1), and equilibrative nucleoside transporter 1 (SLC29

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

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

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

11 the two distinct forms of transketolase at a TK(high):TK(low) ratio that matched those observed previ

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

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

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

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

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

17 the TK(low) subunit of the partially-active TK(high)-TK(low) mixed dimer, where HPA binding to the T

18 ed dimer results in inhibition of the active TK(high) subunit.

19 reased TK(high) activity, while low-activity TK(low) was unmodified.

20 a convolution of binding to the low-activity TK(low)-TK(low) dimer, and the TK(low) subunit of the pa

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

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

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

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

25 f TK with high- (TK(high)) and low-affinity (TK(low)).

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

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

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

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

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

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

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

33 erconversions between apo-/holo-TK(high) and TK(low), and the potential to significantly improve bioc

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

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

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

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

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

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

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

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

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

43 A population semiphysiologically based TK model describing the disposition of BPA and BPS and t

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

45 for the interindividual variability in both TK and TD.

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

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

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

49 receptor signaling seems to be transduced by TK and PI-3K pathways and modulated by CREB, HSF-4a, HDA

50 an intermediate to a preclinical candidate (TK-666) and its derivatives.

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

52 ymidine kinase-deficient CD4(+) T-cells (CEM/TK(-)).

53 ymidine kinase-deficient CD4(+) T-cells (CEM/TK(-)).

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

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

56 nd in CEM/0 cells was completely kept in CEM/TK(-) cells.

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

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

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

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

61 A two-compartment TK model adequately described the biphasic uptake patter

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

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

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

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

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

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

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

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

70 gnostic-compatible triple knock-out DeltaBCG TK strain.

71 The protective efficacy of the DeltaBCG TK was tested in guinea pigs experimentally infected wit

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

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

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

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

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

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

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

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

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

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

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

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

84 shifting can explain this ability to express TK.

85 ta into in silico population models both for TK (such as a physiologically based pharmacokinetic mode

86 ounding cirrhotic tissue and was stained for TK-1 A prospective study was conducted; 18 patients with

87 wn high TPP-affinity and high-activity form, TK(high), in the presence of Mg(2+).

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

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

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

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

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

93 e TK(low) subunit of the mixed dimer to have TK(high)-like properties, but without oxidation.

94 ow) subunit of the partially-active TK(high)-TK(low) mixed dimer, where HPA binding to the TK(low) su

95 istinct forms of transketolase at a TK(high):TK(low) ratio that matched those observed previously via

96 the existence of two forms of TK with high- (TK(high)) and low-affinity (TK(low)).

97 ribes the interconversions between apo-/holo-TK(high) and TK(low), and the potential to significantly

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

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

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

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

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 fficient in killing cells independent of HSV-TK.

110 thesized at key locations in the SV40 or HSV-TK model promoters to determine the location dependency

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

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

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

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

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

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

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

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

119 The HSV1-TK enzyme can act as a suicide gene of transduced cells

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

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

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

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

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

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

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

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

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

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

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

131 Population variability in TK of S-(1,2,2-trichlorovinyl)GSH (TCVG), S-(1,2,2-trich

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

133 tial oxidation was responsible for increased TK(high) activity, while low-activity TK(low) was unmodi

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

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

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

137 as built from these data to estimate the key TK parameters that drive the internal exposure to active

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 KSHV thymidine kinase (TK), the ORF21 gene product, can enhance the production

154 ORF21 encodes KSHV thymidine kinase (TK), which increases the pool of dTTP for viral replicat

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

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

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

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

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

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

161 Tyrosine kinase (TK) inhibitor, genistein and phosphatidylinositol 3-kina

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

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

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

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

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

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

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

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

170 f upstream acting receptor tyrosine kinases (TK).

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

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

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

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

175 90 human TKs; it should detect 92% of known TK fusions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 ution of binding to the low-activity TK(low)-TK(low) dimer, and the TK(low) subunit of the partially-

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

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

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

194 We measured TK activity by plaque autoradiography and expression of

195 gnition receptors BAI1, CD36, Tim-4, and Mer-TK contribute to fertilization.

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

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

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

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

200 arker-assisted selection for the breeding of TK.

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

202 The HPA dissociation constant of TK(low) was comparable to the substrate-inhibition disso

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

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

205 oxidation of TK(low) led to the formation of TK(high), which was 22-fold more active than TK(low).

206 ence indicated the existence of two forms of TK with high- (TK(high)) and low-affinity (TK(low)).

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

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

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

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

211 trometry revealed that chemical oxidation of TK(low) led to the formation of TK(high), which was 22-f

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

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

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

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

216 cases PTPs can potentiate the activation of TKs.

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

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

219 , a known valid model for investigating oral TK.

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

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

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

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

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

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

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

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

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

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

230 6 SNPs were different in high and low rubber TK genotypes.

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

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

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

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

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

236 d analyzed viruses expressing epitope-tagged TK.

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

238 TK(high), which was 22-fold more active than TK(low).

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

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

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

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

243 The TK behavior of BPA and BPS was investigated by administe

244 The TK gene product in combination with the prodrug ganciclo

245 elations between surface/volume area and the TK parameters (sorption and uptake rate constants and th

246 low-activity TK(low)-TK(low) dimer, and the TK(low) subunit of the partially-active TK(high)-TK(low)

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

248 ilarly investigated and found to convert the TK(low) subunit of the mixed dimer to have TK(high)-like

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

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

251 e/depuration rate constants required for the TK model.

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

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

254 ength and the functional group influence the TK.

255 A better understanding of the TK of ionizable test compounds is essential to allow ass

256 e resulting BCF) were found, but none of the TK parameters correlated with sensitivity.

257 We studied the TK of four PFAA (PFOS, PFHxS, PFOA, and PFBA) with diffe

258 K(low) mixed dimer, where HPA binding to the TK(low) subunit of the mixed dimer results in inhibition

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

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

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

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

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

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

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

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

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

268 is more related to the TD parameters than to TK parameters.

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

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

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

272 of associated interindividual toxicokinetic (TK) and toxicodynamic (TD) variability by using the Coll

273 f endocrine disruption if its toxicokinetic (TK) properties, namely its oral availability and systemi

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

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

276 siological traits and modeled toxicokinetic (TK) and toxicodynamic (TD) parameters.

277 iver model with a first-order toxicokinetic (TK) model to predict the concentrations of wastewater-de

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

279 the processes governing its toxicokinetics (TK) are poorly understood.

280 emical structure affects the toxicokinetics (TK) in different organisms.

281 Transketolase (TK) cofactor binding has been studied extensively over m

282 ble loops of Escherichia coli transketolase (TK).

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

284 low-activity form of E. coli transketolase, TK(low), which also binds the cofactor thiamine pyrophos

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

286 gene duplication, as are all known trematode TKs.

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

288 s revealed increased RNA expression of TYMS, TK-1, and SLC29A1 in HCC.

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

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

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

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

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

294 d the yolk sac of the zebrafish embryo using TK experiments, a dialysis approach, thermodynamic calcu

295 y analytical ultracentrifugation at various [TK].

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

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

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

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

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