ライフサイエンスコーパス: Met

1 Met inhibition showed clinical benefit in this model.

2 Met is weakly cationic and targets the mitochondria to i

3 Met mRNA was expressed rhythmically during the reproduct

4 Met need for family planning was greater in the interven

5 Met oxidation studies (pH 7, D2O, 0.01 M phosphate, 25 d

6 Met was markedly overexpressed in both PDA cell lines an

7 Met was specifically required for the assembly of autoph

8 By replacement of the C-terminal Leu(13)-Met(14)-NH2 dipeptide of SB3 by Sta(13)-Leu(14)-NH2, the

9 n prenatal maternal smoking and COMT Val(158)Met in conduct problems and crime in the 1993 Pelotas Bi

10 convergent with human studies of the Val(158)Met polymorphism, and suggest that COMT's effects are mo

11 human gene contains a polymorphism (Val(158)Met) that alters enzyme activity and influences PFC func

12 In a single-pulse TMS study carried on 16 Met (Val/Met and Met/Met) and 16 Val/Val participants se

13 anges in estradiol secretion and BDNF Val(66)Met genotype on measures of hippocampal function and anx

14 n 39 healthy women genotyped for BDNF Val(66)Met, and a confirmatory data set was obtained with fMRI

15 ammary tumours with 9qA1 (Yap1) and/or 6qA2 (Met) amplification(s).

16 recommendations, having e.g. 4.8% Lys, 2.7% Met+Cys, and 7.7% Phe+Tyr.

17 and halogen-bond interactions with Ser-876, Met-915, and Met-956.

18 With the exception of two amino acids (Met and Trp), all other amino acid residues are each enc

19 alamocortical pathway of mice lacking active Met in the cerebral cortex.

20 With aging, Met metabolism changes, and increased plasma homocystein

21 urating concentration of the opioid agonist [Met(5)]-enkephalin (ME) caused significantly less desens

22 without enzyme activity but that retain all Met residues were created.

23 ition, age contributes to oxidation at alpha-Met-32 significantly in all subjects and in nonsmokers.

24 ine kinases (RTKs) from the ErbB, IGF-1R and Met families in breast cancer cells.

25 /Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met (N=19, 26.8%)) received mood ratings before infu

26 egions probed at Leu-17, Leu-34, Val-36, and Met-35 side chains were found to be very pronounced at a

27 bond interactions with Ser-876, Met-915, and Met-956.

28 al. describe the mechanisms linking Axl and Met activation to acquired resistance to sunitinib in re

29 cal rationale for the development of Axl and Met inhibitors including cabozantinib in anti-angiogenic

30 expression in mutant-K-Ras-beta-catenin and Met-beta-catenin HCC.

31 ates two receptor tyrosine kinases, EGFR and Met, in the absence of ligands.

32 lse TMS study carried on 16 Met (Val/Met and Met/Met) and 16 Val/Val participants selected from a lar

33 Blocking CCR5 using the antagonist, (Met)CCL5, abolished the de-phosphorylation of IRS-1(S302

34 peptides containing Arg or Arg-Asn, not Arg-Met, with a 0 or +1 charge, significantly reduced plaque

35 ously, inactivation of the autism-associated Met tyrosine kinase receptor in GABAergic interneurons l

36 ion of CYSTATHIONINE gamma-SYNTHASE (AtCGS), Met's main regulatory enzyme.

37 ates of Pc from the perspective of the axial Met ligand and evidence for perturbation of the Cu site

38 Attenuation of responses in BDNF Met mice indicates that patients with the Met allele may

39 We found that BDNF Met/Met mice have attenuated responses to scopolamine an

40 der individuals who are carriers of the BDNF Met allele displayed no positive association between sle

41 However, advancing age and carrying the BDNF Met allele were both identified as factors that potentia

42 jects carrying at least one copy of the BDNF Met allele, a more consolidated sleep was not associated

43 imming test in BDNF(Val/Val) but not in BDNF(Met/Met) mice.

44 sent or reduced in the dentate gyrus of BDNF(Met/Met) mice.

45 otic 43S preinitiation complex (PIC) bearing Met-tRNAi(Met) in a ternary complex (TC) with eukaryotic

46 eIF2-GTP binds Met-tRNAi to form the eIF2-GTP*Met-tRNAi ternary complex

47 Cyt c H19M, the first bis-Met liganded cyt c, is compared with other axial ligand

48 to block the AnxA1 pathway (by using N-t-Boc-Met-Leu-Phe, a nonselective AnxA1 receptor antagonist, o

49 e frameshift mutation, probably at the BRCA1-Met-297 codon.

50 the cross-beta subunits, which is defined by Met-35 contacts.

51 c-Met expression was assessed by immunofluorescence imagin

52 c-Met immunohistochemistry and real-time polymerase chain

53 tic RF ablation was combined with either a c-Met inhibitor (PHA-665752) or VEGF receptor inhibitor (s

54 Activated c-Met signaling promoted adhesion of tumor cells to brain

55 ve tumors and can be blocked with adjuvant c-Met and VEGF inhibitors.

56 ined the requirement of lipogenesis in AKT/c-Met driven hepatocarcinogenesis using conditional Fatty

57 otype characterizes liver lesions from AKT/c-Met mice, we determined the requirement of lipogenesis i

58 note, hepatocarcinogenesis induced by AKT/c-Met was fully inhibited by FASN ablation.

59 cancer stem cell markers CD44, CD133, and c-Met and the immunologic markers human leukocyte antigen

60 e combined expression of activated AKT and c-Met in the mouse liver.

61 demonstrates that co-activation of AKT and c-Met induces HCC development that depends on the mTORC1/F

62 ted expression of FASN, activated AKT, and c-Met proteins was detected in a subgroup of biologically

63 ular endothelial growth factor (VEGF), and c-Met receptor expression measurement in periablational ri

64 Co-expression of AKT and c-Met triggered rapid liver tumor development and mice req

65 crizotinib (inhibitors of IGF-1R, Src and c-Met/ALK, respectively) led to synergistic effects in som

66 rapeutically targetable receptors, such as c-Met, would be of potential benefit.

67 treatment effectively down-regulated both c-Met phosphorylation and Ras activation in renal cancer c

68 It inhibited the expression of both c-Met- and CNI-induced HO-1, and promoted cancer cell apop

69 reting PNET cell line, MIN6, downregulates c-Met expression.

70 ment promoted c-Met induction and enhanced c-Met-induced Ras activation.

71 in vivo and highlight a promising role for C-Met inhibitors in blocking tumor cell streaming and meta

72 These results establish HGF/C-Met as a central organizing signal in blood vessel-direc

73 subcutaneous tumor growth mediated by HGF/c-Met pathway and VEGF activation.

74 effectively blocked, by inhibiting the HGF/C-Met signaling pathway between endothelial cells and tumo

75 n together, these results suggest that HGF/c-Met-mediated lamellipodia formation, and perhaps motilit

76 ay benefit patients whose tumors show high c-Met expression and who do not respond to PARP inhibition

77 imaging agent with high affinity for human c-Met, for the detection of early-stage locoregional recur

78 in vitro reconstituted system implicating C-Met signaling were confirmed in vivo in mammary tumors u

79 This effect was not observed in c-Met-negative tumors and can be blocked with adjuvant c-M

80 mb repressive complex 2 (PRC2), to inhibit c-Met expression.

81 activation of the receptor tyrosine kinase c-Met and overexpression of the cytoprotective enzyme heme

82 we show that the receptor tyrosine kinase c-Met associates with and phosphorylates PARP1 at Tyr907 (

83 Its receptor tyrosine kinase, c-Met, is expressed in the cochlear epithelium and melanoc

84 ied to function downstream of HGF-mediated c-Met activation in a PI3K dependent manner.

85 3230 tumors for comparison with the native c-Met-positive line.

86 , and that treatment with a combination of c-Met and PARP inhibitors may benefit patients whose tumor

87 The combination of c-Met and PARP1 inhibitors synergized to suppress the grow

88 etic mechanisms underlying Meg3 control of c-Met and the oncogenic consequences of Meg3 loss or c-Met

89 cident with increased expression levels of c-Met and the p85alpha subunit of PI3K.

90 tion of IL1beta secretion by activation of c-Met induced tumor-associated astrocytes to secrete the c

91 Ras activation downstream of c-Met is sufficient to induce clinically relevant HCC in c

92 esulting in compromised KSHV activation of c-Met pathway, and KSHV induction of cell invasion and ang

93 We studied the potential role of c-Met signaling axis on CNI-induced renal tumor growth and

94 a new diagnostic tool for the detection of c-Met-expressing primary tumor and has potential utility f

95 i-tumor activity through the inhibition of c-Met-Ras-HO-1 axis; and it can have significant therapeut

96 epressed CD82, relieving its inhibition on c-Met activation and inducing cell invasion and angiogenes

97 the oncogenic consequences of Meg3 loss or c-Met gain.

98 and it decreased the expression of phospho-c-Met and HO-1 and reduced blood vessel density in tumor t

99 Importantly, CNI treatment promoted c-Met induction and enhanced c-Met-induced Ras activation.

100 ed NRG-GBM-RPA consisting of MGMT protein, c-Met protein, and age revealed greater separation of OS p

101 io of MET to chromosome 7, 4.3) and strong c-Met immunohistochemical expression (mean H score, 253) t

102 cleotides (TFOs), in MIN6 cells suppressed c-Met expression and enhanced cell proliferation, perhaps

103 uld suppress brain metastasis by targeting c-Met signaling.

104 The c-Met expression of individual resected tumor samples, det

105 o unique genomic regions in and around the c-Met gene.

106 xperienced a major partial response to the c-Met inhibitor crizotinib.

107 tumor-associated astrocytes to secrete the c-Met ligand HGF.

108 nvasion and angiogenesis by activating the c-Met pathway.

109 ogen response modifier raloxifene with the c-Met/VEGFR2 kinase inhibitor cabozantinib, dramatically p

110 In the absence of Meg3, these c-Met regions displayed distinctive enhancer-signature his

111 acilitating cytoprotective signals through c-Met signaling to limit bronchial epithelial apoptosis, t

112 GF supports hindlimb motor neurons through c-Met; CNTF supports subsets of axial motor neurons throug

113 Prospective clinical trials with c-Met inhibitors will be necessary to validate MET exon 14

114 anistically, CD82 directly interacted with c-Met to inhibit its activation.

115 attenuated apoptosis by crosstalking with c-Met to potentiate its cytoprotective signals in airway e

116 tic RF ablation was performed in rats with c-Met-negative R3230 tumors for comparison with the native

117 d with isotope-labeled [(13)C]SMM and [(13)C]Met feeding experiments enabled us to reveal that SMM th

118 mor model indicated that breast cancer cells Met-1 with up-regulation of DACH1 were endowed with rema

119 o the native mouse COMT gene to produce COMT-Met mice, which were compared with their wild-type litte

120 ents (the S6 bundle crossing) at a conserved Met residue.

121 s-crossing of the S6 segments at a conserved Met.

122 Mutation of the conserved Met residues in the S6 segments to the negatively-charge

123 (fl/fl)/Apc(fl/+) mice compared with Ah(Cre)/Met(+/+)/Apc(fl/+) control mice.

124 )/Met(fl/fl)/LacZ) and control mice (Ah(Cre)/Met(+/+)/LacZ, Lgr5(Creert2)/Met(+/+)/LacZ) were exposed

125 We also quantified adenomas in Ah(Cre)/Met(fl/fl)/Apc(fl/+) mice compared with Ah(Cre)/Met(+/+)

126 Total epithelial disruption of Met (Ah(Cre)/Met(fl/fl)/Apc(fl/+) mice) resulted in an approximate 50

127 d numbers of proliferating crypts in Ah(Cre)/Met(fl/fl)/LacZ mice.

128 total epithelial disruption of MET (Ah(Cre)/Met(fl/fl)/LacZ) or ISC-specific disruption of MET (Lgr5

129 rt2)/Met(fl/fl)/Apc(fl/fl) and Lgr5(Creert2)/Met(+/+)/Apc(fl/fl) mice.

130 l mice (Ah(Cre)/Met(+/+)/LacZ, Lgr5(Creert2)/Met(+/+)/LacZ) were exposed to 10 Gy total body irradiat

131 GF using adenomas derived from Lgr5(Creert2)/Met(fl/fl)/Apc(fl/fl) and Lgr5(Creert2)/Met(+/+)/Apc(fl/

132 SC-specific disruption of Met (Lgr5(Creert2)/Met(fl/fl)/Apc(fl/fl) mice) caused a twofold increase in

133 Lgr5(Creert2)/Met(fl/fl)/LacZ mice had impaired regeneration of MET-de

134 SC-specific disruption of MET (Lgr5(Creert2)/Met(fl/fl)/LacZ) and control mice (Ah(Cre)/Met(+/+)/LacZ

135 We believe that the ease of [(11)C] D-Met radiosynthesis, coupled with its rapid and specific

136 sis of D-[methyl-(11)C]methionine ([(11)C] D-Met), and showed that it can rapidly and selectively dif

137 Reexpression of wild-type Met, kinase-dead Met, or integrin alpha3 was sufficient to rescue death u

138 In thus report, decreased Met signaling in glutamatergic neurons had no effect on

139 bstrate N5 position in closed and disordered Met(20) loop states and found a strong correlation betwe

140 r distance dynamics in closed and disordered Met(20) loop states.

141 Not only do Met allele carriers exhibit distinct levels of baseline

142 EGFR-ErbB3 associations; non-canonical EGFR-Met interactions are implicated in resistance to anti-ca

143 ers but instead results in formation of EGFR-Met and EGFR-ErbB3 associations; non-canonical EGFR-Met

144 t to rescue death upon removal of endogenous Met.

145 major shrimp allergen of Metapenaeus ensis (Met e 1), and to evaluate their therapeutic effects in a

146 s, methoprene-tolerant transcription factor (Met) and steroid receptor coactivator (SRC), would be ex

147 impaired chemotactic migration toward formyl-Met-Leu-Phe (fMLP) and stromal cell-derived factor 1alph

148 ct level (LOAEL) of supplemented, oral, free Met in healthy older adults by examining the increase in

149 y determinant.We provided capsules with free Met to 15 healthy older adult subjects for 4 wk at climb

150 Free-Met supplements have been claimed to have multiple posit

151 okine responses of splenocytes isolated from Met e 1-sensitized Balb/c mice upon stimulation by 18 sy

152 d at least one copy of the lower functioning Met allele of the BDNF gene.

153 associated with skeletal muscle glutathione/Met/Cys metabolism (2-hydroxybutanoic acid, oxoproline,

154 IF2-GTP binds Met-tRNAi to form the eIF2-GTP*Met-tRNAi ternary complex (TC), which is recruited to th

155 nitiation complex (PIC) bearing the eIF2.GTP.Met-tRNAi(Met) ternary complex (TC) scans the mRNA for a

156 by restricting the levels of active eIF2-GTP/Met-tRNAi ternary complexes (TC).

157 Hepatocyte growth factor (HGF)/Met signaling has critical roles in pancreatic ductal ad

158 bined activation of Wnt/beta-catenin and Hgf/Met signaling in mouse mammary epithelial cells.

159 M1, and the cross talk between FOXM1 and HGF/Met signaling promoted PDA growth and resistance to Met

160 Furthermore, activation of HGF/Met signaling increased the expression and transcription

161 Blockade of HGF/Met, Janus kinase 2 (JAK2)/STAT3 and TGF-beta1 signaling

162 hey also shed light on the effects of higher Met levels on seed physiology and behavior.

163 tivation gate, replacement of the homologous Met residues in human Slo2.1 or Slo2.2 with the negative

164 To determine how Met promotes cell survival, we inhibited Met kinase acti

165 The human Met allele was introduced into the native mouse COMT gen

166 within the first five residues following (i)Met and that the first and second positions are the most

167 terminal acetylation for proteins lacking (i)Met, some of which have not previously been described.

168 for proteins whose initiator methionine ((i)Met) residues have been removed.

169 rian hormones induce cognitive impairment in Met carriers.

170 ects differential hippocampal recruitment in Met carriers but only in the presence of estradiol.

171 scue" pathway induced by targeted therapy in Met-addicted carcinoma cells.

172 learning a short story presented verbally in Met allele carriers (beta = -0.585, p = 0.005).

173 ated activation of several kinases including Met receptor.

174 We found increased Met phosphorylation within both the kinase and the docki

175 to detect possible intolerance to increased Met intake.

176 how Met promotes cell survival, we inhibited Met kinase activity or blocked its expression with RNA i

177 g 609 differentially expressed genes, c-Kit, Met and EphA3 cytokine/tyrosine-kinase (TK) receptors we

178 th bound SAH (a SAM analog) or 5'-dAdo and l-Met (SAM cleavage products) is consistent with the canon

179 ed for L-[methyl-(11)C]methionine ([(11)C] L-Met), we developed an enhanced asymmetric synthesis of D

180 deoxyadenosine (5'-dAdo) and l-methionine (l-Met).

181 synthetic peptides that span the full-length Met e 1.

182 Six major Met e 1 T cell epitopes were identified.

183 sing lower activity BDNF genotypes (Val/Met, Met/Met).

184 icropollutants (MPs), including metaldehyde (Met), provides an ideal space for determining the charac

185 amine (Pur), genistein (Gen), and metformin (Met).

186 l-Methionine (Met) is an essential amino acid for humans and is import

187 participate in the metabolism of methionine (Met) in seeds.

188 tudies to evaluate the impact of methionine (Met) oxidation on the biological functions of IgG1 antib

189 ce DMSP, probably using the same methionine (Met) transamination pathway as macroalgae and phytoplank

190 eactions and participates in the methionine (Met) metabolic pathway.

191 Subjects with the Methionine (Met)/Valine (Val) and Val/Val genotypes showed higher fr

192 78N mutation in combination with methionine (Met) at codon 129 in the mutated allele of PRNP (D178N-1

193 y (15)N-labeled Ras as well as [(13)C]methyl-Met,Ile-labeled Sos for observing site-specific details

194 Mutagenizing Met-915 or Met-956 selectively abolishes activation by i

195 We generated a new Met-blocking antibody which binds outside the ligand-bin

196 ificantly contributed to the accumulation of Met in their seeds at late stages of development.

197 rated a spatiotemporal expressional atlas of Met and gce throughout development.

198 a hydrogen bond to the backbone carbonyl of Met-631.

199 In mice, circuit-specific deletion of Met causes distinct atypical behaviors.

200 Total epithelial disruption of Met (Ah(Cre)/Met(fl/fl)/Apc(fl/+) mice) resulted in an a

201 ISC-specific disruption of Met (Lgr5(Creert2)/Met(fl/fl)/Apc(fl/fl) mice) caused a

202 methyl farnesoate stimulates dissociation of Met multimers with subsequent association with SRC.

203 as activation, which can occur downstream of Met signaling, is sufficient to cause HCC in association

204 T cell epitopes of Met e 1 were first identified based on the proliferation

205 eatic tumor specimens, and the expression of Met correlated directly with that of FOXM1 in human tumo

206 Knockdown of the expression of Met, SRC, EcR, USP, BR-C (Broad-Complex), TOR (target of

207 oss of Met expression, but not inhibition of Met kinase activity, induced apoptosis by reducing integ

208 we showed for the first time interaction of Met(33) (involved in dipyridamole binding) with BCR-ABL

209 Finally, EC-specific KO of Met inhibited vascular transformation, normalized blood

210 s accumulated significantly higher levels of Met compared with control seeds through an as yet unknow

211 Further experiments indicate that loss of Met activity downregulates GABAAreceptors on glutamaterg

212 Loss of Met expression, but not inhibition of Met kinase activit

213 sonance bands are absent, indicating loss of Met-80 coordination.

214 erapeutic effects in a Balb/c mouse model of Met e 1 hypersensitivity.

215 Phloem-specific reconstitution of Met Cycle activity in mti1 and dep1 mutant plants was su

216 how improving the mitochondrial targeting of Met enhances its anticancer activities, including aggres

217 N firing with the mu/delta selective opioid [Met(5)]enkephalin (1 mum) decreased spontaneous dopamine

218 Mutagenizing Met-915 or Met-956 selectively abolishes activation by isoflurane a

219 The Yang or Met Cycle is a series of reactions catalyzing the recycl

220 P1 Met was an interesting exception that was preferred by C

221 ment of parental HeLa cells elevated phospho-Met levels whereas antioxidant treatment of GNPTAB(-/-)

222 were needed to cause an increase in phospho-Met in GNPTAB(-/-) cells.

223 eatment of GNPTAB(-/-) cells reduced phospho-Met levels.

224 ient for spontaneous tumors in mice (Alb-R26(Met) ), conceptually illustrating how the shift from phy

225 ling diversity results obtained from Alb-R26(Met) HCC versus control livers to design an "educated gu

226 that liver tumorigenesis modeled by Alb-R26(Met) mice corresponds to a subset of hepatocellular carc

227 eukemia 1+ signature, deregulated in Alb-R26(Met) tumors, characterizes a subgroup of HCC patients wi

228 hing harmful oxidants through its recyclable Met residues, resulting in oxidant protection to the bac

229 ein-tyrosine phosphatases that down-regulate Met phosphorylation.

230 ee-electron laser, determining that the Fe-S(Met) bond enthalpy is 4 kcal/mol stronger than in the a

231 This Fe-S(Met) bond is too weak to persist in the absence of prote

232 UCP3 Tg mice (e.g., Asp, Glu, Lys, Tyr, Ser, Met) were significantly reduced after an EB; that metabo

233 utation (F142L; numbered including the start-Met), which markedly reduces CaM Ca(2+) binding.

234 The MfR protein subunits Met and SRC, cloned from Daphnia pulex, were fused to th

235 asma homocysteine, the NOAEL of supplemented Met intake is 46.3 and the LOAEL is 91 mg . d(-1) in hea

236 The estimated NOAEL of supplemented Met was set at 46.3 mg . d(-1), and the estimated LOAEL

237 -1), and the estimated LOAEL of supplemented Met was set at 91 mg . d(-1) (on the basis of the actual

238 evated with the highest dose of supplemented Met.

239 e synthesized a set of mitochondria-targeted Met analogues (Mito-Mets) with varying alkyl chain lengt

240 Further, we revealed evidence that Met proteins self-associate in the absence of methyl far

241 en at the very 5' end of mRNA, implying that Met-tRNAi (Met) inspects mRNA from the first nucleotide

242 Molecular dynamics simulations reveal that Met(73)influences beta3-beta4 hairpin loop conformation,

243 Our results show that Met(73) and, to a lesser extent, Ile(75) suppress excisi

244 ering of active site hydration, although the Met(20) loop conformation only has a moderate effect on

245 in the Glu-Xaa8-Glu (double E) loop and the Met-Gln-Trp sequence of the canonical Thr-His-Trp (THW)

246 et, which identifies the binding site as the Met Ig1 domain.

247 thway FA was strongest in women carrying the Met allele, which is linked with decreased activity-depe

248 t manner, and define a critical role for the Met axis in sarcoma initiation.

249 G translation by competing with eIF5 for the Met-tRNAi-binding factor eIF2.

250 dopsis thaliana) mutants with defects in the Met Cycle enzymes 5-METHYLTHIORIBOSE-1-PHOSPHATE-ISOMERA

251 lO extends catalyst lifetime to increase the Met turnover number (TON) 3-fold compared with H2O2, hig

252 In this study, the probe is the Met surrogate azidohomoalanine (Aha), which carries a re

253 nditions and assayed the contribution of the Met Cycle to the regeneration of S for these pathways.

254 examine the most likely conformation of the Met(20) loop during the chemical step, we studied the hy

255 We found that the conformation of the Met(20) loop has a dramatic effect on the ordering of ac

256 ween N5 basicity and the conformation of the Met(20) loop.

257 Results demonstrated that the Met subunit is highly dynamic in controlling the action

258 asic, yet unanswered question is whether the Met(20) loop adopts a closed conformation during the che

259 ydrofolate reductase (ecDHFR) is whether the Met(20) loop is dynamically coupled to the chemical step

260 NF Met mice indicates that patients with the Met allele may be less responsive to scopolamine.

261 r mechanics free energy simulations with the Met(20) loop in a closed and disordered conformation.

262 fter immersion ended, whereas those with the Met/Met genotype did not show these relationships.

263 e exogenously expressing histone 3 Lys-36 to Met mutation (K36M) acts in a dominant-negative manner t

264 (S) compound 5'-methylthioadenosine (MTA) to Met.

265 naling promoted PDA growth and resistance to Met inhibition.

266 s, where higher reconversion rates of SMM to Met were detected.

267 Histone Lys-to-Met (K-to-M) mutations act as gain-of-function mutations

268 hormone (JH) receptor, Methoprene-tolerant (Met), steroid receptor coactivator (SRC) and GATAa but n

269 ed to yield the paralog Methoprene-tolerant (Met).

270 Analysis of TAML/NaClO treated Met solutions employing successive identical catalyst do

271 ranscripts from two plastid loci, psbD-tRNA (Met)-ycf4 and rpl36-rps13-rps11.

272 acid azidonorleucine (Anl) to elongator tRNA(Met) in hamster (CHO), monkey (COS7), and human (HeLa) c

273 demonstrate that m(5)C deficiency in mt-tRNA(Met) results in the lack of 5-formylcytosine (f(5)C) at

274 lly encoded transfer RNA methionine (mt-tRNA(Met)).

275 eport that RPUSD4 binds 16S mt-rRNA, mt-tRNA(Met), and mt-tRNA(Phe), and we demonstrate that it is re

276 Defined in vitro analyses revealed that tRNA(Met(CAU)) and tRNA(Trp(CCA)) are substrates for Cm forma

277 ery 5' end of mRNA, implying that Met-tRNAi (Met) inspects mRNA from the first nucleotide and that in

278 ous tumor allografts was enhanced in 2+tRNAi(Met) mice compared with wild-type littermate controls.

279 ional copies of the tRNAi(Met) gene (2+tRNAi(Met) mouse).

280 is fact, it is not currently known how tRNAi(Met) expression levels influence tumor progression.

281 reinitiation complex (PIC) bearing Met-tRNAi(Met) in a ternary complex (TC) with eukaryotic initiatio

282 complex (PIC) bearing the eIF2.GTP.Met-tRNAi(Met) ternary complex (TC) scans the mRNA for an AUG codo

283 indicated that elevated expression of tRNAi(Met) significantly increased synthesis and secretion of

284 partially rescued by overexpression of tRNAi(Met).

285 To investigate how elevated stromal tRNAi(Met) contributes to tumor progression, we generated a mo

286 se expressing additional copies of the tRNAi(Met) gene (2+tRNAi(Met) mouse).

287 sion of the initiator methionine tRNA (tRNAi(Met)) is deregulated in cancer.

288 e 58 of the initiator methionine tRNA (tRNAi(Met)), a nuclear post-transcriptional modification assoc

289 t in the liver subtle increases in wild-type Met RTK levels are sufficient for spontaneous tumors in

290 Reexpression of wild-type Met, kinase-dead Met, or integrin alpha3 was sufficient

291 =71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met (N=19, 26.8%)) received m

292 cts of scopolamine were assessed in BDNF Val/Met knock-in mice, in which BDNF processing and release

293 on in women that the effects of the BDNF Val/Met polymorphism on hippocampal function are selectively

294 ossessing lower activity BDNF genotypes (Val/Met, Met/Met).

295 ingle-pulse TMS study carried on 16 Met (Val/Met and Met/Met) and 16 Val/Val participants selected fr

296 Feeding and mating working through Vg, Met, SRC, EcR, and GATAa regulate oocyte development.

297 ted from a large pool of healthy volunteers, Met participants showed significantly less muscle-specif

298 h in preclinical mouse models, compared with Met.

299 We show that eIF2B can compete with Met-tRNAi for eIF2-GTP and can destabilize TC.

300 DHD was modulated by COMT polymorphism, with Met-carriers exhibiting significantly lower functional c