ライフサイエンスコーパス: Met

1 Met also promoted antidepressant-like activities as obse

2 Met inhibition showed clinical benefit in this model.

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-lead 1.44 M1 has an apparent dissociation constant (

7 Met-predictor combines a variety of sequence-based featu

8 Met-predictor was tested on two independent test sets, w

9 riptomic information, we showed that Prima-1(Met) activity was independent of its canonical target, m

10 also observed subtype selectivity of Prima-1(Met), which showed higher levels of efficacy in the mese

11 n suffering, TMD patients with the COMT (158)Met substitution had higher pain sensitivity and longer

12 Together, the TMD diagnosis, COMT (158)Met substitution, and pain chronicity explained 52% of u

13 chol-O-methyltransferase (COMT), the Val(158)Met polymorphism (rs4680) markedly affected enzyme activ

14 aggregates by cleaving the cryptic Tyr(1605)-Met(1606) bond in the VWF A2 domain.

15 Lys-27-Met mutations in histone 3 genes (H3K27M) characterize a

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

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

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

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

20 ally conserved among GA 3-oxidases, Tyr(93), Met(106), and Thr(202), respectively, conferred GA 3-oxi

21 nteractions between the Met66 sequence and a Met-rich receptor that initiates neuronal growth cone re

22 mRNA, likely from downstream initiation on a Met residue that comprises the P1 position of NS1-ARF2(1

23 ed a mutant for ORM1 lacking one amino acid (Met-51) near its second transmembrane domain that retain

24 12-mechanism-II requires nhr-114 to activate Met/SAM cycle gene expression, the vitamin B12 transport

25 as glycolysis, and the Calvin and S-adenosyl-Met cycles.

26 way and the methionine/S-adenosylmethionine (Met/SAM) cycle.

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

28 show that the loss of the C-terminal Tyr-Ala-Met-Leu motif is responsible for P0 mislocalization, as

29 Most of the Se-Met (84.0%) and Met (75.8%) were found to be in free form in the fruitin

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

31 this site (Arg(301), Gly(304), His(307), and Met(369)) enable potent activation of the SMAD2/3 pathwa

32 Cez) binds Lys(11)-, Lys(48)-, Lys(63)-, and Met(1)-linked ubiquitin chains in vitro, establishing UB

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

34 odels reveal eIF2beta contacts with eIF1 and Met-tRNAi exclusive to the open complex that should dest

35 a ternary complex (TC) of GTP-bound eIF2 and Met-RNAi scans the mRNA for the start codon.

36 y long-lived ribosome complex with eIF5B and Met-tRNA(i)(Met) immediately before transition into elon

37 at chemoattractant signaling between Hgf and Met is required for vagus innervation of the pharyngeal

38 variants, leading to genomic instability and Met amplification.

39 Cfz was administered at 8 mg/kg (IP) and Met at 140 mg/kg (per os).

40 Phe, Leu, and Met are favored residues, each with a cleavage probabili

41 ical intervention; control, Cfz, Cfz+Met and Met for 2 and 6 days, respectively); and protocol 7 (bor

42 ansporters and genes involved in sulfate and Met metabolism were upregulated, suggesting regulation o

43 c 46-kDa protein (TRbeta2-46) that starts at Met-79.

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

45 n Exon 3, a site that coincides with an AUG (Met) in human CLU.

46 lopment of this circuit is disrupted in BDNF Met carriers due to insufficient BDNF bioavailability, s

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

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

49 variectomized mice heterozygous for the BDNF Met allele (Het-Met) and their matched wild-type (WT) mi

50 Although the BDNF Met genotype intersects the behavioral and transcription

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

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

53 rgy transfer (FRET)-based Pb(2+) biosensor, 'Met-lead 1.44 M1', with excellent performance.

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

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

56 Both Met supplementation and chemically induced glutathione d

57 pecific antibody that is monovalent for both Met and epithelial cell adhesion molecule (EpCAM).

58 on to a closed state with more tightly-bound Met-tRNAi (PIN state).

59 on to a closed state with more tightly-bound Met-tRNAi.

60 nterval and safety of FME using EMI-137, a c-Met-targeted fluorescent peptide, in a population at hig

61 cence was correlated to histopathology and c-Met expression.

62 of the growth factor receptors IGF-1R and c-Met.

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

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

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

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

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

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

69 ncluded the hepatocyte growth factor (Hgf)/c-Met signaling pathway.

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

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

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

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

74 T proto-oncogene receptor tyrosine kinase (c-Met) autocrine feed-forward loop promoting SC proliferat

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

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

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

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

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

80 factor receptor (EGFR) and proto-oncogene c-Met (MET), and shunts their trafficking into late endoso

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

82 R), and hepatocyte growth factor receptor (c-Met), improves the capture of RCC cells by up to 80%.

83 ic and microscopic level, with significant c-Met overexpression in dysplastic mucosa.

84 induction of osteopontin (Opn) stimulated c-Met expression in EC with CEC phenotype, which sensitize

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

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

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

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

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

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

91 Here, we show that installing a canonical Met ligand in lieu of the Tyr found at the heme of MauG

92 rmacological intervention; control, Cfz, Cfz+Met and Met for 2 and 6 days, respectively); and protoco

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

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

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

96 On the contrary, Met stimulated 5-HT neurons excitability and 5-HT neurot

97 leotide exchange factor cytohesin-1 controls Met-dependent cell migration.

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

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

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

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

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

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

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

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

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

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

108 We deployed Met-lead 1.44 M1 to measure Pb(2+) concentrations in dif

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

110 Blocking endocytosis or endosomal Met/beta1-integrin/FAK signaling profoundly inhibits the

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

112 A significant role for Met/Met interactions is consistent with previously-obser

113 i) chemotaxis towards chemoattractant formyl Met-Leu-Phe (fMLP) coupled with their decreased polariza

114 decreased neutrophil chemotaxis to a formyl-Met-Leu-Phe gradient.

115 richia coli and the chemoattractant N-formyl-Met-Leu-Phe (fMLP)-coated beads.

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

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

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

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

120 Furthermore, Met-predictor also attains excellent performance for pre

121 Upon binding JH, Gce/Met activates its target genes.

122 studies, reveal how the flexibility of a Gly-Met-Gly (GMG) motif in the unwound region of transmembra

123 The addition of the inhibitor GS-Met and GS-Hex resulted in hGSTA1-1 to favor the more ri

124 gulate hydrolysis of the GTP in the eIF2*GTP*Met-tRNAiMet complex to GDP and Pi.

125 al for efficient recruitment of the eIF2*GTP*Met-tRNAiMet ternary complex to the ribosome and for its

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

127 ormation and decreases the level of eIF2-GTP-Met-tRNA(i)(Met) ternary complexes.

128 s allows continued formation of the eIF2-GTP-Met-tRNAi ternary complex and unabated global translatio

129 pression, an indicator of defective eIF2-GTP-Met-tRNAiMet complex formation, and, likewise, overexpre

130 57E accelerated dissociation of the eIF2.GTP.Met-tRNAi ternary complex (TC) from reconstituted PICs w

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

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

133 mt, and Th) between hBDNF(Val/Val) and hBDNF(Met/Met) mice, implicating involvement of BDNF in Meth-i

134 ce heterozygous for the BDNF Met allele (Het-Met) and their matched wild-type (WT) mice were administ

135 s markedly different between WT mice and Het-Met mice.

136 ety-like and depression-like behavior in Het-Met mice, but not in WT mice.

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

138 at experimentally altering the timing of Hgf/Met signaling is sufficient to redirect axon targeting a

139 controls the spatiotemporal dynamics of Hgf/Met signaling to coordinate axon targeting with the deve

140 In C. jejuni, TsdA Heme 2 has His/Met ligation and an E(m) of +172 mV.

141 rom His/Lys ligation (E(m) , -129 mV) to His/Met (E(m) , +266 mV), but the rates of interconversion a

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

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

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

145 ribosome complex with eIF5B and Met-tRNA(i)(Met) immediately before transition into elongation.

146 ect positioning of the initiator Met-tRNA(i)(Met) on the ribosome in the later stages of translation

147 decreases the level of eIF2-GTP-Met-tRNA(i)(Met) ternary complexes.

148 Our study also identified Met receptor tyrosine kinases (RTKs), which carry a trun

149 , we propose that the I259M mutation impairs Met-tRNAiMet binding, causing altered control of protein

150 Biochemical analyses revealed a defect in Met-tRNAiMet binding to the mutant yeast eIF2 complexes

151 xidation kinetics point out a minor delay in Met-127 modification, likely due to the effects of AS in

152 rian hormones induce cognitive impairment in Met carriers.

153 nisms lead to inhibition of proliferation in Met-driven cancer cells, inhibition of HGF-mediated canc

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

155 t and beta1-integrin receptors, resulting in Met/beta1-integrin co-internalization and co-accumulatio

156 ated activation of several kinases including Met receptor.

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

158 to detect possible intolerance to increased Met intake.

159 ocks ligand-dependent and ligand-independent Met signaling by inhibiting HGF binding to Met and induc

160 plays critical roles in delivering initiator Met-tRNAiMet to the 40S ribosomal subunit and in selecti

161 tylate N termini starting with the initiator Met followed by acidic amino acids and contributed 20% o

162 in the correct positioning of the initiator Met-tRNA(i)(Met) on the ribosome in the later stages of

163 also can sense and bind uncharged initiator Met tRNA, resulting in the sequestering of the anti-Shin

164 Our findings establish a Tbx1-Isl1-Met genetic hierarchy that uniquely regulates esophagus

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

166 tial dietary restriction or with bacterial l-Met-degrading enzymes exerts potent antitumor effects.

167 However, administration of bacterial l-Met-degrading enzymes has not proven practical for human

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

169 As the human genome does not encode l-Met-degrading enzymes, we engineered the human cystathio

170 ignancies have revealed that l-methionine (l-Met) and its metabolites play a critical role in tumorig

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

172 ) to catalyze the selective degradation of l-Met.

173 ly relevant dosing, hMGL-4.0 reduces serum l-Met levels to >75% for >72 h and significantly inhibits

174 strated that systemic restriction of serum l-Met, either via partial dietary restriction or with bact

175 by artificial microRNA interference using l-Met sulfoximine selection-based gene transformation syst

176 ORM1 lacking Met-51 had strongly impaired interactions with LCB1 in a

177 nd a C-terminal swinging arm, with a Cys-Leu-Met-Cys sequence suggested to act as a shuttle dithiol/d

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

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

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

181 e the cardioprotective potency of metformin (Met).

182 malized by chronic treatment with metformin (Met).

183 Cystine (Cys(2)), methionine (Met), and sulfate were also detected and quantified in a

184 wering homocysteine (Hcy) with a methionine (Met)-restricted diet and betaine supplementation.

185 se to leader peptides containing methionine (Met; M) or threonine (Thr; T), which differentially infl

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

189 s these problems, we propose a novel method, Met-predictor, to predict methylation sites and methylat

190 ompared with other state-of-the-art methods, Met-predictor had 13.1% (3.9%) and 8.5% (16.4%) higher a

191 y generated mouse model in which both murine Met transgene and stabilized beta-catenin are conditiona

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

193 mycelium where 53.4% of Se-Met and 80.5% of Met is incorporated into proteins.

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

195 Coadministration of Met prevented Cfz-induced FS reduction and restored AMPK

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

197 Clinical development of Met-targeted antibodies has been challenging, however, a

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

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

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

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

202 Evaluation of Met, EpCAM, and HGF levels in human tumor samples reveal

203 that vitamin B12 represses the expression of Met/SAM cycle genes by a propionate-independent mechanis

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

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

206 htt(NT)Q(10) by catalyzing the oxidation of Met(7) to a sulfoxide, resulting in an aggregation-incom

207 helix domain but is released by oxidation of Met-8 during reactive oxygen species (ROS) stress.

208 involved in the chain elongation pathway of Met-derived glucosinolates.

209 expressed at high levels in a wide range of Met-positive tumor types, suggesting a broad opportunity

210 ion of FA and glycogen storage regardless of Met supply.

211 The 10 nM sensitivity of Met-lead 1.44 M1 is five times below the World Health Or

212 Besides oxidation at certain sites of Met, His, and Tyr, conversion of histidine to aspartate

213 gle-nucleotide polymorphism substitutions of Met residues by Thr in cancer-related proteins.

214 In addition, a novel type of Met-like RTK with a complete plexin extracellular domain

215 ents with T2DM who were free from CVD and on Met-SU dual therapy and who were intensified with DPP4i

216 ated that, for patients with T2DM who are on Met-SU dual therapy, the addition of DPP4i was a preferr

217 ity, CVD, and SH among patients with T2DM on Met-SU dual therapy intensified with DPP4i, insulin, or

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

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

220 ither methylenetetrahydrofolate reductase or Met synthase deficiency.

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

222 This Pro-Phe Met relay may constitute a structural switch that mediat

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

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

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

226 We pinpointed Met-1669 as the residue in the GBA motif of DAPLE that d

227 te er sensing of 85 scalemic samples of Pro, Met, Cys, Ala, methylpyrrolidine, 1-(2-naphthyl)amine, a

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

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

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

231 of stress-induced damage (e.g., by reducing Met and Cys oxidation products) as well as adjusting met

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

233 ck potency and the capacity to down-regulate Met.

234 Overexpression of tRNAiMet restored Met-tRNAiMet binding to eIF2 in vivo and rescued the gro

235 eIF2beta is also predicted to restrict Met-tRNAi movement into the closed/PIN state, and substi

236 er insights into the susceptibility of CaM's Met residues to oxidation and the resulting structural e

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

238 contrast with the mycelium where 53.4% of Se-Met and 80.5% of Met is incorporated into proteins.

239 Selenomethionine (Se-Met) was found to be the major Se-compound, together wit

240 Most of the Se-Met (84.0%) and Met (75.8%) were found to be in free for

241 ncrease UUG initiation in vivo and stabilize Met-tRNAi binding at UUG codons in vitro with little eff

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

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

244 A1c) control despite metformin-sulfonylurea (Met-SU) dual therapy, a third-line glucose-lowering medi

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

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

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

248 evated with the highest dose of supplemented Met.

249 e potency of a monovalent antibody targeting Met could be dramatically improved by introducing a seco

250 in Lophotrochozoa and Echinodermata (termed Met-LP RTK).

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

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

253 Our results suggest that Met may act by decreasing circulating BCAAs levels to fa

254 The Met receptor tyrosine kinase (RTK) modulates invasive gr

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

256 on calmodulin (CaM), using peroxide and the Met to Gln oximimetic mutations.

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

258 chanism is activated by perturbations in the Met/SAM cycle, genetically or due to low dietary vitamin

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

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

261 Activation of the Met receptor tyrosine kinase, either by its ligand, hepa

262 ten along with frequent amplification of the Met receptor tyrosine kinase, which conferred a stem cel

263 sed 3D cell migration upon activation of the Met receptor tyrosine kinase.

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

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

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

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

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

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

270 NRP1 variants enhance interactions with the Met and beta1-integrin receptors, resulting in Met/beta1

271 ally regulated by Cys oxidation/thioredoxin, Met-SO formation, phosphorylation, or Lys acetylation, b

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

273 t Met signaling by inhibiting HGF binding to Met and inducing receptor down-regulation.

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

275 The Val to Met substitution in the S4-S5 loop induced a larger incr

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

277 Taken together, Met/SAM cycle activity is sensed and transcriptionally a

278 sion of the JH receptor Methoprene tolerant (Met) was unable to induce Kr-h1 in the presence of HDAC1

279 its duplicate paralog, methoprene-tolerant (Met).

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

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

282 idine at position 34 of human elongator tRNA(Met)(CAT) for 2'-O-methylation (C(34)m).

283 4)m prohibits site-specific cleavage of tRNA(Met) (CAT) into tRNA fragments (tRFs) by the stress-resp

284 The presence of tRNA(Met) and tRNA(Trp) in both ceriantharian mitogenomes sup

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

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

287 f glycerophospholipids and amino acids (Trp, Met, and Cys, branched-chain amino acids), as well as ca

288 DOTA-MG11 ((177)Lu-DOTA-dGlu-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)) and (177)Lu-DOTA-PP-F11 ((177)Lu-DOTA

289 -F11 ((177)Lu-DOTA-(dGlu)(6)-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)), and whether the use of protease inhi

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

291 amino acids were composed of Val, Pro, Tyr, Met, Leu, Trp, Phe, Lys and Glu.

292 Based on the UK Met Office's long-term temperature and rainfall records,

293 al recurrences are frequently dependent upon Met gene amplification.

294 =71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met (N=19, 26.8%)) received m

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

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

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

298 d its downstream autophagic targets, whereas Met represents a novel promising intervention against Cf

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

300 ith eIF2Bdelta leading to a competition with Met-tRNA(i).