ライフサイエンスコーパス: MEP

1 MEP amplitude was facilitated during troughs and rising

2 MEP concentrations at 5 and 8 y of age were associated w

3 MEP concentrations were consistently higher when the usa

4 MEP pathway regulation is poorly understood in microorga

5 MEPs could be easily recorded, disappearing after NMB an

6 MEPs decreased by 36 +/- 6% (P < 0.05) from the start of

7 MEPs detect the lowest systemic blood pressure that ensu

8 MEPs evoked from motor cortex were robustly augmented wi

9 MEPs were also measured in one lamb undergoing Neuro-Mus

10 MEPs were only present in individuals who had spasticity

11 t characteristics did not explain additional MEP amplitude variance beyond that explained by mean bet

12 h low iron in the marrow environment affects MEP metabolism, attenuates ERK signaling, slows prolifer

13 After PAS25 alone, MEP amplitude increased while intracortical circuits did

14 Proteins of the Amt/MEP family facilitate ammonium transport across the memb

15 proposed in which the monoterpene blocks an MEP pathway-dependent protein geranylgeranylation necess

16 tensity below the threshold for provoking an MEP.

17 ic stem cell signature and largely retain an MEP signature.

18 y inactivating HMGR, but possibly targets an MEP-derived isoprenoid involved in the early steps of th

19 ations of BPA (1.53; 95% CI: 1.04, 2.25) and MEP (monoethyl phthalate) (1.72; 95% CI: 1.28, 2.30) at

20 siological measures including DTI, fMRI, and MEP being measured.

21 t urine sample adequately classified MBP and MEP concentrations during pregnancy.

22 Moreover, MIP and MEP significantly improved only after magnesium administ

23 Recent advances in both MVA and MEP pathway-based synthetic biology are also illustrated

24 in regulating the formation of both MVA and MEP pathway-derived terpenoid compounds by controlling t

25 titatively follow the cooperation of MVA and MEP reprogrammed upon osmotic stress (sorbitol treatment

26 esent in individuals who had spasticity, and MEP size correlated with the severity of spasticity.

27 ctober 2014 who underwent OTAAR with DAP and MEPs monitoring and had no IP-SCI.

28 a positive feedback loop in multipotent and MEPs.

29 Health and Food Safety Vytenis Andriukaitis, MEP Sirpa Pietikainen, Chair of the European Parliament

30 Afferent input attenuated PA, but not AP, MEPs during voluntary activity compared with rest.

31 calization of TRPV4(EC) channels and eNOS at MEPs, and the absence of Hbalpha, favour TRPV4(EC) -eNOS

32 cortical stimulation of corticospinal axons (MEPs and CMEPs, respectively) and the activity in intrac

33 rtex of healthy human subjects, and baseline MEPs recorded from forearm flexor, forearm extensor and

34 ants and bacteria, other HAD proteins may be MEP pathway regulators.

35 CD71(+) CD105(-) MEPs are erythrocyte-biased MEPs (E-MEPs) and CD71(int/+) CD105(+) cells are EPs.

36 nemia also show thrombocytosis and Mk-biased MEPs.

37 K signaling, slows proliferation, and biases MEPs toward Mk lineage commitment.

38 valonate pathway of isoprenoid biosynthesis (MEP pathway), is a clinically validated antimalarial tar

39 on is much more highly enriched for bipotent MEPs than any previously reported subpopulations.

40 However, both MEPs and TEPs were consistently larger when evoked durin

41 During NOGO trials, both MEPs and CMEPs remained unchanged compared to baseline i

42 e in Allergy and Airways Diseases, hosted by MEP David Borrelli, and with active participation of the

43 potentiation (LTP) after-effect assessed by MEPs, but did not vary at PPC level.

44 the PAS protocol induced LTD as revealed by MEPs, there was a specific increase of the coherence bet

45 erived population of glia we propose calling MEP glia.

46 CD71(+) CD105(-) MEPs are erythrocyte-biased MEPs (E-MEPs) and CD71(int/+

47 Both CD71(-) CD105(-) and CD71(+) CD105(-) MEPs, at least in vitro, still retained bipotency for th

48 es as well as their common progenitor cells (MEPs).

49 monstrate that cortical and cervicomedullary MEP size was reduced during precision grip compared with

50 tical inhibition (SICI) and cervicomedullary MEPs (CMEPs) in neural populations controlling in the ES

51 In contrast, cervicomedullary MEPs and F-waves remained unchanged across conditions, a

52 In all conditions, MEPs in this muscle were elevated upon or following move

53 ains and correlated with individual cortical MEP latency differences.

54 mice exhibited significantly longer cortical MEP latencies (4.5 +/- 0.22 ms versus 3.7 +/- 0.13 ms; P

55 iring caused strong augmentation of cortical MEPs and spinal excitability that lasted up to an hour a

56 otor evoked potentials elicited by cortical (MEPs) and subcortical (CMEPs) stimulation of corticospin

57 from Agrobacterium tumefaciens, which covert MEP to the corresponding eight-membered cyclic diphospha

58 We synthesized five D-MEP analogues-D-erythritol-4-phosphate (EP), D-3-methylt

59 Therefore, conventionally defined MEP are a mixed population, as a minority give rise to m

60 remained unchanged across conditions, as did MEPs evoked during unopposed weak flexion of the index f

61 es was used to inhibit carbon input into DXP/MEP pathway or both input and output.

62 These data indicate that the DXP/MEP pathway is extremely elastic, and the presence of a

63 esidual myeloid differentiation capacity; "E-MEP," strongly biased towards erythroid differentiation;

64 CD105(-) MEPs are erythrocyte-biased MEPs (E-MEPs) and CD71(int/+) CD105(+) cells are EPs.

65 ES MEPs were increased after the arm cycling.

66 min of the arm cycling, the amplitude of ES MEPs increased to a similar extent as with 30 min of the

67 monstrate that the size of cortically evoked MEPs in the first dorsal interosseous, but not in the ab

68 Extended MEPs monitoring was independently associated with decrea

69 e studied the independent effect of extended MEPs monitoring on the risk of developing DP-SCI.

70 with ERG in enhancing the expansion of fetal MEPs and megakaryocytic precursors, resulting in hepatic

71 ted the significant increase in elbow flexor MEP observed from rest to non-fatiguing exercise under c

72 These analyses exposed 18 key genes from MEP, SK, phytol recycling and VTE-core pathways highly a

73 Although a functional MEP pathway is essential for plant viability, the underl

74 and quantitation of primary functional human MEPs from granulocyte colony-stimulating factor-mobilize

75 els of iron deficiency anemia, primary human MEPs exhibit decreased proliferation and Mk-biased commi

76 ur results demonstrate that immunophenotypic MEP comprise three distinct subpopulations: "Pre-MEP," e

77 Comparative expression analyses in MEP, MkP, and ErP populations revealed differential expr

78 with 0.5% predicted after placebo; change in MEP: 11.9% predicted after magnesium compared with 0.8%

79 However, no correlation between changes in MEP amplitudes and functional connectivity was detected.

80 d this negatively correlated with changes in MEP size.

81 he effects of PAS25 with further increase in MEP amplitude and led to reduction in SICI and LICI.

82 Although the increase in MEP amplitudes did not differ between the first and seco

83 score and predicted a 254-1,333% increase in MEP and parabens concentrations.

84 Significant increases in MEP amplitude were seen following all sessions in the as

85 Increases in MEP and parabens were generally greater with PCP use wit

86 the Mk lineage, further defining its role in MEP lineage fate.

87 In MEPs of transmembrane serine protease 6 knockout (Tmprss

88 -E fate decision at the single cell level in MEPs and found that short hairpin RNA-mediated MYB knock

89 Parasites lacking PfHAD1 have increased MEP pathway metabolites, particularly the DXR substrate,

90 iTBS over M1 increased MEP amplitudes compared with sham stimulation after each

91 Extensor imagination with TMS increased MEPs in extensor muscles only.

92 Flexion imagination with TMS increased MEPs in flexors and an intrinsic hand muscle.

93 and differentiation potential of individual MEP cells.

94 rmacological manipulations of the individual MEP pathway metabolite levels demonstrate the high speci

95 -SMA (but not over a control site) inhibited MEPs at an ISI of 40 ms.

96 Immediately after this intervention, MEP measurement was repeated.

97 Post-interventional MEPs were recorded for an hour and compared to sham usin

98 Carbon was rapidly assimilated into MEP pathway intermediates, but not into the mevalonate p

99 This insight into MEP pathway inhibition consequences underlines the risk

100 iTBS-gamma tACS induced a larger MEP facilitation than iTBS-sham tACS in both groups, wit

101 Interestingly, larger MEPs were associated with higher levels of GABA in M1, b

102 Moreover, left MEPs were larger, as soon as the signal appeared, in the

103 As expected, the maximal MEPs increase with subjects at rest was instead obtained

104 d towards erythroid differentiation; and "MK-MEP," a previously undescribed, rare population of cells

105 -2-ethylhexyl (MEHP, 700 nM), and monoethyl (MEP, 1.5muM) phthalates.

106 biotic, and should be effective against most MEP-dependent organisms.

107 n analyses reveal that both human and murine MEP have lower levels of phospho-ERK1/2 in iron-deficien

108 idual TMS SI1mV (stimulus intensity for 1 mV MEP amplitude) sensitivity correlated negatively with 1.

109 We recorded myogenic MEPs after transcranial motor cortex stimulation in 6 la

110 P, overcoming flux limitations of the native MEP pathway.

111 onfidence interval (CI) = 0.21-0.31] for NRS-MEP = 0 to 0.45 (95% CI = 0.36-0.55) for NRS-MEP = 10.

112 MEP = 0 to 0.45 (95% CI = 0.36-0.55) for NRS-MEP = 10.

113 ain score on the Numerical Rating Scale (NRS-MEP) and the patients' opinion whether the pain was acce

114 Ablation of MEP glia resulted in the absence of myelinating glia alo

115 scarriage indicated positive associations of MEP, MEOHP, MEHHP and SigmaHMWP with embryonic loss (dur

116 her creatinine- normalized concentrations of MEP, MBP, MEOHP, MEHHP, SigmaLMWP and SigmaHMWP.

117 e first aimed to evaluate the feasibility of MEP recording in neonatal lambs and test its validity.

118 onsistent with this hypothesis, lethality of MEP pathway inhibition in Arabidopsis thaliana by fosmid

119 r example, the NADPH-dependent production of MEP from 1-deoxy-D-xylulose 5-phosphate in the first com

120 sis was by far (99%) the main carbon sink of MEP pathway intermediates in mature gray poplar leaves,

121 ncluding facilitating mechanistic studies of MEP lineage commitment, improving approaches for in vitr

122 Suppression of MEP/DOXP pathway activity by high CO2 has been explained

123 in (FSM) is light dependent, and toxicity of MEP pathway inhibition is reduced by genetic and chemica

124 ediated MYB knockdown promoted commitment of MEPs to the Mk lineage, further defining its role in MEP

125 itself is sufficient to induce expansion of MEPs in fetal livers.

126 We hypothesized that extension of MEPs monitoring beyond ACI can also help decrease the ri

127 Initial impairment score, presence of MEPs and FA asymmetry were the only predictors of impair

128 We found that the size of MEPs, but not CMEPs, was more suppressed during power gr

129 Notably, the suppression of MEPs was present from the MEP onset, suggesting that ind

130 downstream of Kit to support the survival of MEPs.

131 and the effect of an acoustic startle cue on MEPs elicited by cervicomedullary stimulation (CMEPs) on

132 itory RT, the CS no longer had any effect on MEPs.

133 At and following movement onset, MEPs obtained in the right FCR were smaller in the Visio

134 beneath the threshold of detection in GMP or MEP.

135 Nras(G12D/+)p53(-/-) MEPs are transformed to self-renewing AML-initiating cel

136 ric inhibition correlated with changes in PA MEPs.

137 hate/1-deoxy-d-xylulose 5-phosphate pathway (MEP/DOXP), and its synthesis is directly related to phot

138 mic manner as their minimum energy pathways (MEPs) are separated by a large barrier.

139 m transporter (AMT)/methylammonium permease (MEP)/Rhesus glycoprotein (Rh) family of ammonia (NH(3)/N

140 cerebellar rTMS increased cortico-pharyngeal MEP amplitudes (mean bilateral increase 52%, P = 0.007)

141 Based on the changes in pharyngeal MEPs, the optimal preconditioned 1 Hz and 5 Hz rTMS prot

142 XP into 2-C-methyl-D-erythritol 4-phosphate (MEP) by consecutive isomerization and NADPH-dependent re

143 pendent 2-C-methyl-D-erythritol 4-phosphate (MEP) isoprenoid pathway, unexpectedly down-regulated the

144 ng the 2-C-methyl-d-erythrithol-4-phosphate (MEP) pathway for isoprenoid biosynthesis offers interest

145 use the 2-C-methyl-D-erythritol 4-phosphate (MEP) pathway for the synthesis of their essential isopre

146 astidic 2-C-methyl-d-erythritol-4-phosphate (MEP) pathway genes, geranylgeranyl diphosphate synthases

147 astidic 2-C-methyl-D-erythritol-4-phosphate (MEP) pathway is one of the most important pathways in pl

148 The 2-C-methyl-D-erythritol 4-phosphate (MEP) pathway leads to the biosynthesis of isopentenyl di

149 e (DXP)/2-C-methyl-D-erythritol 4-phosphate (MEP) pathway of isoprenoid synthesis by end products dim

150 The 2-C-methylerythritol 4-phosphate (MEP) pathway supplies precursors for plastidial isopreno

151 via the 2-C-methyl-d-erythritol 4-phosphate (MEP) pathway.

152 VA) and 2-C-methyl-d-erythritol-4-phosphate (MEP) pathways, which have been engineered to produce com

153 D-3-Methylerythritol-4-phosphate (MEP), the first pathway-specific intermediate in the pat

154 lize the 2C-methyl-D-erythritol 4-phosphate (MEP, 5) pathway for the biosynthesis of isopentenyl diph

155 athway involving methylerithritol phosphate (MEP) was discovered in the early 1990s.

156 derived from the methylerythritol phosphate (MEP) and shikimate pathways (SK), respectively.

157 tetrapyrrole and methylerythritol phosphate (MEP) biosynthesis pathways, respectively.

158 y the plastidial methylerythritol phosphate (MEP) pathway and a stress-specific retrograde signal, in

159 esis through the methylerythritol phosphate (MEP) pathway generates commercially important products a

160 The methylerythritol phosphate (MEP) pathway is an essential metabolic pathway found in

161 t enzymes of the methylerythritol phosphate (MEP) pathway of isoprenoid biosynthesis, including the c

162 last step of the methylerythritol phosphate (MEP) pathway which is used for the biosynthesis of essen

163 oids through the methylerythritol phosphate (MEP) pathway, an attractive pathway for antimicrobial dr

164 tic pathway [the methylerythritol phosphate (MEP) pathway] and a modified mevalonic acid (MVA) pathwa

165 lonate (MVA) and methylerythritol phosphate (MEP) pathways, operating in parallel in plants to genera

166 c acid (MVA) and methylerythritol phosphate (MEP) pathways.

167 a the endogenous methylerythritol-phosphate (MEP) pathway, in tandem with the growth of Synechocystis

168 nary concentrations of mono-ethyl phthalate (MEP) decreased by 27.4% (95% CI: -39.3, -13.2) on averag

169 In mothers, monoethyl phthalate (MEP) metabolite concentrations were significantly higher

170 est percent increase in monoethyl phthalate (MEP) was associated with use of cologne/perfume (83%, p-

171 orDEHP) metabolites and monoethyl phthalate (MEP) with child adiposity depended on the timing of expo

172 methyl phthalate (MMP), monoethyl phthalate (MEP), monobutyl phthalate (MBP), monobenzyl phthalate (M

173 enzyl phthalate (MBzP), monoethyl phthalate (MEP), monocarboxyisooctyl phthalate (MCOP), monocarboxyi

174 versely associated with monoethyl phthalate (MEP; the urinary metabolite of DEP) concentration (p < 0

175 e glial segregation at the motor exit point (MEP) transition zone are unknown.

176 Positive associations between postnatal MEP and summation operatorDEHP concentrations depended o

177 Motor evoked potential (MEP) amplitude, recruitment curve, and intracortical cir

178 through recording of motor-evoked potential (MEP) amplitude.

179 nificantly predicted motor-evoked potential (MEP) amplitudes.

180 ed by changes in the motor evoked potential (MEP) following the paired stimulation.

181 over M1 producing a motor-evoked potential (MEP) in the relaxed hand.

182 uisition of baseline motor evoked potential (MEP) recordings from each site as a measure of excitabil

183 lity as measured by motor-evoked potentials (MEPs) and (2) alters functional connectivity measured us

184 trolling latency of motor evoked potentials (MEPs) and clinical onset of experimental autoimmune ence

185 Motor evoked potentials (MEPs) and motor threshold were recorded from extensor ca

186 lation, we examined motor evoked potentials (MEPs) and the activity in intracortical and subcortical

187 examined in humans motor-evoked potentials (MEPs) and the activity in intracortical circuits (suppre

188 taneously recording motor-evoked potentials (MEPs) and TMS-evoked EEG potentials (TEPs).

189 ess was monitored via TMS-evoked potentials (MEPs) during a 25% MVC.

190 Motor evoked potentials (MEPs) elicited by cortical, but not by subcortical, stim

191 thesis, we examined motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation over

192 erve stimulation on motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation over

193 thesis, we examined motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation over

194 Motor-evoked potentials (MEPs) evoked by single-pulse transcranial magnetic stimu

195 ex (M1) we examined motor evoked potentials (MEPs) in the contralateral erector spinae (ES) muscle be

196 or cortex to elicit motor evoked potentials (MEPs) in the quadriceps femoris muscle and structural ma

197 ulus (TS) to elicit motor-evoked potentials (MEPs) in the right hand.

198 T, such that larger motor-evoked potentials (MEPs) measured at rest were associated with faster RTs.

199 Motor evoked potentials (MEPs) monitoring can promptly detect spinal cord ischemi

200 we used the size of motor evoked potentials (MEPs) obtained by transcranial magnetic stimulation (TMS

201 Motor evoked potentials (MEPs) were measured before and for 60 min post-rTMS.

202 pinal cord in rats; motor evoked potentials (MEPs) were measured from biceps.

203 Motor-evoked potentials (MEPs) were obtained by transcranial magnetic stimulation

204 imulation (TMS), 25 motor-evoked potentials (MEPs) were recorded before, and 10 time points up to 2 h

205 Motor-evoked potentials (MEPs) were recorded from the right first dorsal inteross

206 the measurement of motor evoked potentials (MEPs), we have previously demonstrated that corticospina

207 d quantification of motor evoked potentials (MEPs).

208 logical (changes in motor evoked potentials [MEPs]) assessments were performed prior to and following

209 comprise three distinct subpopulations: "Pre-MEP," enriched for erythroid/megakaryocyte progenitors b

210 n 6 h of urine collection strongly predicted MEP and paraben urinary concentrations.

211 During pregnancy, MEP (ICC = 0.50) and MBP (ICC = 0.45) were less variable

212 ssure (MIP) and maximal expiratory pressure (MEP)].

213 The maximum entropy principle (MEP) is a method for obtaining the most likely distribut

214 Maximum entropy production (MEP), rooted in thermodynamics principles, provides a to

215 d at the Megakaryocyte/Erythroid Progenitor (MEP) stage of differentiation and is not observed in non

216 r (CMP), megakaryocyte-erythroid progenitor (MEP), and granulocyte-macrophage progenitor (GMP) cells,

217 sor, the megakaryocyte-erythroid progenitor (MEP), which remains poorly defined.

218 SC) and megakaryocyte-erythroid progenitors (MEP) than low-risk patients, and provided a prognostic m

219 MPs), megakaryocyte-erythrocyte progenitors (MEPs), pre-megakaryocyte-erythrocyte progenitors (PreMeg

220 urified megakaryocyte/erythroid progenitors (MEPs) from W41/41 mice and rescued by the SCL transgene.

221 ipotent megakaryocyte/erythroid progenitors (MEPs) give rise to progeny limited to the megakaryocyte

222 f megakaryocytic (Mk)-erythroid progenitors (MEPs) toward the Mk lineage in both human and mouse.

223 f fetal megakaryocyte-erythroid progenitors (MEPs) triggered by trisomy of chromosome 21 and is furth

224 ), and megakaryocytic-erythroid progenitors (MEPs).

225 nown as megakaryocyte/erythroid progenitors (MEPs).

226 cts the megakaryocyte-erythroid progenitors (MEPs).

227 ence in megakaryocyte-erythroid progenitors (MEPs).

228 (EC) channels at myoendothelial projections (MEPs) in MAs, although they lacked the spatial proximity

229 ffect of iTBS-beta tACS on both single-pulse MEPs and SICI was similar to that obtained in the iTBS-s

230 produced by iTBS-gamma tACS on single-pulse MEPs correlated with disease duration, while changes in

231 iTBS-sham tACS facilitated single-pulse MEPs in HSs, but not in patients.

232 ablished that fosmidomycin inhibits purified MEP synthase (DXR) from F. tularensis LVS.

233 tor agonist baclofen by SCI patients reduced MEP size during precision grip to similar levels as unin

234 PAS25 followed by cTBS150 led to reduced MEP amplitude and increased LICI and SICI.

235 e found that SCI participants showed similar MEPs and maximal voluntary contractions in biceps but sm

236 Highly purified, single MEP cells were analyzed using index fluorescence-activat

237 akefulness and regardless of SO state, sleep MEPs were smaller and delayed whereas sleep TEPs were fu

238 hat participants with spasticity had smaller MEPs and MVCs and larger StartReact compared with partic

239 However, neither stable MEPs during aortic clamp interval (ACI) nor absence of I

240 These results suggest that standardized MEP recording and analysis in neonatal lambs is feasible

241 ending volley from motor cortex stimulation, MEPs were more than doubled.

242 ich engages the reticular system, suppressed MEP size during power grip to a lesser extent than durin

243 hat engages the reticular system, suppressed MEP size during power grip to a lesser extent than durin

244 ut significantly (P < 0.001) suppressed test MEPs with an ISI in the range 18-40 ms.

245 Francisella is demonstrated by the fact that MEP pathway mutations are lethal.

246 We hypothesized that MEP pathway inhibition is lethal because a reduction in

247 The MEP has found hundreds of applications in ergodic and Ma

248 The MEP pathway is used by a number of pathogens, including

249 The MEP pathway, which is absent in animals but present in m

250 f CNS-derived peripheral glia located at the MEP that selectively restrict the migration of OPCs into

251 d suggests new opportunities to engineer the MEP pathway.

252 the suppression of MEPs was present from the MEP onset, suggesting that indirect corticospinal pathwa

253 ate (MEcDP), metabolically isolated from the MEP pathway.

254 A brief overview highlights the MEP pathway's potential as a selective drug target, whic

255 at catalyzes the first committed step in the MEP pathway, producing the essential isoprenoid precurso

256 The antimalarial fosmidomycin inhibits the MEP pathway enzyme deoxyxylulose 5-phosphate reductoisom

257 r long-chain Dols, the relative input of the MEP and MVA pathways remained unchanged, suggesting dive

258 or root axons and an immediate breach of the MEP by OPCs.

259 and the abundance of the first enzyme of the MEP pathway (1-deoxy-D-xylulose 5-phosphate synthase, DX

260 ant mechanism of metabolic regulation of the MEP pathway and indicates that thiamine pyrophosphate-de

261 numerous organisms, makes the enzymes of the MEP pathway attractive drug targets for the development

262 hematical model of diurnal regulation of the MEP pathway in Arabidopsis thaliana.

263 The contribution of the MEP pathway increased significantly (reaching 100%) excl

264 phosphate in the first committed step of the MEP pathway is catalyzed by 1-deoxy-D-xylulose-5-phospha

265 nderstanding the metabolic regulation of the MEP pathway is important considering the numerous applic

266 The effect of different metabolites of the MEP pathway on PtDXS activity was tested.

267 The importance of the MEP pathway to Francisella is demonstrated by the fact t

268 review, we describe the seven enzymes of the MEP pathway, along with their discoveries, three-dimensi

269 se (IspD), the third catalytic enzyme of the MEP pathway.

270 rol of DXS for the diurnal regulation of the MEP pathway.

271 is an important regulatory mechanism of the MEP pathway.

272 t DXS is the major controlling enzyme of the MEP pathway.

273 ary stimulation was used, suppression of the MEP was only evident 1-3 ms after its onset.

274 or LytB) catalyzes the terminal step of the MEP/DOXP pathway where it converts (E)-4-hydroxy-3-methy

275 ew, we summarize mechanistic insights on the MEP pathway enzymes.

276 We demonstrate that the MEP is a perfectly consistent concept for nonergodic and

277 istribution, together with the fact that the MEP pathway is essential in numerous organisms, makes th

278 Therefore, the MEP pathway is a target for the development of new antim

279 e, we analyzed the carbon fluxes through the MEP pathway and into the major plastidic isoprenoid prod

280 Our data show that flux through the MEP pathway is accelerated in light due to the photosynt

281 -methyl-d-erythritol-4-phosphate through the MEP pathway.

282 - in hematopoietic cells, contributes to the MEP lineage commitment bias observed in Tmprss6-/- mice.

283 efore controls substrate availability to the MEP pathway.

284 extend processes into the periphery via the MEP and immediately upon contact with spinal motor root

285 They are synthesized in the plastids via the MEP pathway.

286 y reduced the overall carbon flux within the MEP pathway.

287 (int)/+) CD105(+) subset of cells within the MEP population was completely restricted to the erythroi

288 ng of cell proliferation, and biasing of the MEPs toward megakaryocyte commitment, which ultimately r

289 of IR in erythroid cells and MKs compared to MEPs.

290 hanced oncogenic Nras signaling to transform MEPs and drive AML development.

291 how that during AML development, transformed MEPs acquire overexpression of oncogenic Nras, leading t

292 equencing analysis revealed that transformed MEPs gain a partial hematopoietic stem cell signature an

293 Notably, during GO trials, MEPs increased to a similar extent in both groups but CM

294 oy a forward genetics approach to understand MEP pathway regulation in the malaria parasite, Plasmodi

295 nd task and that performance correlated with MEP amplitudes in the upper limb motor region.

296 ndex finger sensory function correlated with MEP size during precision grip in SCI patients.

297 f spasticity were negatively correlated with MEP-max and MVC values and positively correlated with sh

298 impairment resolved by 70% in patients with MEPs regardless of their initial impairment, and ipsiles

299 K) pathways are enriched in Tmprss6-/- vs WT MEPs.

300 sed proliferation relative to wild-type (WT) MEPs.