ライフサイエンスコーパス: MPT

1 MPT cells become resistant to rapamycin after prolonged

2 MPT inhibitors, cyclosporin A (CsA), and NIM811 temporar

3 MPT is caused by the opening of permeability transition

4 MPT, observed in situ as Deltapsi(m) loss, was prevented

5 MPT-based portfolios can also have 21% less uncertainty

6 MPT-guided diversification can work to reduce the climat

7 ubling the screw speed when processing a 10% MPT formulation does not affect the solid state of the p

8 At a 10% MPT load, increasing the extrusion temperature does not

9 Second malignancies were observed in 18 MPT-T patients vs 14 mPR-R patients.

10 Thus, methenyl-dH(4)MPT accumulation inhibits H(4)F-dependent assimilation.

11 nt strain, predicted to reduce methenyl-dH(4)MPT accumulation, enhances growth on methylamine.

12 in its kinetic properties for methylene-dH(4)MPT and for methenyl-H(4)F during growth on single-carbo

13 Putative functions of these genes in dH(4)MPT biosynthesis are discussed.

14 Methenyl-dH(4)MPT is shown to be a competitive inhibitor of the reduct

15 size dH(4)MPT, and six were found to be dH(4)MPT negative.

16 cs of dephosphotetrahydromethanopterin (dH(4)MPT) biosynthesis.

17 te is dephosphotetrahydromethanopterin (dH(4)MPT) dependent, while the assimilation of carbon into bi

18 re dehydrogenases able to use methylene-dH(4)MPT, an intermediate in the oxidation of formaldehyde to

19 analyzed for the ability to synthesize dH(4)MPT, and six were found to be dH(4)MPT negative.

20 ts role in oxidative metabolism via the dH(4)MPT-dependent pathway and its apparent inability to repl

21 results in the accumulation of methenyl-dH(4)MPT.

22 ovide the first biochemical evidence for H(4)MPT biosynthesis genes in bacteria.

23 Thus the first two enzymes involved in H(4)MPT biosynthesis in the archaea are Fe(2+) dependent.

24 te synthase, the first committed step of H(4)MPT biosynthesis.

25 suggesting a role for these two genes in H(4)MPT biosynthesis.

26 R that is required for the final step of H(4)MPT biosynthesis.

27 ization of four mutants defective in the H(4)MPT pathway and place them into three different phenotyp

28 These results define the role of the H(4)MPT pathway as the primary formaldehyde oxidation and de

29 ght to be essential, indicating that the H(4)MPT pathway is not absolutely required during growth on

30 ates; however, mutants defective for the H(4)MPT pathway reveal a unique phenotype of being inhibited

31 Unlike mutants defective for the H(4)MPT pathway, the ftfL mutant strain does not exhibit phe

32 D(+) can successfully substitute for the H(4)MPT pathway.

33 H(4)MPT was detectable in wild-type cells but not in strains

34 n bond before the appearance of methenyl-H(4)MPT(+) (MPT(+)).

35 e 5,10-methenyl tetrahydromethanopterin (H(4)MPT) cyclohydrolase, was constructed in vitro and recomb

36 oped to measure tetrahydromethanopterin (H(4)MPT) levels in wild-type and mutant cells of Methylobact

37 pathway and the tetrahydromethanopterin (H(4)MPT) pathway, and both are required for growth on C(1) c

38 tions linked to tetrahydromethanopterin (H(4)MPT) were analyzed in a variety of proteobacteria and in

39 erin portion of tetrahydromethanopterin (H(4)MPT), a C(1) carrier coenzyme first identified in the me

40 ns defective in tetrahydromethanopterin (H(4)MPT)-dependent formaldehyde oxidation.

41 pathway and the tetrahydromethanopterin (H(4)MPT)-linked pathway.

42 a precursor of both tetrahydrofolate and H(4)MPT, and afpA apparently encodes a novel dihydromethanop

43 anogenic Archaea and Bacteria possessing H(4)MPT-linked functions, orfY, orf1, and afpA were shown to

44 ted that the evolution of genes encoding H(4)MPT-linked reactions in Proteobacteria involved lateral

45 the enzymes involved in C(1) metabolism (H(4)MPT/H(4) F pathways, formate oxidation and serine cycle)

46 When extruding a formulation with a 40% MPT concentration, the broadening of MPT peaks indicates

47 Per-protocol response rates were 63.6% (MPT-T) and 59.9% (mPR-R) (P = .557).

48 smembrane potential within 2 h, indicating a MPT.

49 active MPT synthase and 4117 A(2) for active MPT synthase.

50 for the binding of MoaD-SH to MoaE in active MPT synthase.

51 l killing was prevented by cyclosporin A, an MPT blocker, and by pancaspase and caspase 3 inhibition,

52 llapse in Deltapsi(m) is a consequence of an MPT and that the timing of the victorin-induced MPT is p

53 ddition, we observed that the presence of an MPT inhibitor did not attenuate the activation of caspas

54 itochondrial depolarization, cell death, and MPT were detected by intravital confocal/multiphoton mic

55 se results suggest that NAD(+) depletion and MPT are necessary intermediary steps linking PARP-1 acti

56 , mitochondrial membrane depolarization, and MPT.

57 in, a common intermediate in both folate and MPT biosynthesis.

58 d increased mitochondrial ROS production and MPT.

59 ROS and MPT have been implicated in myocardial stunning associat

60 used them to investigate the role of ROS and MPT in cell death caused by t-butylhydroperoxide (tBHP)

61 leading to the formation of precursor Z and MPT, respectively.

62 a combination chemical and physical barrier MPT.

63 peak shifts indicating interactions between MPT and the carrier) between sections 5 and 6, due to fo

64 teria, this form is modified to form the bis-MPT guanine dinucleotide cofactor with two MPT units coo

65 ria depolarization by more than 60%, blocked MPT onset, and prevented cell death.

66 olar concentrations of cyclosporin A blocked MPT and cell death, suggesting that MPT is a necessary s

67 Blocking MPT diminished p53 translocation and apoptosis.

68 hondrial membrane potential and blocked both MPT and cell death.

69 We used BU.MPT cells, a mouse kidney epithelial cell line, as our p

70 sulfur- and metal-free precursor Z to MPT by MPT synthase involves the transfer of sulfur atoms from

71 moters to regulate transcription and control MPT.

72 Cultured MPT cells exposed to rapamycin for 7 days were approxima

73 lling and cytochrome c release and decreased MPT and antimycobacterial activity.

74 an existing bioenergetics model to describe MPT induction under a variety of conditions.

75 t C-7 and C-9 of the pterin ring distinguish MPT from all other pterin-containing natural products.

76 We exposed MPT cells to 0.2 dynes/cm(2) FSS for 3 h and performed c

77 ochondria subjected to conditions that favor MPT.

78 e >/=3 nonhematologic toxicity was 59.5% for MPT-T vs 40.0% for mPR-R (P = .001).

79 phosphorus ratios, time-dependent assays for MPT and MGD detection, and determination of the numbers

80 des the three basic necessary conditions for MPT: a high calcium load, alkaline matrix pH and circums

81 The results also suggest a new model for MPT in which the central pore protein ANT is regulated b

82 gets and evaluate potential therapeutics for MPT mitigation.

83 ontrast, protection of the mitochondria from MPT favors apoptosis of M. tuberculosis-infected macroph

84 Further, MPT-inducing conditions permitted victorin access to the

85 nd step is catalyzed by the heterotetrameric MPT synthase protein consisting of two large (MoaE) and

86 d upon formation of the subunit interface in MPT synthase was estimated to be 2378 A(2) for inactive

87 role of c-Jun N-terminal kinase 2 (JNK2) in MPT-induced liver injury.

88 of the interaction between MoaE and MoaD in MPT synthase using a H/D exchange and matrix-assisted la

89 e was estimated to be 2378 A(2) for inactive MPT synthase and 4117 A(2) for active MPT synthase.

90 for the binding of MoaD to MoaE in inactive MPT synthase and a dissociation constant of 2.6 +/- 0.9

91 alcein into mitochondria after MHX indicated MPT onset.

92 +) depletion is necessary for PARP-1-induced MPT, NAD(+) was restored to near-normal levels after PAR

93 In addition, they inhibited 3NP-induced MPT in isolated mitochondria and prevented mitochondrial

94 The protective effect against Ca-induced MPT was most evident under conditions in which the abili

95 me inactivation is observed for Ca2+-induced MPT.

96 reased susceptibility to the calcium-induced MPT in liver mitochondria isolated from a knock-in HD mo

97 The manganese-induced MPT in astrocytes was blocked by pretreatment with antio

98 The mutant huntingtin protein-induced MPT pore opening was accompanied by a significant releas

99 and that the timing of the victorin-induced MPT is poised to influence the cell death response.

100 t can scavenge mitochondrial ROS and inhibit MPT, suggesting that it may protect against ischemic ren

101 Exogenous H(2)O(2) inhibited MPT, because of its activation of PKCepsilon, with an IC

102 he K(+) ionophore valinomycin also inhibited MPT opening and that this inhibition required reactive o

103 s of PKG or protein kinase C (PKC) inhibited MPT opening.

104 ased mitochondrial ROS production, inhibited MPT and swelling, and prevented cytochrome c release ind

105 Heat shock inhibited MPT pore opening induced by 50 microm CaCl(2) plus 5 mic

106 r 3 to 6 hours followed by a CsA-insensitive MPT 9 to 16 hours after acetaminophen.

107 )-independent and cyclosporin A-insensitive) MPT pore opening induced by higher doses of HgCl(2) and

108 /kg, n = 7), a calcineurin inhibitor lacking MPT activity, followed in 30 min by LPS.

109 rmeability transition pore complex, to limit MPT induction is the general mechanism of cardiomyocyte

110 suggested the distinctness of CypD-mediated MPT from RIPK1/RIPK3-mediated necroptosis.

111 Methanopterin (MPT) and its analogs are coenzymes required for methanog

112 opy enabled identification of a novel bis-Mo-MPT intermediate on MobA prior to nucleotide attachment.

113 ddition of Mg-GTP to MobA loaded with bis-Mo-MPT resulted in formation and release of the final bis-M

114 n, which involves 1) the formation of bis-Mo-MPT, 2) the addition of two GMP units to form bis-MGD on

115 s via a dithiolene function, thus forming Mo-MPT.

116 of the fragments of the Mo-molybdopterin (MO-MPT) binding site and nitrate reduction active site and

117 d tungsten are coordinated by molybdopterin (MPT), a tricyclic pyranopterin containing a cis-dithiole

118 MOCS2A, the small subunit of molybdopterin (MPT) synthase.

119 basic form comprises a single molybdopterin (MPT) unit, which binds a molybdenum ion bearing three ox

120 The molybdopterin (MPT) synthase complex in Escherichia coli consists of tw

121 rom a pyranopterindithiolate (molybdopterin, MPT) cofactor.

122 onths, from 32.7 months (MP) to 39.3 months (MPT).

123 Overall survival was 52.6 months (MPT-T) vs 47.7 months (mPR-R) (P = .476).

124 efore the appearance of methenyl-H(4)MPT(+) (MPT(+)).

125 8 kcal/mol lower than that in the absence of MPT+, a result that explains why the isotopic H2/D2O exc

126 t is essential for the catalytic activity of MPT synthase.

127 /H(2)O exchange take place as the arrival of MPT(+) triggers the breaking of the strong Fe-H(delta-).

128 (3) Only upon the arrival of MPT(+) with its strong hydride affinity can D(2)/H(2)O e

129 h a 40% MPT concentration, the broadening of MPT peaks indicates melting of MPT between sections 2 an

130 release of cytochrome c is a consequence of MPT, the results of our time course experiments suggest

131 d 668 patients between nine 4-week cycles of MPT followed by thalidomide maintenance until disease pr

132 ion-free survival (PFS) hazard ratio (HR) of MPT-T/mPR-R </=0.82.

133 lted in mitoK(ATP)-independent inhibition of MPT opening, whereas activation of PKCepsilon by PKG or

134 se caused mitoK(ATP)-dependent inhibition of MPT opening.

135 ow that cyclosporin A (CsA), an inhibitor of MPT, protects the mitochondria from release of cytochrom

136 broadening of MPT peaks indicates melting of MPT between sections 2 and 3, caused by the first kneadi

137 t heat shock causes resistance to opening of MPT pores, which may contribute to heat shock protection

138 e barrier for H2 cleavage in the presence of MPT+ is 18 kcal/mol lower than that in the absence of MP

139 Hmd is strictly dependent on the presence of MPT+.

140 ng must ultimately involve the prevention of MPT.

141 n essential component and a key regulator of MPT induction.

142 Use of MPT-T or mPR-R in elderly patients with untreated MM dem

143 rates (partial response or better was 59% on MPT and 37% on MP).

144 Median PFS was 21 months on MPT-T and 18.7 months on mPR-R (HR, 0.84; 95% confidence

145 l permeability transition (MPT)-dependent or MPT-independent mechanisms.

146 MPR-R has no advantage over MPT-T concerning efficacy.

147 demonstrated by the ability of pharmacologic MPT inhibitors to completely protect PLC/PRF/5 cells.

148 utations confirmed that Vp15 encodes a plant MPT synthase small subunit (ZmCNX7).

149 cene (LPT, 2.5 to 3 Ma) and mid-Pleistocene (MPT, 1.2 to 0.85 Ma) climate transitions.

150 eet dynamics and that longer and deeper post-MPT ice ages were sustained by carbon cycle feedbacks re

151 Its recovery into the post-MPT 100-thousand-year world is characterized by continue

152 ted and the activities of the four predicted MPT-containing enzymes were assayed in the presence of m

153 gulated Deltapsi(m), and diazoxide prevented MPT by inhibiting the driving force for Ca uptake.

154 n after MHX, at least in part, by preventing MPT onset and subsequent compromised energy supply and p

155 In conclusion, NO prevents MPT-dependent necrotic killing of ischemic hepatocytes a

156 predicted to contain a metal binding pterin (MPT), with the metal being either molybdenum or tungsten

157 8 patients were randomly assigned to receive MPT-T, and 319 received MPR-R.

158 ed cortical neurons had a delayed or reduced MPT as compared with astrocytes.

159 t-D+TPEN, and rOx production did not require MPT or caspase activation.

160 The MPT inhibitor sanglifehrin A reversed MPT markers and increased respiration in LM7 and 143B ce

161 clusion, after acetaminophen a CsA-sensitive MPT occurred after 3 to 6 hours followed by a CsA-insens

162 ngs suggest that the development of specific MPT inhibitors may be an interesting therapeutic avenue

163 ed [Ca(2+)](m), blocked necrosis, stabilized MPT, decreased mitochondrial cytochrome c release, lower

164 In summary, these results support MPT as an upstream target for pharmacologic intervention

165 Metoprolol tartrate (MPT) concentration (10 and 40% in Eudragit RSPO), extrus

166 itiated, multipurpose prevention technology (MPT) that simultaneously reduces their risk of acquiring

167 l (LTD) nuclei of the mesopontine tegmentum (MPT).

168 at 33 degrees C (male producing temperature: MPT) yields male offspring, whereas incubation temperatu

169 n of melphalan, prednisone, and thalidomide (MPT) is considered standard therapy for newly diagnosed

170 ared melphalan, prednisone, and thalidomide (MPT-T) with melphalan, prednisone, and lenalidomide (mPR

171 ombination melphalan-prednisone-thalidomide (MPT) is considered a standard therapy for patients with

172 prednisone alone (MP) and with thalidomide (MPT).

173 e of cytochrome c occurred much earlier than MPT; hence, the former is unlikely to be a consequence o

174 ility to MPT, increasing the likelihood that MPT will occur on reperfusion (the MPT trigger phase).

175 el was corroborated and used to predict that MPT in an acidic environment is mitigated by an increase

176 blocked MPT and cell death, suggesting that MPT is a necessary step linking PARP-1 activation to cel

177 The MPT containing enzymes nitrate reductase, sulphite oxida

178 The MPT induction model was able to reproduce the expected b

179 The MPT inhibitor sanglifehrin A reversed MPT markers and in

180 The MPT ocean circulation crisis facilitated the coeval draw

181 The MPT then induces ATP depletion-dependent necrosis or cas

182 The MPT was critical for TRAIL-induced apoptosis as demonstr

183 tely 43 to approximately 75 muatm across the MPT, mainly because of lower glacial CO2 levels.

184 of the RIPK1 inhibitor necrostatin-1 and the MPT inhibitor sanglifehrin A confirmed the results with

185 h manganese acetate (10-100 microM), and the MPT was assessed by changes in the mitochondrial membran

186 ing, the shift to 100,000-year cycles at the MPT is more likely to be a response to an additional cha

187 Because the MPT is a cell death-inducing phenomenon, we hypothesized

188 Minocycline blocked the MPT by decreasing mitochondrial Ca(2+) uptake, whereas N

189 and NIM811 but not tetracycline blocked the MPT.

190 7), a calcineurin inhibitor that blocks the MPT, or tacrolimus (FK506, 0.1 mg/kg, n = 7), a calcineu

191 crotic cell death after reperfusion, but the MPT is also implicated in apoptosis.

192 that apoptotic signaling is initiated by the MPT and further amplified by downstream caspases, probab

193 mohaline circulation (THC) system during the MPT between marine isotope stages (MISs) 25 and 21 at ~9

194 nor CO2 change in isolation can explain the MPT.

195 Following the MPT high-amplitude lake level variations dominate the re

196 with a previously proposed mechanism for the MPT synthase reaction.

197 approved (FDA-approved) drugs identified the MPT antagonist tigecycline (TIG) as a potent inhibitor o

198 lar acetylcholine transporter (VAchT) in the MPT of rat brain to identify the potential sites for M2R

199 east grade 3 was significantly higher in the MPT-T arm: 16% vs 2% in MPR-R, resulting in a significan

200 holinergic and noncholinergic neurons in the MPT.

201 rons and astrocytes to manganese induces the MPT.

202 Instead, the MPT promotes caspase-and ATP-dependent apoptosis.

203 During ischemia (the MPT priming phase), factors such as intracellular Ca2+ a

204 amine methyl ester to visualize onset of the MPT and mitochondrial depolarization, respectively.

205 optotic effect of CypD is independent of the MPT but is due to its interaction with some key apoptosi

206 Induction of the MPT by manganese and associated mitochondrial dysfunctio

207 ng atmospheric CO2 levels as a driver of the MPT has proven difficult with available observations.

208 n treated with mastoparan, an inducer of the MPT in rat liver mitochondria.

209 The framework of the MPT induction model includes the potential states of the

210 This difference is a result of the MPT+ triggering the pyridone to provide electron density

211 f autophagy proteins, prevented onset of the MPT, and decreased cell death after reoxygenation.

212 CsA delayed these changes, indicative of the MPT, to approximately 11 hours after acetaminophen admin

213 release from mitochondria independent of the MPT.

214 losporin A, consistent with induction of the MPT.

215 ed ischemia/reperfusion despite onset of the MPT.

216 Quantification of the MPT/molybdenum and molybdenum/phosphorus ratios, time-de

217 poptosis and delayed but did not prevent the MPT.

218 hood that MPT will occur on reperfusion (the MPT trigger phase).

219 osis, suggesting that apoptosis requires the MPT, and that caspase activation is downstream to the MP

220 Our data suggest that the MPT may play a role in suppression of mitochondrial func

221 Instead, we infer that the MPT was initiated by a change in ice sheet dynamics and

222 Our results suggest that the MPT was initiated by an abrupt increase in Antarctic ice

223 Thus, the MPT is a common mechanism responsible for both necrosis

224 a proton while transferring a hydride to the MPT+.

225 that caspase activation is downstream to the MPT.

226 l for investigators to use to understand the MPT induction phenomenon, explore alternative hypotheses

227 mitochondria, which is not mediated via the MPT.

228 increased mitochondrial dysfunction via the MPT.

229 me inactivation linearly correlates with the MPT onset and propagation.

230 d the pathway that links mitoK(ATP) with the MPT.

231 We adapt Modern Portfolio Theory (MPT) to optimal spatial targeting of conservation activi

232 e crystal structures of non-thiocarboxylated MPT synthase from Staphylococcus aureus in its apo form

233 protein catalyzes the nucleotide addition to MPT, but the mechanism of the biosynthesis of the bis-MG

234 alyses showed that RB1-E2F complexes bind to MPT gene promoters to regulate transcription and control

235 al autophagy, and this subsequently leads to MPT-dependent hepatocyte death after A/R.

236 or 72 weeks (18 cycles; 541 patients), or to MPT for 72 weeks (547 patients).

237 s lenalidomide-dexamethasone was superior to MPT for all secondary efficacy end points, including ove

238 ely increase mitochondrial susceptibility to MPT, increasing the likelihood that MPT will occur on re

239 of the sulfur- and metal-free precursor Z to MPT by MPT synthase involves the transfer of sulfur atom

240 isease progression or unacceptable toxicity (MPT-T) and the same MP regimen with thalidomide being re

241 Here, we use multiple-particle tracking (MPT) microrheology and traction force cytometry to probe

242 microscopy, and multiple particle tracking (MPT) to investigate the intracellular trafficking of hig

243 r environment by multiple particle tracking (MPT).

244 f the mitochondrial permeability transition (MPT) 5 hours after rhTRAIL plus actinomycin D, which was

245 h the mitochondrial permeability transition (MPT) and cytochrome c loss from the intermembrane space.

246 iated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-med

247 n and mitochondrial permeability transition (MPT) are sequential and necessary steps in PARP-1-mediat

248 e the mitochondrial permeability transition (MPT) as a key factor in acetaminophen-induced necrotic a

249 f the mitochondrial permeability transition (MPT) can initiate necrotic cell death after reperfusion,

250 r the mitochondrial permeability transition (MPT) in cardiomyocytes and that cell survival is steeply

251 ty to mitochondrial permeability transition (MPT) induction that may contribute significantly to HD p

252 Mitochondrial permeability transition (MPT) is a highly regulated complex phenomenon that is a

253 The mitochondrial permeability transition (MPT) is a marker of impaired mitochondrial function that

254 The mitochondrial permeability transition (MPT) mediates hepatic necrosis after ischemia and reperf

255 duced mitochondrial permeability transition (MPT) pore opening in isolated mouse liver mitochondria,

256 f the mitochondrial permeability transition (MPT) pore, resulting in mitochondrial depolarization, de

257 ng of mitochondrial permeability transition (MPT) pores, mitochondria from heat-preconditioned rat li

258 f the mitochondrial permeability transition (MPT) process], z-VAD (a pan-caspase inhibitor) and inhib

259 d the mitochondrial permeability transition (MPT) were assessed in isolated rat liver mitochondria.

260 f the mitochondrial permeability transition (MPT) with N-methyl-4-isoleucine cyclosporine (NIM811) im

261 duced mitochondrial permeability transition (MPT), an effect that was reversed by KT5823.

262 f the mitochondrial permeability transition (MPT), but not FK506, a calcineurin inhibitor, abolished

263 se of mitochondrial permeability transition (MPT), mitochondrial cytochrome c release, and caspase-9

264 of a mitochondrial permeability transition (MPT), on a per cell basis, did not occur simultaneously

265 f the mitochondrial permeability transition (MPT), such as mitochondrial swelling, depolarization, an

266 n the mitochondrial permeability transition (MPT), which is associated with increased release of cyto

267 d via mitochondrial permeability transition (MPT)-dependent or MPT-independent mechanisms.

268 f the mitochondrial permeability transition (MPT).

269 h the mitochondrial permeability transition (MPT).

270 n and mitochondrial permeability transition (MPT).

271 o the mitochondrial permeability transition (MPT).

272 f the mitochondrial permeability transition (MPT).

273 f the mitochondrial permeability transition (MPT).

274 with mitochondrial permeability transition (MPT).

275 f the mitochondrial permeability transition (MPT).

276 The mid-Pleistocene transition (MPT) marked a fundamental change in glacial-interglacial

277 observed at the Mid-Pleistocene Transition (MPT), consistent with far-field climate forcing, which s

278 d years ago, the mid-Pleistocene transition (MPT), when the dominant periodicity of climate cycles ch

279 During the Mid-Pleistocene Transition (MPT; 1,200-800 kya), Earth's orbitally paced ice age cyc

280 drial membrane permeability pore transition (MPT) and consequent cytochrome c release in these cells.

281 ce of mitochondrial permeability transition [MPT]).

282 on of the mitochondrial protein translation (MPT) gene pathway relative to tumors harboring p53 delet

283 ased the Ca2+ threshold necessary to trigger MPT pore opening.

284 ulture filtrate proteins of M. tuberculosis, MPT 32, and the 81-kDa GlcB protein were detectable in p

285 Cultured mouse proximal tubular (MPT) cells were used to compare the antiproliferative ef

286 s study, we have used mouse proximal tubule (MPT) cells as a model to study the role of fluid shear s

287 s-MPT guanine dinucleotide cofactor with two MPT units coordinated at one molybdenum atom, which addi

288 We find that using MPT instead of simple diversification in the PPR can ach

289 continuous lenalidomide-dexamethasone versus MPT.

290 NP, and ROS mediate cytochrome c release via MPT.

291 or continuous lenalidomide-dexamethasone vs. MPT and 0.70 for continuous lenalidomide-dexamethasone v

292 tuberculosis, and this may be enhanced when MPT is stabilized.

293 of lenalidomide-dexamethasone, and 51% with MPT.

294 mitoK(ATP) and the other in association with MPT.

295 As compared with MPT, continuous lenalidomide-dexamethasone given until d

296 As compared with MPT, continuous lenalidomide-dexamethasone was associate

297 lidomide-dexamethasone, and 21.2 months with MPT (hazard ratio for the risk of progression or death,

298 er a median follow-up of 36 months, PFS with MPT-T was 20 months (95% confidence interval [CI], 18-23

299 tinuous lenalidomide-dexamethasone than with MPT (70% vs. 78%).

300 s H(2) capture and hydride formation without MPT(+) while the pyridone's special role involves the pr