ライフサイエンスコーパス: MPF

1 MPF (%WC, -2.06 (95% confidence interval (CI), -2.99, -1

2 MPF activation and its subcellular localization are depe

3 MPF activation further boosts Cdc25 and represses Wee1.

4 MPF is inhibited by Wee1-related kinases and activated b

5 MPF macromolecular proton fraction in SPMS secondary pro

6 MPF macromolecular proton fraction mapping enables quant

7 MPF macromolecular proton fraction outperforms MT magnet

8 MPF strongly correlated with quantitative histology in a

9 MPF-induced phosphorylation of CDK7 results in inhibitio

10 y in MPF release, ranging from 210 to 72,000 MPF/g textile per wash.

11 est resulting from the inability to activate MPF.

12 cked the enzymatic activity of the activated MPF kinase present in those extracts.

13 PF; or Cdc25. the phosphatase that activates MPF).

14 ntal consequences of precociously activating MPF in oocytes prior to fertilization.

15 Active MPF was able to phosphorylate p27C only in the absence o

16 generation of a critical "trigger" of active MPF promotes a positive feedback loop that employs Polo

17 arrest cdc55 mutants in mitosis with active MPF and unseparated sister chromatids.

18 he recycling approach significantly affected MPF release (p < 0.05), whereas the fabric type did not

19 ations of protein phosphatase activity allow MPF to be inactivated by inhibitory phosphorylation inst

20 , implying that Greatwall participates in an MPF autoregulatory loop.

21 Particularly, an MPF incorporating polar N-acetyl azepane moieties (Ag-5M

22 B-type cyclins and MPF activity are required to maintain c-mos and MAP kina

23 Integrated EMG and MPF remained relatively constant and at the same level t

24 ements are regulated by PKA inactivation and MPF activation, respectively.

25 cessary for the activation of MAP kinase and MPF, the resumption of meiosis, and maturation of the oo

26 d the relative contributions of the MAPK and MPF signaling pathways to Mos mRNA polyadenylation.

27 aternal mRNA polyadenylation by the MAPK and MPF signaling pathways.

28 aturation through the activation of MAPK and MPF, and also leading to the premature activation of cdk

29 s with an increase in the levels of MAPK and MPF.

30 By differentially inducing Mos, MAPK, and MPF, we demonstrate that the activation of MPF is necess

31 We discuss the interdependence of c-mos and MPF, and reveal an important role for translational cont

32 y composition changes between UPF -> MPF and MPF -> UPF groups.

33 omain prevented complete phosphorylation and MPF-mediated repression.

34 was found according to both LFB staining and MPF in all anatomical structures (corpus callosum, anter

35 ent between histological myelin staining and MPF suggests that fast MPF mapping enables robust and ac

36 [Ca2+]i oscillations entrain the autonomous MPF oscillator.

37 e showed previously that p34(cdc2)/cyclin B (MPF) hyperphosphorylates poly(A) polymerase (PAP) during

38 ated cyclin B degradation and Cdc2/cyclin B (MPF) inactivation between Meiosis I and II.

39 s activated during M phase by Cdk1/cyclin B (MPF), but once activated, Gwl promotes PP2A/B55delta inh

40 the sensitivity and specificity of qMT-based MPF as a non-invasive biomarker for LOAD risk.

41 wortmannin, inhibitors of PI-3 kinase, block MPF and MAP kinase activation and entry into meiosis.

42 Mechanisms to block MPF activation in developing oocytes must exist to preve

43 PF activity is low and are present when both MPF and MAP kinase activity are elevated.

44 Whole-brain MPF maps were obtained in vivo on an 11.7T animal MRI sc

45 ll-cycle transition at G2-M is controlled by MPF (M-phase-promoting factor), a complex consisting of

46 phosphorylation between the two elements by MPF and the NIMA kinase Fin1 blocked PP1(Dis2) recruitme

47 leads to the inactivation of MPF followed by MPF reactivation.

48 We show further that hyperphosphorylation by MPF dramatically reduces the activity of purified PAP, a

49 that preactivated SOCE is not inactivated by MPF, suggesting that MPF does not block Ca(2+) influx th

50 ed using a [2 + 2 + 2] strategy modulated by MPF.

51 nsensus cdk sites that are phosphorylated by MPF.

52 ent for Gwl activation is phosphorylation by MPF of the proline-directed sites T193 and T206 in the p

53 taphase II arrest is maintained primarily by MPF levels only.

54 Mitosis is regulated by MPF (maturation promoting factor), the active form of Cd

55 omatid separation appears to be regulated by MPF activity rather than by protein degradation.

56 of maternal cyclin B1 mRNA was stimulated by MPF in a MAPK-independent manner, thus revealing a diffe

57 an be phosphorylated in vivo and in vitro by MPF.

58 regulated by a protein kinase complex called MPF.

59 s the accumulation of active cyclin B1/Cdk1 (MPF) complexes in the nucleus to activate mitosis, the i

60 In animal cells, MPF is cytoplasmic in interphase and is translocated int

61 utions which have the possibility to control MPF formation throughout the textile manufacturing chain

62 Conversely, MPF levels appear to modulate both ER structure and the

63 The medial prefrontal cortex (MPF) regulates autonomic and neuroendocrine responses to

64 s, we find that injection of egg cytoplasm ("MPF activity") into G2-arrested X. tropicalis oocytes in

65 ks2(-/-) oocytes display reduced and delayed MPF activity during meiotic progression, leading to defe

66 Three-dimensional MPF macromolecular proton fraction maps were reconstruct

67 se a unified network model in which distinct MPF areas orchestrate physiological and behavioural resp

68 es, respectively, [Ca2+]i oscillations drive MPF activation cycles.

69 B1-GFP, or cyclin B1-GFP bound to CDK1 (i.e. MPF), into interphase nuclei it is rapidly exported into

70 thway, MAP kinase is not required for either MPF activation or subsequent oocyte maturation in starfi

71 Activation of either MPF or the mitogen-activated protein kinase cascade inde

72 rto unrecognized source of the environmental MPF contamination and highlights the need to evaluate ex

73 ) and activation of M-phasepromoting factor (MPF).

74 helin and megakaryocyte potentiating factor (MPF).

75 se studies that maturation promoting factor (MPF) activation stimulates vesicle association with micr

76 attenuation of maturation-promoting factor (MPF) activation, and severely compromised meiotic resump

77 uses failure of maturation-promoting factor (MPF) activation.

78 correlates with maturation promoting factor (MPF) activation.

79 reduced (P < 0.05) M-phase-promoting factor (MPF) activity and promoted (P < 0.05) progression to met

80 duces maturation (M-phase)-promoting factor (MPF) activity and securin degradation allows sister chro

81 es two waves of maturation promoting factor (MPF) activity corresponding to meiosis I and meiosis II.

82 1) to generate the M phase-promoting factor (MPF) activity essential for progression through mitosis

83 Maturation Promoting Factor (MPF) activity is elevated in the metaphase I (MI)-arrest

84 inactivation of maturation promoting factor (MPF) and egg activation.

85 rotein level of maturation promoting factor (MPF) by inhibiting ubiquitin ligase anaphase promoting c

86 M phase-promoting factor (MPF) in turn activates Greatwall, implying that Greatwal

87 indicates that maturation promoting factor (MPF) is an upstream kinase.

88 n kinase (MAPK)-maturation-promoting factor (MPF) kinase cascade, which drives Xenopus oocyte maturat

89 ion of the MAPK-maturation promoting factor (MPF) kinase cascade.

90 ases (MAPKs) or maturation-promoting factor (MPF) prior to confocal microscopic analyses.

91 nase (MAPK) and maturation-promoting factor (MPF) signaling pathways have been proposed to mediate pr

92 se component of maturation promoting factor (MPF) triggers germinal vesicle breakdown after the lutei

93 atory molecules of mitosis-promoting factor (MPF) were compared in parallel synchronized cultures of

94 the cell cycle is M-phase promoting factor (MPF), a complex composed of cdc2 and a B-type cyclin.

95 Maturation promoting factor (MPF), a complex of cyclin-dependent kinase 1 and cyclin

96 The activity of maturation-promoting factor (MPF), a protein kinase complex composed of p34cdc2 and c

97 is is initiated by M phase promoting factor (MPF), composed of B-type cyclins and their partner prote

98 lex, also known as mitosis-promoting factor (MPF), drives commitment to mitosis.

99 an inhibitor of maturation-promoting factor (MPF), prevented GVBD, indicating that maturing oocytes e

100 rior activation of M-phase promoting factor (MPF), suggesting that Plo1 does not act as a mitotic tri

101 ism that regulates M-phase promoting factor (MPF), the major enzymatic activity controlling mitotic c

102 a component of the M-phase promoting factor (MPF), which promotes entry into and progression through

103 ty at the heart of mitosis-promoting factor (MPF), yet fundamental questions concerning its role in m

104 ne component of maturation-promoting factor (MPF).

105 the activation of M-phase promoting factor (MPF).

106 nent of maturation/M phase promoting factor (MPF).

107 n as maturation or M-phase promoting factor (MPF).

108 se to activated maturation-promoting factor (MPF).

109 he activity of the M-phase-promoting factor (MPF).

110 the activity of maturation-promoting factor (MPF).

111 lure to inactivate M-phase promoting factor (MPF).

112 omplex (APC) by maturation promoting factor (MPF).

113 target proteins by M phase-promoting factor (MPF); Gwl is thus essential for M phase entry and mainte

114 rylation of the maturation promoting factor (MPF, p34cdc2/cyclin B complex) kinase associated with ge

115 s is controlled by mitosis-promoting factor (MPF; Cdc2/cyclin B) activity.

116 al regulator of maturation-promoting factor (MPF; CDK1-cyclin A/B) activity in meiosis.

117 clin B complex (maturation-promoting factor [MPF]).

118 nactivation of maturation-promoting factor [(MPF) Cdk1/Cyclin B] is a key event in the exit from mito

119 clin B (maturation/mitosis-promoting factor, MPF).

120 l myelin staining and MPF suggests that fast MPF mapping enables robust and accurate quantitative ass

121 an important source of microplastic fibers (MPF) released to the environment.

122 This 'multiple-probability fluctuation' (MPF) analysis gave an estimate of 510 +/- 50 for the num

123 Eatwell Guide: (1) minimally processed food (MPF) and (2) UPF, in a random order.

124 ients and compared minimally processed food (MPF) with ultraprocessed food (UPF) diets.

125 ugh degradation of Cyclin B is important for MPF inactivation, recent studies indicate that Cdk1 phos

126 a inhibition with no further requirement for MPF.

127 A new additive, methyl(phenyl)formamide (MPF), is introduced for the glycosylation of 2-azido-2-d

128 s, a process known as mating pair formation (MPF).

129 had a lower macromolecular proton fraction (MPF) in the left thalamus.

130 method, fast macromolecular proton fraction (MPF) mapping demonstrated a promise as a myelin biomarke

131 egrated EMG (iEMG) and mean power frequency (MPF) response of the vastus lateralis with the VO2 respo

132 only the trend in the percent of grams from MPF remained.

133 r significantly across processing levels: GI-MPF: 54.1 +/- 19.5, PRF: 53.2 +/- 18.9, UPF: 49.3 +/- 18

134 +/- 18.9, UPF: 49.3 +/- 18.1 (P = 0.712); GL-MPF: 17.1 +/- 10.3, PRF: 15.8 +/- 12.4, UPF; 11.5 +/- 7.

135 As a percent of grams, MPF increased and UPF decreased with a higher urbanizati

136 a percent of energy and a percent of grams, MPF increased and UPF decreased with higher urbanization

137 , or body composition changes between UPF -> MPF and MPF -> UPF groups.

138 -> UPF) diets or the opposite order (UPF -> MPF).

139 at generates and maintains sufficiently high MPF activity levels to support mitosis.

140 ll stages, dye removal generated the highest MPF count, averaging nearly 10,055 MPFs g(-1) of textile

141 cle resumption with concomitant decreases in MPF and MAP kinase activities, and recruitment of matern

142 ed the reaction conditions as key factors in MPF fragmentation, with blend ratios influencing the num

143 Among youth, there was no trend in MPF or UPF as a percent of energy by the urbanization le

144 2 textiles demonstrated great variability in MPF release, ranging from 210 to 72,000 MPF/g textile pe

145 -type cyclins, cdc55 mutant cells inactivate MPF.

146 is, whereas cyclin B destruction inactivates MPF and drives cells out of mitosis.

147 orylation of Cdc2 by Wee1 kinase inactivates MPF until Cdc25 removes this phosphate to promote mitosi

148 degradation: Wee1, the kinase that inhibits MPF; or Cdc25. the phosphatase that activates MPF).

149 act as a mitotic trigger kinase to initiate MPF activation during mitotic commitment.

150 Interphase MPF is inhibited through phosphorylation of Cdk1 by Wee1

151 Therefore, during interphase MPF constantly shuttles between the nucleus and the cyto

152 This study investigated MPF release across different stages of two chemical recy

153 Thus, mWee1B is a key MPF inhibitory kinase in mouse oocytes, functions downst

154 a kinase cascade culminating in cdc2 kinase (MPF) activation.

155 nd the activities of two cell cycle kinases (MPF activity and MAP kinase activity) at fertilisation o

156 probability flow-Boltzmann Machine Learning (MPF-BML), for performing fast and accurate inference of

157 ts in rural areas consumed more UPF and less MPF than those in urban areas in terms of both energy an

158 main unclear due to incomplete circuit-level MPF characterization(7).

159 cytes remained arrested at prophase with low MPF activity.

160 eatwall from mitotic extracts rapidly lowers MPF activity due to the accumulation of inhibitory phosp

161 regulation of the cell cycle machinery (MAPK-MPF cascade) is due to Ca(2+)(cyt) acting downstream of

162 tively regulating the initiation of the MAPK-MPF cascade.

163 ted with clinical scores than GM gray matter MPF macromolecular proton fraction (P < .05).

164 had lower WM white matter and GM gray matter MPF macromolecular proton fraction than controls, with p

165 Mean MPF macromolecular proton fraction , R1, and MT magnetiz

166 The median MPF length ranged from 165 to 841 mum.

167 rms long filamentous structures that mediate MPF and describe its cryoelectron-microscopic (cryo-EM)

168 On the basis of the mesoscale MPF connectome, we propose a unified network model in wh

169 ing either the N-terminal part of mesothelin/MPF (D1Ig), reported to be easily cleaved off, or a nonc

170 Soluble molecules of the mesothelin/MPF family may provide useful new marker(s) for diagnosi

171 A new member of the mesothelin/MPF family was discovered, which has an 82-bp insert in

172 lly degrading PET can significantly minimize MPF emissions during recycling.

173 hain by using cutting methods which minimize MPF formation.

174 gral part of the core controls that modulate MPF activation in S. pombe.

175 ionally, injection of MPF plus CKS2, but not MPF alone, restored normal GVBD in cks2(-/-) oocytes, de

176 with DNA damage accumulate inactive nuclear MPF.

177 imilar observations regarding the ability of MPF to prevent sister chromatid separation have recently

178 of endogenous Mos protein in the absence of MPF signaling.

179 However, this action of MPF required MAPK activity.

180 een proposed to be involved in activation of MPF [3], general interactions of MPF with its mitotic su

181 yladenine (1-MA), leads to the activation of MPF and MAP kinase, resumption of the meiotic cell cycle

182 minal vesicle breakdown showed activation of MPF and MAPK, completed the first meiotic division extru

183 into Cdc25b-/- oocytes caused activation of MPF and resumption of meiosis.

184 eiosis I and consequently, the activation of MPF for meiosis II requires new cyclin synthesis, princi

185 d MPF, we demonstrate that the activation of MPF is necessary for SOCE inactivation during oocyte mat

186 Activation of MPF, by injection of cyclin B1 RNA or purified cyclin B1

187 ivated G alpha i, leads to the activation of MPF, entry into meiosis, and oocyte maturation.

188 dependent process dictates the activation of MPF.

189 and increased the protein kinase activity of MPF in SV40-infected CV-1 cells.

190 The activity of MPF is regulated by Wee1/Myt1 kinases and Cdc25 phosphat

191 tly involved in the initial amplification of MPF through the activating phosphorylation on Cdc25 phos

192 destruction, resulting in an attenuation of MPF activation and a delay of entry into the first meiot

193 e nucleus and the cytoplasm, but the bulk of MPF is retained in the cytoplasm by rapid nuclear export

194 to histologically validate the capability of MPF mapping to quantify myelin loss in brain tissues usi

195 The rate and capability of MPF production generally increased with increasing rough

196 The comparison of MPF release from laser-cut samples, which had sealed edg

197 in vitro at a 10-fold lower concentration of MPF than the non-consensus sites.

198 This was a direct consequence of MPF activity because separation was induced following ap

199 The effects of MPF dimensions and elasticity on their mobility and rete

200 The nuclear export of MPF is mediated by a nuclear export sequence in cyclin B

201 age-induced G2 arrest and over-expression of MPF attenuated the DNA damage-induced G2 delay.

202 BD is driven by a CKS2-dependent function of MPF.

203 itotic substrates [4] and/or inactivation of MPF [5,6].

204 e contraction phase required inactivation of MPF and was blocked when MPF activity was maintained at

205 has an essential role in the inactivation of MPF during early C. elegans embryogenesis.

206 This leads to the inactivation of MPF followed by MPF reactivation.

207 for cyclin B destruction and inactivation of MPF, is present at prophase I and undergoes Skp1-Cul1-F-

208 n of mitotic cyclins and the inactivation of MPF.

209 Additionally, injection of MPF plus CKS2, but not MPF alone, restored normal GVBD i

210 Injection of MPF restored meiotic cell cycle progression to >60% of t

211 tivation of MPF [3], general interactions of MPF with its mitotic substrates [4] and/or inactivation

212 hat M phase requires not only high levels of MPF function, but also the suppression, through a Gwl-de

213 checkpoint by regulating the localization of MPF.

214 The mechanism of MPF nuclear localization remains unclear since it contai

215 The decrease in the number of MPF released is likely caused by depletion of the produc

216 amples released 3-21 times higher numbers of MPF than the laser-cut samples.

217 esent a standalone cross-platform package of MPF-BML which features an easy-to-use graphical user int

218 cial for improving models and predictions of MPF behavior in porous systems.

219 lts show that CKS2 is a crucial regulator of MPF functions in meiosis and that its paralog, CKS1, mus

220 tile recycling industries can be a source of MPF release into the environment, but recovering PET thr

221 each of the hypothesized dynamical states of MPF.

222 he synthesis of cyclin B, the suppression of MPF activity before mitosis has been attributed to the p

223 To facilitate seamless use of MPF-BML and encourage more widespread application to dat

224 haride was assembled to prove the utility of MPF.

225 t the SCWs are a local response to a wave of MPF activation and inactivation.

226 We also found that a wave of MPF activity traveled within the cell from the animal to

227 Findings indicate greater weight loss on MPF than UPF diets and needing dietary guidance on food

228 ight loss, with significantly greater %WC on MPF (Delta%WC, -1.01 (95% CI, -1.87, -0.14), P = 0.024;

229 but does not stimulate MAPK phosphorylation, MPF activation, or oocyte maturation, indicating that XG

230 e proteins are protein kinases (CaMKII, PKC, MPF, MAPK, MLCK) whose activity is directly or indirectl

231 rotein synthesis is required to activate pre-MPF, and we show here that this does not require new B-t

232 Frog oocytes contain a pool of inactive "pre-MPF" consisting of cyclin-dependent kinase 1 bound to B-

233 ycles that govern the cell cycle, namely Pre-MPF-MPF, Cdc25P-Cdc25, Wee1P-Wee1 and APCP-APC.

234 CCNB2 is required to assemble sufficient pre-MPF for timely meiosis re-entry and progression.

235 n response to 1-methyladenine which precedes MPF activation, making PRK2 a candidate regulator of ear

236 ks the cell in interphase until Cdc25 pushes MPF activity through this barrier to initiate mitosis.

237 ic platforms (Solo-MFP, Duet-MFP and Quintet-MPF, respectively).

238 Alkaline hydrolysis reduced MPF release during the treatment stage by 87.55% compare

239 iber alterations, raising concerns regarding MPF emissions throughout the process.

240 he sequestration of components that regulate MPF activity in distinct subcellular compartments is ess

241 elucidates a novel mechanism that regulates MPF localization and function.

242 The number of released MPF was influenced by the cutting method, where scissor-

243 f phosphatase(s) that would otherwise remove MPF-driven phosphorylations.

244 show that Thr-1136 phosphorylation requires MPF activation.

245 th respect to other reports on ER structure, MPF cycling and Ca(2+) signaling in oocytes of deuterost

246 Reduced thalamic MPF may reflect inflammation-related tissue swelling and

247 in ultraprocessed grains and vegetables than MPF.

248 n-uniform release probability, indicate that MPF analysis provides a reliable estimate of quantal par

249 Functional data show that MPF activation during oocyte maturation is required for

250 E is not inactivated by MPF, suggesting that MPF does not block Ca(2+) influx through SOCE channels,

251 n of Mos or Ccnb1 reporters, suggesting that MPF is required for their translation in mouse oocytes.

252 The MPF activity is elevated again 15 minutes after fertilis

253 The MPF activity then remains elevated for an extended perio

254 The MPF quantity and fiber length were determined using imag

255 7C formed a complex with, and activated, the MPF kinase in lysates of immature oocytes, although this

256 nd 20 adults randomly assigned to either the MPF followed by the UPF (MPF -> UPF) diets or the opposi

257 sperm-triggered Ca2+ oscillations follow the MPF activity.

258 Active Cdk1 then initiates the MPF autoamplification loop that occurs independently of

259 MAP kinase is an essential component of the MPF activation pathway, MAP kinase is not required for e

260 One of the enduring mysteries of the MPF complex has been the role of Cks/Suc1, a highly cons

261 express significantly reduced levels of the MPF components CDK1 and cyclins A1/B1.

262 le types to investigate the source(s) of the MPF during washing.

263 ion was induced following application of the MPF inhibitor roscovitine.

264 On an average, 84% (range 49-95%) of the MPF release originated from the edges, highlighting the

265 We hypothesize three dynamical states of the MPF system and choose parameter sets to represent each.

266 struct a comprehensive wiring diagram of the MPF, focused on the dorsal peduncular area (DP)-a poorly

267 ions that pause for 5 minutes while only the MPF activity is low and are present when both MPF and MA

268 m oscillations is required to reactivate the MPF activity that precedes extrusion of the second polar

269 and -2A inhibitor okadaic acid restores the MPF activity and induces entry into M phase and the form

270 For all textiles, the MPF release decreased with repeated wash cycles, and a s

271 first polar body (pb1) is extruded when the MPF activity is low.

272 n the second and third hypotheses, where the MPF system rests in excitatory and bistable states, resp

273 ing oocytes eventually need to elevate their MPF levels, as has been documented for other animals.

274 ndomized to MPF then UPF, and 27 to UPF then MPF; 50 participants comprised the intention-to-treat sa

275 ligand mixture (1 and ent-1) yields a third MPF (Ag-rac-1PM).

276 The components that connect G beta gamma to MPF and MAP kinase activation in oocytes are unknown.

277 PK and Cdc25C signaling cascades, leading to MPF activation, germinal vesicle breakdown and arrest at

278 Twenty-eight people were randomized to MPF then UPF, and 27 to UPF then MPF; 50 participants co

279 sites, and their differential sensitivity to MPF, provide a mechanism to link repression specifically

280 This is effected by treating MPF as a time-delayed variable in the activation step of

281 igned to either the MPF followed by the UPF (MPF -> UPF) diets or the opposite order (UPF -> MPF).

282 We used MPF analysis to identify those quantal parameters that c

283 red inactivation of MPF and was blocked when MPF activity was maintained at elevated levels.

284 ted at M phase, times in the cell-cycle when MPF is known to be active.

285 Gwl, PP2A/B55delta remains active even when MPF levels are high.

286 ite demonstrated strongest correlations with MPF macromolecular proton fraction in GM gray matter (r

287 current and the quantal size (estimated with MPF analysis) to a similar degree, but did not affect th