ライフサイエンスコーパス: MPF

1 MPF activation and its subcellular localization are depe

2 MPF activation further boosts Cdc25 and represses Wee1.

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

4 MPF macromolecular proton fraction in SPMS secondary pro

5 MPF macromolecular proton fraction mapping enables quant

6 MPF macromolecular proton fraction outperforms MT magnet

7 MPF strongly correlated with quantitative histology in a

8 MPF-induced phosphorylation of CDK7 results in inhibitio

9 est resulting from the inability to activate MPF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 omain prevented complete phosphorylation and MPF-mediated repression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 nsensus cdk sites that are phosphorylated by MPF.

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

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

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

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

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

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

51 regulated by a protein kinase complex called MPF.

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

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

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

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

56 Three-dimensional MPF macromolecular proton fraction maps were reconstruct

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

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

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

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

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

62 helin and megakaryocyte potentiating factor (MPF).

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

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

65 correlates with maturation promoting factor (MPF) activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 a inhibition with no further requirement for MPF.

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

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

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

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

113 -type cyclins, cdc55 mutant cells inactivate MPF.

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

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

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

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

118 Interphase MPF is inhibited through phosphorylation of Cdk1 by Wee1

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

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

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

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

123 cytes remained arrested at prophase with low MPF activity.

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

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

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

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

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

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

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

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

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

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

134 with DNA damage accumulate inactive nuclear MPF.

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

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

137 However, this action of MPF required MAPK activity.

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

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

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

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

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

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

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

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

146 dependent process dictates the activation of MPF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 n of mitotic cyclins and the inactivation of MPF.

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

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

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

166 checkpoint by regulating the localization of MPF.

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

168 each of the hypothesized dynamical states of MPF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 show that Thr-1136 phosphorylation requires MPF activation.

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

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

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

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

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

189 The MPF activity is elevated again 15 minutes after fertilis

190 The MPF activity then remains elevated for an extended perio

191 7C formed a complex with, and activated, the MPF kinase in lysates of immature oocytes, although this

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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