ライフサイエンスコーパス: mitotic kinase

1 all eukaroytes requires inactivation of the mitotic kinase.

2 nd delays mitosis by affecting the p34(cdc2) mitotic kinase.

3 be a regulator or substrate of the p34(cdc2) mitotic kinase.

4 (PLK1), a tumor suppressor and multitasking mitotic kinase.

5 -loop phosphatase for Aurora A, an essential mitotic kinase.

6 ith overexpression of Aurora A, an important mitotic kinase.

7 RASSF1A interacts with Aurora-A, a mitotic kinase.

8 consequent degradation of Plk1, a prominent mitotic kinase.

9 tion during cytokinesis under the control of mitotic kinases.

10 al definition of candidate substrates of key mitotic kinases.

11 t have been phosphorylated by Cdc2 and other mitotic kinases.

12 ol is the interplay between OGT and OGA with mitotic kinases.

13 ed protein degradation, and was unique among mitotic kinases.

14 5/Tws), which dephosphorylates substrates of mitotic kinases.

15 at are commonly observed when blocking other mitotic kinases.

16 , and that PP1 counteracts the activities of mitotic kinases.

17 ng capacity of MAP65-1 in concert with other mitotic kinases.

18 on through mitosis are regulated by multiple mitotic kinases.

19 suggest there are at least two undiscovered mitotic kinases.

20 of this study further define a link between mitotic kinase activation and the apoptotic machinery in

21 the normal downstream events associated with mitotic kinase activation.

22 This leads to high mitotic kinase activity and prevents mitotic exit.

23 On exit from mitosis, the cdc2p mitotic kinase activity falls, stabilizing cdc18p, which

24 destruction of cyclin B, indicating that the mitotic kinase activity inhibits prereplication complex

25 hosphorylated specifically in anaphase, when mitotic kinase activity starts to decline, has remained

26 ch eventually leads to a switch-like rise in mitotic kinase activity that triggers mitotic entry.

27 prolonged mitotic arrest, elevated levels of mitotic kinase activity, hyperphosphorylation of Bcl-2,

28 o-epitopes produced as a result of increased mitotic kinase activity.

29 PLK1 (polo-like kinase 1) is a key mitotic kinase and a therapeutic target in the treatment

30 This transition is shown to require the Cdk1 mitotic kinase and be promoted prematurely by ectopic ex

31 of Molecular Cell, Yata et al. show that the mitotic kinase and cell-cycle regulator Plk1 can directl

32 tastasis of PCs by coordinated regulation of mitotic kinases and blockade of a putative tumor suppres

33 oring protein Gravin restricts the action of mitotic kinases and cell-cycle effectors to defined mito

34 Treatment of Golgi membranes with mitotic kinases and COPI coat proteins efficiently disas

35 y organized process is controlled by various mitotic kinases and molecular motors.

36 cle oscillator using heterozygous mutants of mitotic kinases and phosphatases revealed that the durat

37 protects a centromeric pool of cohesin from mitotic kinases and the cohesin inhibitor Wapl.

38 rogression require the activation of several mitotic kinases and the proper regulation and localizati

39 olgi-associated proteins that are targets of mitotic kinases, and they have also been implicated in t

40 toxin can still be activated by its upstream mitotic kinases, and this form is fully active in the Go

41 Mitotic kinases are major regulators of protein function

42 yces cerevisiae member of the Polo family of mitotic kinases, are cell cycle regulated.

43 at human nuclear PABPN1 is phosphorylated by mitotic kinases at four specific sites during mitosis, a

44 e-specific genes of Arabidopsis encoding the mitotic kinase AtAurora 1, the microtubule-associated pr

45 The mitotic kinase Aurora A (Aur-A) is required for formatio

46 The mitotic kinase Aurora A (AurA) is regulated by a complex

47 The essential mitotic kinase Aurora A (AURKA) is controlled during cel

48 ining a senescence-inducing inhibitor of the mitotic kinase Aurora A (AURKA) with an MDM2 antagonist

49 e microtubule associated protein TPX2 to the mitotic kinase Aurora A induces a conformational change.

50 The mitotic kinase Aurora A is an important therapeutic targ

51 Amplification of the mitotic kinase Aurora A or loss of its regulator protein

52 diverse effects through upregulation of the mitotic kinase Aurora A, which is encoded by the AURKA g

53 y in embryonic fibroblasts and regulates the mitotic kinase Aurora A, which is frequently upregulated

54 ochore fiber formation and activation of the mitotic kinase Aurora A.

55 e in a transient complex at M phase with the mitotic kinase Aurora B and protein phosphatase 1.

56 omosomal passenger complex (CPC), containing mitotic kinase Aurora B as a catalytic subunit, ensures

57 The mitotic kinase Aurora B is concentrated at the anaphase

58 at coordinate this process, showing that the mitotic kinase aurora B phosphorylates MgcRacGAP to conv

59 Inhibition or depletion of the mitotic kinase Aurora B, which phosphorylates serine 10

60 ncoding RNAs contribute to activation of the mitotic kinase Aurora B.

61 imaging of the functional properties of the mitotic kinase Aurora B.

62 phase of the cell cycle coincident with the mitotic kinase Aurora B.

63 Oncogenic hyperactivation of the mitotic kinase Aurora-A (AurA) in cancer is associated w

64 ional implications because it highlights the mitotic kinase Aurora-A as a novel promising therapeutic

65 re we show that p53 is phosphorylated by the mitotic kinase Aurora-A at serine 215.

66 We show that the mitotic kinase Aurora-A directly interacts with and phos

67 The mitotic kinases Aurora A/B and Cdk1/Cyclin B phosphoryla

68 Here we show that the mitotic kinases Aurora B and Cyclin-dependent kinase 1 (

69 We further demonstrate that the mitotic kinases Aurora-A and -B phosphorylate KIBRA both

70 reported that KIBRA is phosphorylated by the mitotic kinases Aurora-A and -B.

71 e module, whose assembly depends on multiple mitotic kinases (Aurora B, Mps1, and Plx1) and is suppre

72 he scaffolding protein Gravin/AKAP12 and the mitotic kinases, Aurora A and Plk1, that is down regulat

73 se of cohesin is completely blocked when two mitotic kinases, aurora B and polo-like kinase (Plx1), a

74 The conserved mitotic kinase Bub1 performs multiple functions that are

75 Kinetochore targeting of the mitotic kinases Bub1, BubR1, and Mps1 has been implicate

76 demonstrate that the kinetochore-associated mitotic kinase BubR1 phosphorylates itself in human cell

77 Although the mitotic kinase Cdc2 appears to directly phosphorylate an

78 Mik1, two tyrosine kinases that inhibit the mitotic kinase Cdc2.

79 ion changes rapidly at anaphase onset as the mitotic kinase, Cdc2-cyclin B, is inactivated [4].

80 Unstacking is mediated by two mitotic kinases, cdc2 and plk, which phosphorylate the G

81 n target in rat liver Golgi membranes of two mitotic kinases, cdc2-cyclin B and polo-like kinases, wh

82 through multiple sites phosphorylated by the mitotic kinases, cdc2/B1, and the polo-like kinase.

83 C, thereby counteracting the activity of the mitotic kinase Cdc28.

84 Here, we show that the mitotic kinase CDK-1 phosphorylates Suppressor of Par-Tw

85 However, it was discovered recently that the mitotic kinase Cdk1 (Cdc2a) compensates for the loss of

86 rminus of SETD2 serves as a scaffold for the mitotic kinase CDK1 and lamins, facilitating lamin phosp

87 resulting inhibitory phosphorylation of the mitotic kinase Cdk1 create a G2 pause in interphase 14.

88 Furthermore, a mutant form of the mitotic kinase Cdk1 that cannot be inhibited by phosphor

89 e have also found that overexpression of the mitotic kinase Cdk1, which phosphorylates survivin, is u

90 Here we show that in mitosis, the mitotic kinase CDK1-CyclinB binds STIL and prevents form

91 The activation of the mitotic kinase Cdk1/cyclin B, which was detected as earl

92 is sequentially phosphorylated by the master mitotic kinases CDK1 and PLK1.

93 a Cdc25-type phosphatase that activates the mitotic kinase, Cdk1 (Cdc2).

94 Here we show that two mitotic kinases, Cdk1 and polo-like kinase 1 (Plk1), pho

95 Aurora A heterodimer, nominally considered a mitotic kinase complex, as a novel binding partner of 53

96 It was proposed that the inactivation of the mitotic kinase complex, p34(cdc2)/cyclin B, induces a G(

97 Regulation by mitotic kinases controls this entire process.

98 nd it reveals a scaffolding role for the key mitotic kinase, Cyclin B1:CDK1, which ultimately helps t

99 s with open mitosis, the concerted action of mitotic kinases disassembles nuclei and promotes assembl

100 of proteins protect centromeric cohesin from mitotic kinases during prophase.

101 Aurora A is a mitotic kinase essential for cell proliferation.

102 Inhibitors of essential mitotic kinases exemplify this paradigm shift, but intol

103 ary, our work demonstrates a crucial role of mitotic kinases for nuclear delivery of viral DNA and pr

104 HOTPAM9 comprised 7 mitotic kinase genes overexpressed in metastatic PCs, TR

105 AURKA, AURKB, and PLK1, which fall into the mitotic kinase group.

106 Whereas mitotic kinases have been implicated in NEBD, how they c

107 Although two mitotic kinases have been implicated in this process, it

108 ic functions for E2F-2 and suggest that some mitotic kinases have specialized roles supporting enucle

109 function was in the absence of regulation by mitotic kinases, highlighting the intrinsic ability of t

110 l inhibitors of Polo-like kinase 4 (PLK4), a mitotic kinase identified as a potential target for canc

111 PBK/TOPK is a mitotic kinase implicated in haematological and non-haem

112 Aurora kinases (AURKs) are mitotic kinases important for regulating cell cycle prog

113 This suggests PfArk1 is the main Aur mitotic kinase in proliferative stages of Plasmodium, ch

114 This supports a function of the mitotic kinases in both entry into mitosis, and also in

115 Here we delineate the role of mitotic kinases in receptor trafficking during asymmetri

116 itor Sic1 by the phosphatase Cdc14, allowing mitotic kinase inactivation and mitotic exit.

117 was hyperphosphorylated at the N terminus by mitotic kinases, including Aurora kinase B.

118 d removal of cohesin from chromosome arms by mitotic kinases, including Plk1, during prophase, and (2

119 Mitotic kinases, including polo-like kinases (Plk), infl

120 assical chemotherapeutics and the potency of mitotic kinase inhibitors to generate a class of high-pr

121 How mitotic kinases interact with each other and coordinatel

122 nase 1 (Plk1) and Aurora kinase A, important mitotic kinases involved in cell proliferation and cilio

123 ast, kinetochores harboring mutations in the mitotic kinase Ipl1 fail to bind chromosomes in a bipola

124 AuroraA, a mitotic kinase, is reported to be amplified and overexpr

125 The inhibition of the mitotic kinases leads to a reduction in the histone H1 a

126 of kinetochore-microtubule attachment, other mitotic kinases likely contribute to Hec1 phosphorylatio

127 megakaryocyte maturation, and inhibition of mitotic kinases may in fact promote megakaryocyte matura

128 that phosphorylation of Golgi components by mitotic kinases may regulate mechanisms of Golgi inherit

129 mbly checkpoint proteins MAD1, MAD2, and the mitotic kinase MPS1.

130 mitosis, suggesting that TBK1 functions as a mitotic kinase necessary for microtubule dynamics and mi

131 ecifically, dual targeting of CDK4/6 and the mitotic kinase NEK2 in vitro drives centrosome amplifica

132 systematic exploration of inhibitors of the mitotic kinase Nek2.

133 The mitotic kinases NEK6 and NEK7 phosphorylated the EML4 N-

134 that the phosphorylation-site motifs for the mitotic kinases Nek6, Nek7 and Nek9 are essentially iden

135 The mitotic kinase NEK7 licenses the assembly and activation

136 n, driven by the coordinated activation of a mitotic kinase network and repression of counteracting p

137 se 3 (JNK3) and protein interacting with the mitotic kinase, never in mitosis A I (Pin1), the actions

138 a physiological relationship between NFT and mitotic kinase, NFT proteins co-purified with and became

139 1] and as a protein (Pin2) that can bind the mitotic kinase NIMA and suppress its ability to induce m

140 eptor and thereby promotes expression of the mitotic kinase NIMA-related kinase 7 (NEK7).

141 HeLa cells, this repression is mediated by a mitotic kinase other than cdc2-cyclin B and is antagoniz

142 r data suggest that Cdk1, Aurora A, and Plk1 mitotic kinases participate in a feedback activation loo

143 In Schizosaccharomyces pombe, a late mitotic kinase pathway called the septation initiation n

144 onserved "STP" motif in BUB-1 that docks the mitotic kinase PLK-1(14) is necessary for CDC-20 kinetoc

145 ell polarity via the enrichment in AB of the mitotic kinase PLK-1, which itself limits the cortical l

146 LNCaP-AI, are reprogrammed to upregulate the mitotic kinase Plk1 (Polo-like kinase 1) and other M-pha

147 The mitotic kinase Plk1 contributes to the DNA damage respon

148 We propose to understand how the mitotic kinase PLK1 drives chromosome segregation errors

149 Inhibitors of the mitotic kinase PLK1 yield objective responses in a subse

150 We describe a pathway involving the mitotic kinase PLK1, the anaphase-promoting complex/cycl

151 metry depends on a cenexin-bound pool of the mitotic kinase Plk1, which favors the preferential accum

152 ylated tuberin co-immunoprecipitate with the mitotic kinase Plk1.

153 ating the proper concentration of active key mitotic kinases Plk1 and Aurora A at centrosomes and spi

154 s required for the optimal activation of the mitotic kinases PLK1 and Aurora B and thereby the proper

155 dependent manner, independent of the classic mitotic kinase, Plk1.

156 fly neural stem cells (neuroblasts) that the mitotic kinase Polo and its centriolar protein substrate

157 Here we show the mitotic kinase Polo, which regulates all steps of mitosi

158 identified the polo-box domain (PBD) of the mitotic kinase polo-like kinase 1 (Plk1) as a specific p

159 One of these genes is the mitotic kinase Polo-like kinase 1 (Plk1).

160 Genes for the mitotic kinases Polo and Aurora A were first identified

161 The mitotic kinase, polo-like kinase 1 (PLK1), facilitates t

162 we could dissect functions of a pleiotropic mitotic kinase, Polo-like kinase 1 (Plk1), via distinct

163 It is unknown whether any mitotic kinases positively regulate the localization of

164 Comparable levels of the mitotic kinase protein, Cdc2, were detected during the m

165 Mitotic kinase purified from AD and normal brain, using

166 l domains of p60 have maintained hotspots of mitotic kinase regulation.

167 Aurora-A kinases are highly conserved mitotic kinases required for cell division.

168 Aurora B (AurB) is a mitotic kinase responsible for multiple aspects of mitot

169 uction of diverse cytokines, and shutdown of mitotic kinases, resulting in cell cycle arrest.

170 Here, we found that Aurora-A kinase, a major mitotic kinase, specifically binds to and phosphorylates

171 h promotes condensation in cis by recruiting mitotic kinases such as Aurora B kinase.

172 a unique gene expression profile enriched in mitotic kinases such as polo-like kinase 1 (PLK1).

173 entify Sgo1 as a possible partner of Mps1, a mitotic kinase suggested to have an Aurora B-independent

174 ted BLM interacts with polo-like kinase 1, a mitotic kinase that binds to phosphoserine/threonine thr

175 hanism of HURP regulation by Aurora A, a key mitotic kinase that controls the assembly and function o

176 tion system to discover that Cdk1, the major mitotic kinase that drives the cell cycle, phosphorylate

177 Polo-like kinase 1 (Plk1) is a mitotic kinase that has been implicated in microtubule-k

178 PLK1 is a key mitotic kinase that is overexpressed in various cancers

179 Aurora A is a mitotic kinase that localizes to centrosomes.

180 Aurora-A is a mitotic kinase that regulates mitotic spindle formation

181 s stabilization and accumulation of Aurora-A mitotic kinase that ultimately drives the transition fro

182 formed cells are not, in contrast with other mitotic kinases that are commonly essential in all cell

183 show that it is phosphorylated in mitosis by mitotic kinases that include Plk1.

184 n is governed by the combinatorial action of mitotic kinases that neutralizes Haspin autoinhibition t

185 Mitotic kinases that regulate the proliferation of the p

186 ndings therefore link an important oncogenic mitotic kinase to regulate RASSF1A tumor suppressor.

187 ndergo closed mitosis and locate tubulin and mitotic kinases to nuclei only during mitosis.

188 he PBD integrates signals arising from other mitotic kinases to target the activated kinase towards d

189 t phosphatases oppose the addition of PCM by mitotic kinases, ultimately catalyzing the dissolution o

190 Aurora B is an essential mitotic kinase, which is involved in regulation of micro

191 Cdk5 is a post-mitotic kinase with complex roles in maintaining neurona

192 Aurora kinases (AURKA and AURKB) are mitotic kinases with an important role in the regulation