ライフサイエンスコーパス: mitotic kinase

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

2 all eukaroytes requires inactivation of the mitotic kinase.

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

4 be a regulator or substrate of the p34(cdc2) 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 al definition of candidate substrates of key mitotic kinases.

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

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

12 on through mitosis are regulated by multiple mitotic kinases.

13 suggest there are at least two undiscovered mitotic kinases.

14 tion during cytokinesis under the control of mitotic kinases.

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

16 the normal downstream events associated with mitotic kinase activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 The mitotic kinase Aurora A is an important therapeutic targ

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

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

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

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

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

44 The mitotic kinase Aurora B is concentrated at the anaphase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 The conserved mitotic kinase Bub1 performs multiple functions that are

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

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

64 Although the mitotic kinase Cdc2 appears to directly phosphorylate an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 Regulation by mitotic kinases controls this entire process.

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

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

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

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

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

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

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

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

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

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

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

93 How mitotic kinases interact with each other and coordinatel

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

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

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

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

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

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

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

101 systematic exploration of inhibitors of the mitotic kinase Nek2.

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

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

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

105 1] and as a protein (Pin2) that can bind the mitotic kinase NIMA and suppress its ability to induce m

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

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

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

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

110 The mitotic kinase Plk1 contributes to the DNA damage respon

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

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

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

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

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

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

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

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

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

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

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

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

123 Mitotic kinase purified from AD and normal brain, using

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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