ライフサイエンスコーパス: Cdc2 kinase

1 umulation of the hyperphosphorylated form of cdc2 kinase.

2 ion and M phase, in particular cyclin B1 and cdc2 kinase.

3 sly been correlated with inactivation of the Cdc2 kinase.

4 inase activity or in the activation state of cdc2 kinase.

5 ry into mitosis requires the activity of the Cdc2 kinase.

6 e (wt) Greatwall or a noninhibitable form of Cdc2 kinase.

7 Entry into mitosis is catalyzed by cdc2 kinase.

8 n, neural cell adhesion molecule (NCAM), and CDC2 kinase.

9 se activity has the characteristic traits of cdc2 kinase.

10 phosphatases, which results in inhibition of Cdc2 kinase.

11 2 and U(L)13) that mediate the activation of cdc2 kinase.

12 cumulation of inhibitory phosphorylations on Cdc2 kinase.

13 the cytoplasm and co-immunoprecipitated with cdc2 kinase.

14 ecipitates with mitogen-activated protein or cdc2 kinases.

15 motif homologous to that found in eukaryotic cdc2 kinases.

16 ation sites are possibly substrates for CDK5/CDC2 kinases.

17 results in the inhibition of the mitotic p34(cdc2) kinase.

18 rogression by serving as a substrate for p34(cdc2) kinase.

19 ut does not involve viral protein kinases or cdc2 kinase activated by the virus late in infection, an

20 s, desynapsis abnormalities and reduction of Cdc2 kinase activation at the end of meiotic prophase.

21 meiotic arrest is accompanied by a defect in Cdc2 kinase activation at the G2--M transition, raising

22 Cdc2 kinase activation is delayed in p21-deficient cells

23 are polyadenylated later, around the time of cdc2 kinase activation.

24 d by cyclin D(1), A, and B(1) induction, and Cdc2 kinase activation.

25 ry, followed by S phase pause and absence of Cdc2 kinase activation.

26 nduced Xenopus oocyte meiotic maturation and cdc2 kinase activation; the effect of KSR and 14-3-3 on

27 ied the effect of Herceptin treatment on p34(Cdc2) kinase activation and apoptosis in Taxol-treated h

28 ements showed an inverse correlation between Cdc2 kinase activities and KLF4 levels.

29 cip1/waf1) accompanied by inhibition of Cdk2/Cdc2 kinase activities.

30 This resulted in complete inhibition of cdc2 kinase activity and accumulation of cells in G(2).

31 erized wild-type cells had impaired Cdk2 and Cdc2 kinase activity and failed to phosphorylate the che

32 Cyclin B1-Cdc2 kinase activity and G2/M progression in p21-/- cell

33 ws proper maintenance of Cyclin B levels and Cdc2 kinase activity during CSF arrest.

34 link between HSP70-2 heat-shock protein and CDC2 kinase activity during this phase of spermatogenesi

35 ink between an HSP70 molecular chaperone and CDC2 kinase activity essential for the meiotic cell cycl

36 Although CDC2 kinase activity for histone H1 was present in the t

37 Cyclin B-dependent CDC2 kinase activity has a key role in triggering the G2

38 dles attached to condensed chromosomes after Cdc2 kinase activity has returned to the interphase leve

39 Higher Cdc2 kinase activity in MI than MII allows sufficient Em

40 Previous studies reported that most CDC2 kinase activity in the mouse testis is present in p

41 ly reflects an inability to induce cyclin B1/cdc2 kinase activity in the presence of p21Waf1/Cip1, al

42 B1 complex formation but also reconstituted CDC2 kinase activity in vitro.

43 , and examined for their ability to regulate CDC2 kinase activity in vitro.

44 carboxyl-terminal domain of p27 may activate CDC2 kinase activity in vivo during G2/M and that this e

45 phase and becomes maximal in G(2) and M when Cdc2 kinase activity is required to prevent reinitiation

46 Cyclin B1/Cdc2 kinase activity oscillated, peaking before each cle

47 inal domain of Cp27 diminished activation of CDC2 kinase activity otherwise stimulated by Cp27.

48 cytes, thereby preventing development of the CDC2 kinase activity required to trigger G2/M-phase tran

49 Therefore, GADD45 inhibition of Cdc2 kinase activity through alteration of cyclin B1 sub

50 ng endomitosis; however, cyclin B1-dependent Cdc2 kinase activity was largely abolished in the polypl

51 A parallel increase in cyclin B1/Cdc2 kinase activity was observed during p53-mediated ap

52 15 phosphorylation, and cyclin B1-associated Cdc2 kinase activity were examined.

53 , whereas KM12 cells down-regulated cyclin B/cdc2 kinase activity within 30 min to 20 % of control le

54 Cyclins are required for Cdc2 kinase activity, and mutations in cyclin A and cycl

55 G(2) arrest despite high levels of cyclin B/CDC2 kinase activity, at least some of which translocate

56 in B protein levels and dramatically reduces CDC2 kinase activity, leading to a G2/M blockade.

57 se mutant caldesmon did not inhibit cyclin B/cdc2 kinase activity, our results suggest that alteratio

58 that correlated with high and low cyclin B1/Cdc2 kinase activity, respectively.

59 SW620 cells failed to down-regulate cyclin B-cdc2 kinase activity, whereas KM12 cells down-regulated

60 At an early stage in HR, a defect in Cdc2 kinase activity, which is caused by a single amino

61 tion together with an increase in associated cdc2 kinase activity.

62 data showed that both p27 and Np27 inhibited CDC2 kinase activity.

63 inase 2 activity induced by CPT and enhanced Cdc2 kinase activity.

64 wever, in marked contrast, Cp27 enhanced the CDC2 kinase activity.

65 HN2, Vpr-induced arrest led to a decrease in cdc2 kinase activity.

66 yclin B1 is not required for cdc2 binding or cdc2 kinase activity.

67 A, pCdc2 (Tyr15), Cdc2, and an inhibition of Cdc2 kinase activity.

68 n B and phospho-H3, but a decreased level of Cdc2 kinase activity.

69 chk1, wee1, and GADD45 are known to inhibit cdc2 kinase activity.

70 ition arrest resulting from an inhibition of cdc2 kinase activity.

71 nd Cdk5/p25, but had no effect on endogenous cdc2 kinase activity.

72 is II with stable cyclin B and high cyclin B/Cdc2 kinase activity.

73 1 causes G(2)/M arrest through inhibition of CDC2 kinase activity.

74 t may be caused in part by the inhibition of Cdc2 kinase activity.

75 d45 interacts with Cdc2 protein and inhibits Cdc2 kinase activity.

76 45 is also required for Gadd45 inhibition of Cdc2 kinase activity.

77 yclin B1, which results in the inhibition of cdc2 kinase activity.

78 y failed to block cell cycle progression and Cdc2 kinase activity.

79 higher levels of cyclin B and its associated cdc2 kinase activity.

80 Taxol treatment led to higher levels of p34(Cdc2) kinase activity and apoptosis in ErbB2-overexpress

81 or cells and that sequential ablation of p34(cdc2) kinase activity may remove the survivin viability

82 g hyperphosphorylation and inhibition of p34(cdc2) kinase activity, phosphorylation of cdc25C, and al

83 phorylation of EBNA-2 and an increase in p34(cdc2) kinase activity; and (iii) ability of purified p34

84 n B1 and the activity of cyclin B1-dependent Cdc2 kinase, although detectable, are reduced as compare

85 omoting factor), a complex consisting of the Cdc2 kinase and a B-type cyclin.

86 enriched in E5 cells included genes encoding cdc2 kinase and a Ser/Thr kinase.

87 physiologically fragmented during mitosis by Cdc2 kinase and current Cdk5-specific chemical inhibitor

88 t triggers inhibitory phosphorylation of the Cdc2 kinase and mediates resistance to replication inhib

89 signalings, which leads to the inhibition of Cdc2 kinase and subsequent G2/M cell cycle arrest.

90 Both Cdc2 kinase and the DNA-dependent protein kinase (DNA-PK

91 tg(cdc25) phosphatase in G2 activates cyclin/cdc2 kinases and triggers mitosis.

92 ility of EBNA-LP to be phosphorylated by p34(cdc2) kinase and casein kinase II exclusively on serines

93 ivation of two cyclin-dependent kinases (p34(cdc2) kinase and Cdk2 kinase) induced by PDGF, but not b

94 cronuclear histone H1 is phosphorylated by a cdc2 kinase, and H1 phosphorylation regulates CDC2 expre

95 c-AMP dependent protein kinase (PKA) but not Cdc2 kinase, and some data have been presented implicati

96 activation and inactivation of NIMA and p34(cdc2) kinases, and accumulation and degradation of NIMA,

97 fic, as it does not suppress the activity of cdc2 kinase, another proline-directed kinase.

98 low-grade luminal tumours whereas BUB1B and CDC2 kinases are preferentially expressed in high-grade

99 cell cycle control system, cyclin D1 and the Cdc2 kinase, are present in the proliferating precursor

100 negatively regulating the activation of the Cdc2 kinase at the G2-M transition.

101 a G(2)/M arrest and its inactivation of the Cdc2 kinase but not its binding to Cdc2, PCNA, or p21(wa

102 This demonstrates that cdc2 kinase can induce cytoplasmic polyadenylation in th

103 roliferating cell nuclear antigen (PCNA) and Cdc2 kinase (Cdc2 k) can arrest cell cycle progression a

104 Activation of the Cyclin B/Cdc2 kinase complex triggers entry into mitosis in all e

105 Entry into mitosis is regulated by the Cdc2 kinase complexed to B-type cyclins.

106 Activation of the Cdc2-kinase component of maturation promoting factor (MP

107 Point mutation of a p34(cdc2) kinase consensus motif within the nuclear localiza

108 one TPTK motif that resemble established p34(cdc2) kinase consensus sequences.

109 Caldesmon is phosphorylated by cdc2 kinase during mitosis, resulting in the dissociatio

110 onclude that sustained activation of the p34(cdc2) kinase during mitotic arrest is required for subse

111 ar antigen (PCNA) and cell division cycle 2 (cdc2) kinase elaborated significantly more nitric oxide

112 s have demonstrated a requirement for active Cdc2 kinase for apoptosis to occur.

113 In fission yeast, Cdc2 kinase has both positive and negative roles in regu

114 se (PAP) is negatively regulated by cyclin B-cdc2 kinase hyperphosphorylation in the M phase of the c

115 observations suggest that phosphorylation by cdc2 kinase in early to mid-mitosis and inhibition of PP

116 Thus, hyperphosphorylated p21 activates the Cdc2 kinase in the G2/M transition.

117 To investigate a possible role of cdc2 kinase in this process, cyclin B was injected into

118 e role of phosphorylation of stathmin by p34(cdc2) kinase in the assembly of the mitotic spindle is w

119 an be phosphorylated by MAPK, but not by p34(Cdc2) kinase, in vitro.

120 thermore, as phosphorylation of caldesmon by cdc2 kinase inhibits actin binding of caldesmon, phospho

121 Cdc2 kinase is a master regulator of cell cycle progress

122 Earlier studies have shown that cdc2 kinase is activated during herpes simplex virus 1 i

123 Earlier reports have shown that cdc2 kinase is activated in cells infected with herpes s

124 the hypophosphorylated or active form of the Cdc2 kinase is not required for Vpr-induced apoptosis.

125 ng serotype 3 reovirus-induced inhibition of cdc2 kinase is presented, and reovirus-induced perturbat

126 a motif found in ICK/KRP (for Interactors of Cdc2 kinase/Kip-related protein) cell cycle inhibitor pr

127 light of its normal functions, the activated cdc2 kinase may play a role in the changes in the morpho

128 In each case, Cdc2 kinase measurements showed an inverse correlation b

129 ecessary for a kinase cascade culminating in cdc2 kinase (MPF) activation.

130 with decreased inhibitory phosphorylation of cdc2 kinase on tyrosine 15.

131 her GADD45beta nor GADD45gamma inhibited the Cdc2 kinase or induced G(2)/M arrest.

132 Although it is well established that Cdc2 kinase phosphorylates the DNA damage checkpoint pro

133 We show here that Cdc2 kinase phosphorylates the serines located in or nea

134 In vitro, our previous studies showed that cdc2 kinase phosphorylates Thr-320 (T320) in PP-1, and t

135 We also identified Ser-29 as the major Cdc2 kinase phosphorylation site in the p34 subunit.

136 s and regenerating liver, and as an in vitro cdc2 kinase phosphorylation site.

137 rincipal G2-M regulators, string(cdc25), and cdc2 kinase, rather than solely by regulators of the G1-

138 nitiated arrest in G(2) with active cyclin B/CDC2 kinase, regardless of p53 status.

139 be mediated by mitogen-activated protein and cdc2 kinases, respectively.

140 Ca(2+)/calmodulin or by phosphorylation with cdc2 kinase reverses the inhibitory effect of caldesmon

141 er, in vitro kinase assays using recombinant cdc2 kinase showed that RUNX2 was phosphorylated at Ser(

142 o-IL-16 are protein kinase CK2 substrate and cdc2 kinase substrate sites which, along with the NLS, c

143 by further comparing the activation state of cdc2 kinase, the kinetics of G2 arrest, and the ability

144 Our data link a potent inhibitor of Cdc2 kinase to a key protein required for the initiation

145 is correlated with diminished expression of cdc2 kinase, topoisomerase IIalpha, BUB3, and BUB2-like

146 -29) are known to be sites phosphorylated by Cdc2 kinase; two others (Thr-21 and Ser-33) are consensu

147 cdc2 kinase was activated, but mitogen-activated protein

148 To isolate novel activators of Cdc2 kinase, we screened synthetic lethal mutants in a c

149 sistent G(2) delay in the face of active p34(Cdc2) kinase, we determined the location of the kinase a

150 of G(2) arrest is followed by inhibition of cdc2 kinase, which is also prevented by SB202190.

151 in part, be due to inactivation of cyclin B/Cdc2 kinase, which is needed for entry into the G2/M pha

152 ese defects, we first examined the status of cdc2 kinase, which regulates the G2/M transition, and un