ライフサイエンスコーパス: CDK1

1 CDK1 deficiency inhibited mitosis, but did not prevent D

2 CDK1 is the only essential cell cycle CDK in human cells

3 ions, we show how cyclin-dependent kinase 1 (CDK1) activates the APC/C through coordinated phosphoryl

4 nded with delayed cyclin-dependent kinase 1 (CDK1) activation.

5 ted with the high cyclin-dependent kinase 1 (CDK1) activities.

6 ot due to altered cyclin-dependent kinase 1 (CDK1) activity, DNA damage responses, or unscheduled DNA

7 ges are driven by cyclin-dependent kinase 1 (CDK1) activity, yet how cytoplasmic and nuclear CDK1 act

8 ine 592 (T592) by cyclin-dependent kinase 1 (CDK1) and cyclin A2 impairs its HIV-1 restriction activi

9 yclin B activates cyclin-dependent kinase 1 (CDK1) at mitosis, but conflicting views have emerged on

10 ro and in vivo by cyclin-dependent kinase 1 (CDK1) at Ser(119) and Ser(175) during the G2/M phase of

11 phosphorylated by cyclin-dependent kinase 1 (CDK1) at threonine residues 345 and 487 in a cell cycle-

12 hosphorylation by Cyclin-dependent kinase 1 (CDK1) at two conserved sites in this region destabilizes

13 ro and in vivo by cyclin-dependent kinase 1 (CDK1) during antimitotic drug-induced mitotic arrest and

14 t NSun2 regulates cyclin-dependent kinase 1 (CDK1) expression in a cell cycle-dependent manner.

15 Cyclin-dependent kinase 1 (CDK1) inhibitory phosphorylation controls the onset of m

16 scovered that the cyclin-dependent kinase 1 (CDK1) pathway is also affected by internal tandem duplic

17 of cyclin A2 and cyclin-dependent kinase 1 (CDK1) recapitulated this phenotype.

18 demonstrate that cyclin-dependent kinase 1 (CDK1) specifically phosphorylates FOXO1 at serine 249 (S

19 During mitosis, cyclin-dependent kinase 1 (CDK1) substitutes for mTOR and fully phosphorylates 4E-B

20 eukaryotic cells, cyclin-dependent kinase 1 (CDK1), in combination with either activator cyclins A or

21 ion and survival: cyclin dependent kinase 1 (CDK1), inhibitor of growth 4 (ING4), and early B-cell fa

22 bition of cyclin-dependent protein kinase 1 (CDK1), the enzyme required to enter mitosis, induced dif

23 with loss of cell-cycle-dependent kinase 1 (CDK1), which mediates lamin phosphorylation.

24 ation of Thr92 by cyclin-dependent kinase 1 (CDK1)-cyclin B1 initiates degradation of Mcl-1 in cells

25 Gwl requires both cyclin-dependent kinase 1 (CDK1)-dependent phosphorylation and its autophosphorylat

26 and metaphase by cyclin-dependent kinase 1 (CDK1)-mediated phosphorylation and only occurs after ana

27 Cyclin-dependent kinase 1 (CDK1)-mediated phosphorylation of REV-ERBalpha is necess

28 ation of the G2/M cyclin-dependent kinase 1 (CDK1).

29 ed by the mitotic cyclin-dependent kinase 1 (CDK1).

30 and controlled by cyclin-dependent kinase 1 (CDK1).

31 uentially, higher cyclin-dependent kinase 1 (CDK1)/cyclin B activity, and accordingly they have an in

32 is presented that cyclin-dependent kinase 1 (CDK1)/cyclin B catalyzes mitotic-arrest-induced Bcl-x(L)

33 A CDK1-dependent mechanism that blocks CRL4(CDT2) activity

34 70 and Ser-271 of CREB cophosphorylated in a CDK1-dependent manner during G2/M phase.

35 Here we show that a CDK1-mediated negative-feedback loop attenuates cyclin p

36 Collectively, we unveil a CDK1-dependent regulation of the WRN-DNA2-mediated resec

37 irradiated mitotic cells were treated with a CDK1 inhibitor.

38 r-295) acts as a competitor substrate with a CDK1-activating phosphatase in late interphase.

39 the cell cycle regulatory proteins cyclin A, CDK1, and CDK2, which mediates phosphorylation of SAMHD1

40 Relative to CDK2-cyclin A, CDK1-cyclin B is less thermally stable, has a smaller in

41 SAMHD1 is able to interact with the cyclin A-CDK1-CDK2 complexin monocytic THP-1 cells and primary mo

42 tion of CDC25B, a phosphatase that activates CDK1, is responsible for precocious meiotic resumption a

43 e presence of CDK1 and cyclin B1, and active CDK1 and cyclin B1 were present in the VZV tegument with

44 Ectopic expression of constitutively active CDK1 also inhibits FOXO1-induced apoptosis in PCa cells.

45 After CDK1-CyclinB inactivation upon mitotic exit, PLK4 can bi

46 t kinase (CDK)1/2 inhibitors, siRNAs against CDK1/2, and the clinical CDK1/2 inhibitor roscovitine al

47 cyclin B threshold, and CDC25, which allows CDK1 to escape the WEE1/MYT1 inhibition.

48 ession of NSun2 elevated it without altering CDK1 mRNA levels.

49 ed by the down-regulation of cyclin B(1) and CDK1.

50 44 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.

51 at combinatorial inhibition of GSK-3beta and CDK1 augment the apoptotic sensitivity of hypoxic tumors

52 ith other host proteins in the cyclin A2 and CDK1 complex and whether mouse SAMHD1 shares similar cel

53 )/M in the induction of cyclins A and B, and CDK1.

54 aired transcription of the CCNB1, CCNA2, and CDK1 genes, encoding cyclin B1, cyclin A, and Cdk1, resp

55 the downstream signaling proteins CDC25C and CDK1.

56 roles, as pRb inactivation induces CDK1, and CDK1 phosphorylates lamin A/C on serine 22.

57 -> Cdc25 -> CDK1; CDK1 -/ Wee1 -/ CDK1; and CDK1 -/ Myt1 -/ CDK1) that collectively function as a bi

58 that selectively inhibit CDK4 over CDK2 and CDK1 activities.

59 c RNAi sensitivity mutations in the CDK2 and CDK1 genes resulted in a >85% site-specific recombinatio

60 y and selectively inhibit CDK4 over CDK2 and CDK1.

61 clin A), cyclin-dependent kinases (CDK4, and CDK1/2), p-ERK1/2, and p-AKT.

62 ine (P173), which is not present in CDK6 and CDK1/2.

63 eal a mechanism involving PP1alpha, CDK9 and CDK1 that is used by AR to initiate and sustain P-TEFb a

64 tal structures of complexes of CDK1-Cks1 and CDK1-cyclin B-Cks2.

65 ential cell-cycle proteins CyclinA, CKS1 and CDK1.

66 ncerted action of DDK, Polo-like kinase, and CDK1 promotes efficient SC destruction at the end of pro

67 nd GNB1, the kinases PKCbeta, PAK2, Lck, and CDK1, and the chaperone HSPA5.

68 t, along with loss of expression of MCM2 and CDK1, and reduction in dNTP levels.

69 lated event requiring entry into S phase and CDK1 activity.

70 caused induction in UBC9 phosphorylation and CDK1 activation specifically in Kupffer cells in vivo an

71 fill-in is under the control of polalpha and CDK1.

72 h as mother-daughter centriole proximity and CDK1-CyclinB interaction with centriolar components, ens

73 Thus, CDC6 behaves as CDK1 inhibitor regulating not only the M-phase exit, but

74 as on related essential components, such as CDK1, CDK2, cell size, and DNA damage.

75 In addition, instead of inhibiting cyclin B-CDK1 through destruction of Cdc25A phosphatase, oocytes

76 vation, which coincides with higher cyclin B/CDK1 and Polo-like kinase 1 (PLK1) activities in an S-ph

77 leads to hyperactivation of Cdc25C, cyclin B/CDK1, and PLK1 in a G(2)-M-enriched population, LMW-E ov

78 tivates cyclin-dependent kinase 1/cyclin B1 (CDK1/CYCB1) to directly hyperphosphorylate eukaryotic in

79 ically interacted with cyclin A2, cyclin B1, CDK1, and CDK2.

80 e inhibitory effect of TSPX on the cyclin B1-CDK1 complex has been mapped to its carboxyl acidic doma

81 enhances while TSPX represses the cyclin B1-CDK1 phosphorylation activity.

82 dic activation and inactivation of cyclin B1-CDK1.

83 its encoding RNA, which precludes cyclin B1/CDK1 complex function, thus preventing mitotic entry.

84 nd its encoding RNA that precludes cyclin B1/CDK1 complex functions necessary for mitotic entry.

85 which prevented activation of the cyclin B1/CDK1 complex.

86 leads to mitochondrial fission by cyclin B1/CDK1-dependent phosphorylation of DRP1 at serine 616.

87 Here, we identify that cyclin B1/CDK1-phosphorylates iASPP, which leads to the inhibition

88 o phosphorylated by CDK1, and blocking basal CDK1-mediated S81 phosphorylation markedly suppresses AR

89 esign of inhibitors that distinguish between CDK1 and CDK2.

90 ese findings show that the interplay between CDK1, Wee1/Myt1, and Cdc25 is required for the establish

91 racter of the cycle is imposed by a bistable CDK1/Wee1/Myt1/Cdc25 system.

92 Both CDK1 and CDK2 are potential cancer targets for which sel

93 B1 is recruited to kinetochores through both CDK1-dependent and -independent mechanisms.

94 Thus, phosphorylation of Mcl-1 by CDK1-cyclin B1 and its APC/C(Cdc20)-mediated destruction

95 rylation of human SAMHD1 at threonine 592 by CDK1 and cyclin A2 negatively regulates its HIV-1 restri

96 eplication stress and damage, accompanied by CDK1-independent apoptosis and downregulation of RRM1 an

97 Meiotic progression is controlled by CDK1 activity and is accompanied by dynamic epigenetic c

98 Phosphorylation of the loop domains by CDK1 in complex with p9/Cks2 (a CDK regulatory subunit)

99 xample, we show most cells arrested in G2 by CDK1 inhibition express abnormally high levels of replic

100 ion is generally sustained during mitosis by CDK1 phosphorylation of 4E-BP1 even under conditions of

101 AR S81 is also phosphorylated by CDK1, and blocking basal CDK1-mediated S81 phosphorylati

102 ) demonstrate that CENP-A phosphorylation by CDK1 inhibits its association with the chaperone protein

103 r dependent on its Ser727 phosphorylation by CDK1.

104 ring meiosis I, attachments are regulated by CDK1 activity, which gradually increases through prometa

105 translation, which is partially reversed by CDK1/CYCB1 phosphorylation of 4E-BP1.

106 e demonstrate that phosphorylation of WRN by CDK1 is essential to perform DNA2-dependent end resectio

107 e regulatory genes, such as CCNB1 and CCNB2, CDK1, and TOP2A.

108 in (pRb) which coincided with increased cdc2/CDK1 kinase activity, but which further conflicted with

109 ic (TH), and cell-cycle genes (e.g., CDC25A, CDK1).

110 s, as the sites phosphorylated by the CDC28 (CDK1)-encoded cyclin-dependent kinase.

111 sites in Ace2 by the G1 CDKs Pho85 and Cdc28/CDK1 and 2) an unknown mechanism mediated by Pho85 that

112 However, activity of CDC2A (CDK1) kinase is dramatically reduced in mutant spermatoc

113 We report that CDC2A (CDK1)-mediated phosphorylation of MSY2 triggers this tra

114 ative feedback loops (CDK1 -> Cdc25 -> CDK1; CDK1 -/ Wee1 -/ CDK1; and CDK1 -/ Myt1 -/ CDK1) that col

115 During S/G2 phases, CDK1 and CDK2 (CDK1/2) phosphorylate RECQL4 on serines 89 and 251, enha

116 with preference for CDK2 and CDK5 over CDK9, CDK1, CDK4, and CDK6.

117 In CHO cells, CDK1/2-dependent phosphorylation of Ubc2/Rad6 at Ser(120

118 ors, siRNAs against CDK1/2, and the clinical CDK1/2 inhibitor roscovitine all cooperated with the PI3

119 ivation of the maturation-promoting complex, CDK1/cyclin-B1.

120 ual-specificity phosphatase that counteracts CDK1 activity during anaphase to promote mitotic exit in

121 Throughout the cell cycle, CDK1 phosphorylates the SUMO-specific enzyme, ubiquitin-

122 , and its recruitment requires B-type cyclin/CDK1 activity.

123 CyclinA2-CDK1/2 phosphorylates SAMHD1 at Thr-592, but how this mo

124 In vitro phosphorylation of GNU by CyclinB/CDK1 blocks activation of PNG.

125 dependent kinases that promote cell cycling (CDK1, 2), neuronal development (CDK5) and control transc

126 fic responses (i.e., starvation, DNA damage, CDK1 inhibition), rather than physiological cell cycle r

127 mised G(2)/M transition due to the decreased CDK1 (cyclin-dependent kinase 1) activity and upregulate

128 lasticity that might be exploited to develop CDK1-selective inhibitors.

129 A pulse-driven CDK1-anaphase-promoting complex (APC) model corroborated

130 lthough there are conditions in which either CDK1/cyclinB1 activity or securin can prevent sister chr

131 tion assays demonstrate that both endogenous CDK1 and ectopically expressed CDK1 form a protein compl

132 Enhanced CDK1 activity due to deregulation of APC leads in turn t

133 relapsed AML patients resulted from enhanced CDK1-dependent phosphorylation of EZH2 at Thr487.

134 cells and that methylation by NSun2 enhanced CDK1 translation.

135 th endogenous CDK1 and ectopically expressed CDK1 form a protein complex with FOXO1 in prostate cance

136 putatively metastable neural proteins; FEN1, CDK1, and TDP-43.

137 In support of our findings, CDK1 inhibitors largely suppressed cell motility mediate

138 that this bistable trigger is essential for CDK1 oscillations in the early embryonic cell cycle.

139 these results establish a novel function for CDK1-mediated Ezh2 phosphorylation and provide a mechani

140 ide library of approximately 100 members for CDK1, CDK7, and CDK9.

141 ate that the Ser-251 residue is required for CDK1-dependent phosphorylation of FoxM1 as well as its i

142 poptotic Bcl-2 proteins acts as a sensor for CDK1 signal duration and as a functional link coupling m

143 ing transcription factor, as a substrate for CDK1.

144 Thus, IE62 is a substrate for CDK1/cyclin B1, and virions could deliver the active cel

145 Furthermore, CDK1-dependent phosphorylation of CREB in vitro inhibite

146 es, BCL2 and BIRC5, and proliferation genes, CDK1 and CCND2, were repressed by miR-143 and miR-145.

147 le-negative feedback loops (CDK1 -> Cdc25 -> CDK1; CDK1 -/ Wee1 -/ CDK1; and CDK1 -/ Myt1 -/ CDK1) th

148 ggest that the DDR is suppressed by the high CDK1 activity in mitotic mammalian cells.

149 Accordingly, inhibitors of HSP90, CDK1 and the proteasome prevented EZH2 degradation, decr

150 Based on IE62/CDK1/cyclin B1 colocalization near viral assembly region

151 A recent study implicates CDK1 function in releasing mitotic telomeres from the nu

152 were dependent on BaP-mediated alteration in CDK1 kinase activity for maintaining their infectivity.

153 involved activation of p53, p21, decrease in CDK1 expression, and SAMHD1 dephosphorylation.

154 ifference has been attributed to the drop in CDK1/cyclin B activity that accompanies anaphase and cau

155 aratus is observed, but it is not focused in CDK1-deficient lenses.

156 e results indicate that the slow increase in CDK1 activity in meiosis I acts as a timing mechanism to

157 attachments, whereas a premature increase in CDK1 activity led to precocious formation of stable atta

158 eferred in CDK2 but has not been observed in CDK1.

159 Similarly, FGF4 deprivation resulted in CDK1 inhibition by overexpressing two CDK-specific inhib

160 The activity of several kinases, including CDK1 (cyclin-dependent kinase 1) and protein kinase C (P

161 ative roles in adhesion signalling including CDK1, inhibition of which reduces adhesion complex forma

162 As cyclin B concentrations increase, CDK1 activates in a three-stage nonlinear response, crea

163 V status, since BaP treatment also increased CDK1 activity in tissues derived from primary keratinocy

164 e cancer (CRPC) cells is driven by increased CDK1-mediated S81 phosphorylation.

165 for these roles, as pRb inactivation induces CDK1, and CDK1 phosphorylates lamin A/C on serine 22.

166 Inhibiting CDK1 permitted continual cyclin B synthesis, whereas add

167 d to trigger endoreduplication by inhibiting CDK1, while p21 suppressed expression of the checkpoint

168 xtract delays the M-phase entry and inhibits CDK1 during the whole M-phase.

169 p21(Cip1) in the context of MBV activity is CDK1.

170 in vitro substrates for the cellular kinase CDK1/cyclin B.

171 n vitro and in vivo by the cell-cycle kinase CDK1 at T119, S289, and S367 during the G2-M phase of th

172 we show that in mitosis, the mitotic kinase CDK1-CyclinB binds STIL and prevents formation of the PL

173 activity of the major M-phase protein kinase CDK1.

174 n of phosphorylated cyclin-dependent kinase (CDK1) in skin biopsies.

175 be regulated by the cyclin-dependent kinase, CDK1, which phosphorylates Ezh2 at threonines 345 and 48

176 nzyme activities of cyclin-dependent kinases CDK1, -2, or -5.

177 equential action of cyclin-dependent kinases CDK1, CDK2, CDK4, and CDK6.

178 ression, including cyclin-dependent kinases (CDK1 and CDK4) and Aurora kinases A, B, and C, were foun

179 hibitor of the key cyclin-dependent kinases (CDK1-4), and has been thought to be the main mediator of

180 apoptosis protein BIRC5 (survivin), a known CDK1 target, is required for the survival of cells overe

181 Although most post-mitotic cells lack CDK1 and cyclins, lens fiber cells maintain these protei

182 positive and double-negative feedback loops (CDK1 -> Cdc25 -> CDK1; CDK1 -/ Wee1 -/ CDK1; and CDK1 -/

183 In this manner, CDK1-dependent CRL4(CDT2) inactivation contributes to ef

184 Among them, we verify that MAPK1, CDK1, CDK4, PRMT5, beta-catenin, and UbxD8 are directly

185 CDC6 and counterbalancing cyclin B-mediated CDK1 activation.

186 rther studies revealed that NSun2 methylated CDK1 mRNA in vitro and in cells and that methylation by

187 CDK inhibitor NU2058 (CDK2 IC(50)=17 microM, CDK1 IC(50)=26 microM), in comparison with the antiandro

188 ylation, these findings suggest that mitotic CDK1-directed phosphorylation of delta-4E-BP1 may yield

189 omplexes upon phosphorylation by the mitotic CDK1:Cyclin B complex at three distinct CENP-T sites.

190 anipulate clock amplitude via small molecule CDK1 inhibition.

191 t apoptosis when treated with small-molecule CDK1 inhibitors.

192 1; CDK1 -/ Wee1 -/ CDK1; and CDK1 -/ Myt1 -/ CDK1) that collectively function as a bistable trigger.

193 ty is primarily regulated by securin and not CDK1/cyclin B1.

194 primarily regulated by securin binding, not CDK1/cyclin B1.

195 1) activity, yet how cytoplasmic and nuclear CDK1 activities are coordinated is unclear.

196 Grp(Chk1) prevents nuclear CDK1 activation by delaying CycB nuclear accumulation th

197 findings suggest that aberrant activation of CDK1 may contribute to tumorigenesis by promoting cell p

198 ompetitive inhibitor and identify aspects of CDK1 structure and plasticity that might be exploited to

199 eport the crystal structures of complexes of CDK1-Cks1 and CDK1-cyclin B-Cks2.

200 ot and RT-PCR demonstrated downregulation of CDK1 and CDK4 and upregulation of Hsp72.

201 hase in hepatoma cells via downregulation of CDK1, induction of p21(cip1/waf1) expression, and inhibi

202 a model whereby a switch in the duration of CDK1 activation, from transient during mitosis to sustai

203 We analyze the effects of CDK1 and CKD2 inhibitors on population growth, time-depe

204 We examined the effects of CDK1 inhibition in the context of different oncogenic si

205 was accompanied with decreased expression of CDK1 and cyclin B1 and activation of p21 in a p53-indepe

206 yperactivated, and the altered expression of CDK1 was further validated by Western analysis.

207 s), as well as by dominant-negative forms of CDK1 and CDK2 and the pan-CDK inhibitor, p21(Cip1/Waf1)

208 (M-Phase)-Promoting Factor, a heterodimer of CDK1/cyclin B1.

209 c stem cells, revealing that inactivation of CDK1 triggers endoreduplication only in cells programmed

210 e Cdc25C level, which led to inactivation of CDK1.

211 chromatin and centrosomes is independent of CDK1 binding.

212 Importantly, we found that inhibition of CDK1 activity relieves the differentiation block in cell

213 Finally, inhibition of CDK1 and CDK9 decreased AR Ser-81 phosphorylation, chrom

214 Inhibition of CDK1 leads to accumulation of lengthened G-overhangs and

215 n TS cells is triggered by p57 inhibition of CDK1 with concomitant suppression of the DNA damage resp

216 ion of purvalanol A, a specific inhibitor of CDK1 kinase, to BaP-treated cultures, resulted in the pr

217 body we designed to block the interaction of CDK1/cyclin B1 with separase, both failed to induce sist

218 itor of WEE1, a negative regulator kinase of CDK1, could counter the defective apoptosis of tumor cel

219 kinase activation and increases the level of CDK1 activity during the M-phase.

220 ry and progression via limiting the level of CDK1 activity.

221 A positive-feedback loop of CDK1-mediated phosphorylation of MSY2 that leads to degr

222 Here, we show that loss of CDK1 from the lens inhibited the phosphorylation of nucl

223 First, loss of CDK1-mediated phosphorylation of the mitochondrial divis

224 t is blocked completely by overexpression of CDK1 and cyclin B1.

225 Accordingly, overexpression of CDK1 inhibits the transcriptional activity of FOXO1 in P

226 broblasts is diminished by overexpression of CDK1.

227 gulate the cell cycle via phosphorylation of CDK1 and are considered potential drug targets.

228 mediating the activating phosphorylation of CDK1, CDK2, CDK4, and CDK6.

229 e with increased tyrosine phosphorylation of CDK1/2, but show no significant change in apoptosis.

230 alyzed by immunoblotting for the presence of CDK1 and cyclin B1, and active CDK1 and cyclin B1 were p

231 In the presence of CDK1, a single focus of the phosphonuclear mitotic appar

232 Partial reduction of CDK1 activity delayed formation of stable attachments, w

233 s provide new insight into the regulation of CDK1 during the cell division cycle.

234 Importantly, NSun2-mediated regulation of CDK1 expression had an impact on the cell division cycle

235 f purine C-8 substitution within a series of CDK1/2-selective O(6)-cyclohexylmethylguanine derivative

236 segregation through the activation state of CDK1.

237 We also describe the first structure of CDK1 bound to a potent ATP-competitive inhibitor and ide

238 identified serine 216 of Abi1 as a target of CDK1/cyclin B kinase that is phosphorylated in cells at

239 BaP targeting of CDK1 occurred independently of HPV status, since BaP tre

240 nase cascade, culminating in upregulation of CDK1 with subsequent SAMHD1 T592 phosphorylation and dea

241 Significant selectivity for CDK4/6 over CDK1 and CDK2 was demonstrated with several compounds in

242 chieving selectivity of binding to CDK2 over CDK1.

243 Cyclin B plateaus before peak CDK1 activation, and proteasome inhibition caused minima

244 During S/G2 phases, CDK1 and CDK2 (CDK1/2) phosphorylate RECQL4 on serines 8

245 xemplified by a lack of both overt premature CDK1 activation and S-phase mitotic entry.

246 ns, Chk1 becomes active to prevent premature CDK1 activation and mitotic entry until DNA is properly

247 checkpoint-defective context, upon premature CDK1 activation.

248 ing Bcl-x(L) as a key target of proapoptotic CDK1 signaling.

249 cell cycle promotion and cancer progression (CDK1, CDK2, CDK8, CHEK1, CHEK2, GSK-3 beta, NPM, PAK1, P

250 d cells, was also phosphorylated by purified CDK1/cyclin B1.

251 amino acid sequence, we found that purified CDK1/cyclin B1 phosphorylated IE62 at residues T10, S245

252 so promoted by phosphorylation at a putative CDK1 phosphorylation site located within its microtubule

253 human cell extract system that recapitulates CDK1 activation and nuclear envelope breakdown in respon

254 , our findings suggested that reconstituting CDK1 activity to threshold levels may be sufficient to r

255 o restrict AurA phosphorylation and regulate CDK1 activation, whereas a dual phosphatase topology bes

256 Although the signalling pathways regulating CDK1 activity are well defined, the functional significa

257 homologue of the major cell cycle regulator CDK1, yet definitive genetic evidence for an essential r

258 n the activity of the core mitotic regulator CDK1, either by pharmacologic inhibition or siRNA attenu

259 of regulators of proliferation/self-renewal (CDK1, EZH2) and recruit them to EIF4E to facilitate thei

260 a cell line G361 that correlated with robust CDK1 and CDK2 inhibition and caspase activation.

261 A specific CDK1 inhibitor blocked VZV spread, indicating an importa

262 C1 degradation is modulated by a stabilizing CDK1-dependent phosphorylation site within the degradati

263 t activated p90RSK and its downstream target CDK1.

264 co-expression strategy, we demonstrate that CDK1 controls Mis18 complex recruitment to centromeres b

265 oorly characterized, we now demonstrate that CDK1 phosphorylates MCM3 at Ser-112, Ser-611, and Thr-71

266 We further demonstrated that CDK1 phosphorylates C/EBPalpha on serine 21, which inhib

267 We find that CDK1 and PKC act in concert to mediate phosphorylation-d

268 Given that CDK1 and cyclin B1 are often overexpressed in human canc

269 vely target the MYC pathway, we propose that CDK1 inhibition might therefore be useful in the treatme

270 We report that CDK1-cyclin B1 phosphorylates the RNMT regulatory domain

271 We reported that CDK1-mediated phosphorylation of UBC9 enhanced its stabi

272 In vitro protein binding assays reveal that CDK1 interacts directly with FOXO1.

273 Furthermore, we show that CDK1 transiently and incompletely phosphorylates these p

274 Together, these data show that CDK1-mediated phosphorylation of serine 216 in Abi1 serv

275 molecular, and cellular approaches show that CDK1/Cyclin B1 phosphorylates Gravin on threonine 766 to

276 The combined results suggest that CDK1-dependent phosphorylation of CREB on Ser-270/Ser-27

277 These observations suggest that CDK1-dependent phosphorylations required for the initiat

278 n binding for transcription and suggest that CDK1-mediated Ser-81 phosphorylation during mitosis prov

279 Knockdown of NSun2 decreased the CDK1 protein level, while overexpression of NSun2 elevat

280 wn configuration as potent inhibitors of the CDK1 and CDK5 kinases.

281 e changes are triggered by activation of the CDK1 kinase and have been studied extensively.

282 es both the efficiency and robustness of the CDK1-APC oscillator.

283 Our data strongly suggest that targeting the CDK1 pathway might be applied in the treatment of FLT3IT

284 Thus the CDK1 inhibitor roscovitine and an antibody we designed t

285 This CDK1-FBXW7 pathway controlling REV-ERBalpha repression d

286 Thus, CDK1 activation proceeds with concomitant inhibition by

287 re, our results suggest that, in addition to CDK1 and cyclin A2, CDK2 phosphorylates T592 of human SA

288 -fold greater inhibition of CDK2 compared to CDK1.

289 SNP rs2456778, which maps to CDK1 ('cyclin-dependent kinase 1'), was associated with

290 s approximately 2000-fold less active toward CDK1 (IC50 86 muM).

291 In parallel, upregulated CDK1 activity also targets Dbf4.

292 In vivo, CDK1-dependent phosphorylation of Ser-112 triggers the a

293 oops (CDK1 -> Cdc25 -> CDK1; CDK1 -/ Wee1 -/ CDK1; and CDK1 -/ Myt1 -/ CDK1) that collectively functi

294 CDK2 is required for endoreduplication when CDK1 is inhibited.

295 on and only occurs after anaphase onset when CDK1 activity is down-regulated.

296 ut also elucidate a novel mechanism by which CDK1/2 inhibitors can enhance the effectiveness of the c

297 stent with the cell cycle phase during which CDK1 exhibits peak activity, Ezh2 phosphorylation is enr

298 on increases during mitosis, coincident with CDK1 activation.

299 Since IE62 colocalized with CDK1/cyclin B1 by confocal microscopy, we investigated w

300 Clinical trials with CDK1 inhibitors are currently under way for various mali