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 CDK1 was identified as a positive regulator of global tr

4 CDK1-CCNB1 is therefore an integral component of the spi

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

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

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

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

9 y is dependent on cyclin-dependent kinase 1 (CDK1) activity.

10 was dependent on cyclin-dependent kinase 1 (CDK1) activity.

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

12 the activities of Cyclin-dependent kinase 1 (CDK1) and Polo-like kinase 1 (PLK1), transitions through

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

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

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

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

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

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

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

20 We found that cyclin-dependent kinase 1 (CDK1) phosphorylated a threonine residue on the catalyti

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

22 e kinase 1 (PLK1)/cyclin-dependent kinase 1 (CDK1) signaling pathway was the main driver of PI3K inhi

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

24 cyclin-dependent serine/threonine kinase 1 (CDK1) to generate the M phase-promoting factor (MPF) act

25 ure activation of cyclin-dependent kinase 1 (CDK1), early onset to S-phase and mitosis, and increased

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

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

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

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

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

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

32 h from mTORC1- to cyclin-dependent kinase 1 (CDK1)-mediated regulation.

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

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

35 A, Aurora B, and cyclin-dependent kinase 1 (CDK1).

36 at Ser1456 by the cyclin-dependent kinase 1 (CDK1).

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

38 h the activity of cyclin-dependent kinase 1 (CDK1)/cyclin B rather than through canonical mTOR kinase

39 bolic function of cyclin-dependent kinase 1 (CDK1)/cyclin B1-the activation of mitochondrial respirat

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

41 ia-preconditioning, was largely reduced by a CDK1 inhibitor.

42 70 and Ser-271 of CREB cophosphorylated in a CDK1-dependent manner during G2/M phase.

43 ors induce RIF1 Ser2205 phosphorylation in a CDK1-dependent manner, which disrupts an interaction bet

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

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

46 irradiated mitotic cells were treated with a CDK1 inhibitor.

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

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

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

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

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

52 In addition, CDK1 fails to activate, possibly due to persistent WEE1

53 In addition, CDK1/2 inhibition impairs TRAPP complex/COPII relocation

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

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

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

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

58 44 including MCT-1, c-Myc, Bcl-2, Mcl-1, and CDK1/2.

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

60 Furthermore, we demonstrate that CDK4/6 and CDK1 play a key role not only in the transition but also

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

62 in cell survival, such as c-Myc, CDC25, and CDK1.

63 the downstream signaling proteins CDC25C and CDK1.

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

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

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

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

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

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

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

71 ties of target genes including cyclin D1 and CDK1.

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

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

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

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

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

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

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

79 is directly mediated by cyclin B1-associated CDK1, and indirectly by Aurora B, and is antagonized by

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

81 5, the phosphatase counterbalancing cyclin B/CDK1 activity during mitosis.

82 Cyclin B:CDK1 is the master kinase regulator of mitosis.

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

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

85 When mitotic CDK (Cyclin B1-CDK1) is used to drive interphase egg extracts into a mi

86 ading to increased activity of the cyclin B1/CDK1 complex confirmed by qRT-PCR and immunoblot analysi

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

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

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

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

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

92 Successful mitosis requires that cyclin B1:CDK1 kinase activity remains high until chromosomes are

93 g role for the key mitotic kinase, Cyclin B1:CDK1, which ultimately helps to inhibit its own degradat

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

95 esign of inhibitors that distinguish between CDK1 and CDK2.

96 us adding a layer to the interaction between CDK1 and PP2A in regulating mitotic entry.

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

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

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

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

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

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

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

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

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

106 This direct phosphorylation by CDK1 was in addition to a previously reported indirect m

107 r dependent on its Ser727 phosphorylation by CDK1.

108 ast cells, growth in prophase is promoted by CDK1 through increased phosphorylation of 4E-BP1 and cap

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

110 because PP2A-B55 is negatively regulated by CDK1-CCNB1 and only becomes fully active once CCNB1 conc

111 APC/C(CDC20) is regulated by CDK1-cyclin B and counteracting PP1 and PP2A family phos

112 ed mitochondrial homeostasis is regulated by CDK1-mediated SIRT3 phosphorylation, which in turn deace

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

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

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

116 selected 10, i.e. TOP2A, AURKA, CKS2, CCNB2, CDK1 SLC19A1, E2F8, E2F1, PRC1, KIF11 for in depth valid

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

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

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

120 lated to eumetazoan cell-cycle-related CDKs (CDK1) were identified as well as transcription-related C

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

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

123 icantly reduced levels of the MPF components CDK1 and cyclins A1/B1.

124 in the ratio of cyclin B1 to CDK1 to control CDK1 activity; early cyclin B1 destruction reflects the

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

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

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

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

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

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

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

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

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

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

135 cells and that methylation by NSun2 enhanced CDK1 translation.

136 uirement for PP1 is lost in cells expressing CDK1 phosphorylation-defective CDC20(6A) mutants.

137 e that tumor development in liver expressing CDK1(AF) is inhibited.

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

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

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

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

142 ing transcription factor, as a substrate for CDK1.

143 EE1i treatment through activation of a FOXM1-CDK1 circuit that drives mitotic gene expression and DNA

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

145 lso exhibited altered DNA methylation (e.g., CDK1, FICD, TPX2, and TYMS).

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

147 vation, including no separase activity, high CDK1 activity, and high cyclin B1 and securin levels.

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

149 benzaldehyde, AKT3-vandetanib, BCR-imatinib, CDK1 and 20-palbociclib, CASP1-imexon, and FGFR3-pazopan

150 bolic remodeling in beta-cells and implicate CDK1 as a regulator of complex I that enhances beta-cell

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

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

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

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

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

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

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

158 mechanisms that impede cell proliferation in CDK1(AF) expressing cells differ partially from the acti

159 ecurin promotes anaphase entry, inactivating CDK1 and permitting chromosome segregation, respectively

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

163 olog of the yeast and animal mitotic inducer CDK1, regulates the critical size for commitment.

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

165 We show that WEE1i induces CDK1-dependent RIF1 phosphorylation and CDK2- and CDC7-d

166 Inhibiting CDK1 permitted continual cyclin B synthesis, whereas add

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

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

169 I to SGs only occurs in cycling cells and is CDK1/2-dependent, being driven by the interaction of TRA

170 ix mostly changed hub genes including KIF14, CDK1, AURKA, LCN2, TGM1, and DSG1.

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 Cyclin B-dependent kinase (CDK1-CCNB1) promotes entry into mitosis.

176 rylation of Sae2 by cyclin-dependent kinase (CDK1/Cdc28) activates the Mre11 endonuclease, while the

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

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

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

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

181 py via a prolonged G2 delay induced by lower CDK1/CyclinB1 activity, thus preventing cells from mitot

182 dent inhibitory phosphorylation of mammalian 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 ylation, these findings suggest that mitotic CDK1-directed phosphorylation of delta-4E-BP1 may yield

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

189 anipulate clock amplitude via small molecule CDK1 inhibition.

190 gulator of maturation-promoting factor (MPF; CDK1-cyclin A/B) activity in meiosis.

191 In the near absence of mTOR, CDK1 activates eIF4E-dependent translation in MPs throug

192 uction reflects the loss of an excess of non-CDK1-bound cyclin B1 in late prometaphase, while CDK1-bo

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

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

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

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

197 controlling global translation downstream of CDK1.

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

199 rotenone mimicked the restrictive effects of CDK1 inhibition on mitochondrial respiration, NADH turno

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

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

202 We uncovered that monoallelic expression of CDK1(AF) is early embryonic lethal in mice and induces S

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

204 wed that this is an extramitotic function of CDK1.

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

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

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

208 Inhibition of CDK1-driven mitotic translation reduces daughter cell gr

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

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

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

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

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

214 e assay showed that increased methylation of CDK1 directly reduces its transcription in pancreatic be

215 To study the outcome of CDK1 loss and blocked hepatocyte proliferation on lipid

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

217 This MPS1 and MAD1-dependent pool of CDK1-CCNB1 creates a positive feedback loop necessary fo

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

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

220 Reduction of CDK1 activity relieves inhibition of the CDK1-counteract

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

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

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

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

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

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

227 g at known repressive sites, is dependent on CDK1 but independent of mTOR.

228 RP1 phosphorylation is strongly dependent on CDK1.

229 selectivity for CDK2 and CDK5 over not only CDK1, but transcriptional CDKs (CDK7 and CDK9) and cell

230 chieving selectivity of binding to CDK2 over CDK1.

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

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

233 nase responsible for SAMHD1 phosphorylation, CDK1, exhibited lower levels of expression in female-der

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

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

236 checkpoint-defective context, upon premature CDK1 activation.

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

238 prometaphase, ensuring a period of prolonged CDK1 activity sufficient to achieve optimal chromosome a

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

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

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

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

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

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

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

246 where complex I flux dominates respiration, CDK1 inhibition is sufficient to restrict the duty cycle

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

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

249 synaptic dopamine signaling in the striatum, CDK1-modulated transcriptional regulation, and the genet

250 Thus, ATR and CHK1 signaling suppresses CDK1 kinase activity throughout the S phase and stabiliz

251 WEE1 suppresses CDK1 and CDK2 kinase activities to regulate the G1/S tra

252 ish a unique mitotic collapse with sustained CDK1 activity, consistent with known mechanisms of virus

253 t activated p90RSK and its downstream target CDK1.

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

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

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

257 We find that CDK1-CCNB1 localizes to unattached kinetochores and like

258 We find that CDK1/2 targets exhibit hyperphosphorylation selectively

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

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

261 We show that CDK1-CCNB1 and a counteracting phosphatase PP2A-B55 regu

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

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

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

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

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

267 nistic detail limited to the suggestion that CDK1 phosphorylates VPS34.

268 This suggests that CDK1-CCNB1 is an integral component and not only an upst

269 Moreover, Ribo-Seq analysis uncovered that CDK1 exerts a particularly strong effect on the translat

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

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

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

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

274 of CDK1 activity relieves inhibition of the CDK1-counteracting phosphatases PP1 and PP2A-B55, allowi

275 This protects the CDK1-bound fraction from destruction in prometaphase, en

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

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

278 Thus, CDK1 activation proceeds with concomitant inhibition by

279 Thus, CDK1 provides a direct means to couple cell proliferatio

280 Thus, CDK1 substitutes for inhibited mTORC1 as the master regu

281 Thus, CDK1, YTHDF2, and WEE1 form a feedforward regulatory loo

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

283 it an imbalance in the ratio of cyclin B1 to CDK1 to control CDK1 activity; early cyclin B1 destructi

284 -fold greater inhibition of CDK2 compared to CDK1.

285 its failure to localize to lysosomes due to CDK1-dependent RAPTOR phosphorylation.

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

287 d 49% of state 3 respiration is sensitive to CDK1 inhibition.

288 lin B1 and exhibited a higher sensitivity to CDK1 blockade, which reduced complex I flux by 76% and s

289 By acting together, CDK1-CCNB1 and PP2A-B55 thus create a spindle checkpoint

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

291 In parallel, upregulated CDK1 activity also targets Dbf4.

292 ents mitochondrial metabolic homeostasis via CDK1-SIRT3-CPT2 cascade.

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

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

295 -bound cyclin B1 in late prometaphase, while CDK1-bound cyclin B1 is destroyed only during metaphase.

296 on increases during mitosis, coincident with CDK1 activation.

297 but masked when cyclin B1 is in complex with CDK1.

298 Cyclin B3 forms active kinase complexes with CDK1, and meiotic progression requires cyclin B3-associa

299 ATP-binding site shares high similarity with CDK1, a related kinase whose inhibition causes toxic eff

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