ライフサイエンスコーパス: CDK

1 CDK inhibitors specifically blocked HIV-1 infection at t

2 CDK phosphorylation of the replication factor TICRR (Top

3 CDK-4/CYD-1 phosphorylates specific residues in the LIN-

4 CDK-mediated phosphorylation of CtIP on T847 is required

5 The cyclin-dependent kinase 5 (CDK-5) activating protein, p35, is important for acute h

6 A CDK inhibitor blocks p53-RS's nuclear translocation in H

7 p domains by CDK1 in complex with p9/Cks2 (a CDK regulatory subunit) controlled loading of coactivato

8 The structures revealed novel features for a CDK, including a large beta4-beta5 loop insertion that c

9 SLD-2 is a CDK target in vivo, and phosphorylation regulates the in

10 This was prevented by the addition of a CDK inhibitor.

11 Expression of a CDK-insensitive version of PAH1 with a serine 162 to ala

12 ATR site, and hypo-phosphorylation of S64, a CDK site.

13 )/stathmin double-KO mice, suggesting that a CDK-independent function of p27(kip1) contributes to the

14 gase was able to specifically ubiquitinate a CDK inhibitor-p21(Cip1) at K16, K154, K161 and K163 but

15 In addition, treatment with a CDK inhibitor, flavopiridol, partially restored the arse

16 by ATR, ATR promotes HR by orchestrating a "CDK-to-ATR switch" post-resection, directly coupling the

17 ad reduced ability to interact with cyclin A-CDK complexes and to form the tetramer.

18 quired priming by cyclin/Cdk1 at an adjacent CDK consensus site.

19 EXO1 are proficient in resection even after CDK inhibition and favour HR over NHEJ.

20 Here, we show that ATR promotes HR after CDK-driven DNA end resection.

21 ting MCM, and can act either before or after CDK.

22 Selectivity of shortlisted compounds against CDKs and other kinases was tested.

23 T220/T179 linker residue independent of Akt, CDK and Erk activity.

24 that DNA damage-activated mitotic arrest and CDK activation lead to the phosphorylation of Vps34, whi

25 clin A, cyclin B, cyclin E, cdc2, cdc25c and CDK-1.

26 umber of cyclin-dependent kinases (CDKs) and CDK inhibitors (CKIs), the expression of which is often

27 onserved centrosome protein SPD-2/CEP192 and CDK activity from the mitotic cell.

28 Using co-immunoprecipitation and CDK kinase activity assays, we found that PIN1 binds the

29 Importantly, the combination of PI3K and CDK 4/6 inhibitors overcomes intrinsic and adaptive resi

30 21, as loss of other checkpoint proteins and CDK inhibitors did not affect apoptosis.

31 quiescence is dependent on SOX9, RARbeta and CDK inhibitors.

32 pendent kinase (CDK) consensus sequence, and CDK inhibitors decrease T387 phosphorylation.

33 cated by decreased expression of cyclins and CDKs and increased expression of p21 and p27.

34 kinases and kinase families, including ATM, CDKs, GSK-3, MAPKs, PKA, PKB, PKC, and SRC.

35 n of cyclin-binding sites on EXO1 attenuates CDK binding and EXO1 phosphorylation, causing a resectio

36 hibits CDKs during checkpoint responses, but CDK activity is required for efficient HR.

37 hermore, CI antagonized senescence caused by CDK inhibitors.

38 activities are likely directly controlled by CDK activity, thus allowing co-ordinate regulation of ca

39 e microscopy in single cells, is dictated by CDK-APC/C.

40 Sequential phosphorylations of Eco1 by CDK, DDK, and Mck1 create a phosphodegron that is recogn

41 dic acid phosphatase of the lipin family, by CDK phosphorylation is both necessary and sufficient to

42 PAT-1 version that is nonphosphorylatable by CDK-1 and that is defective in PLK-1 binding in vitro pr

43 p107 and p130, which, when phosphorylated by CDK-cyclin complexes, play a role in permitting cell pro

44 ivision processes and metabolic processes by CDK activity may be a general phenomenon important for c

45 In summary, phosphorylation of EXO1 by CDKs is a novel mechanism regulating repair pathway choi

46 ated by the phosphorylation of the canonical CDK sites at the distal NSD.

47 d, thus, in highly proliferating tumor cells CDK inhibitors are gaining interest as potential antican

48 apping activities between pUL97 and cellular CDKs.

49 yclin-dependent kinase (CDK) inhibitor (CKI)-CDK-retinoblastoma protein (Rb) pathway.

50 ty to PI3K inhibitors revealed that combined CDK 4/6-PI3K inhibition synergistically reduces cell via

51 es to the development of non-ATP-competitive CDK inhibitors, and evidence that CDK inhibitors may hav

52 he development of novel, non-ATP-competitive CDK inhibitors.

53 t UL97 phosphorylates 11 of the 16 consensus CDK sites in Rb.

54 CKS1, therefore, encodes a conserved CDK-binding partner, essential for appressorium-mediated

55 nase A (CDKA) is an evolutionarily conserved CDK.

56 CDK1 is the only essential cell cycle CDK in human cells and is required for successful comple

57 tent with on-target inhibition of cell cycle CDKs.

58 activating phosphorylation of all cell cycle CDKs.

59 t by the action of multiple different cyclin-CDK complexes.

60 Distinct cyclin-CDK complexes are specialized to drive different cell-cy

61 ve cyclin-binding motif found in many cyclin-CDK complex substrates.

62 h wild-type cells expressing multiple cyclin-CDK complexes reveals how cyclin-substrate specificity w

63 Thus, PARK2 regulates cyclin-CDK complexes, as does the CDK inhibitor p16, but acts a

64 red during the cell cycle by a single cyclin-CDK.

65 and p27, and inhibition of correlated cyclin/CDK network.

66 method was developed for identifying cyclin/CDK substrates together with their sites of phosphorylat

67 Inactivation of the bipartite cyclinA2-CDK-binding site in the SAMHD1 C terminus described here

68 which phosphorylation of Thr-592 by cyclinA2-CDK down-modulates, but does not inactivate, SAMHD1 dNTP

69 ass of miRNAs that target nearly all cyclins/CDKs, which are very effective in inhibiting cancer cell

70 rgeting miRNAs," that target several cyclins/CDKs, reduce tumor cell growth, and induce apoptosis.

71 o identify means of interfering with cyclins/CDKs, we performed nine genome-wide screens for human mi

72 he essential requirement of CDK4/6-cyclin D (CDK-4/CYD-1) in C. elegans.

73 volved in cellular proliferation (cyclin D1, CDKs) and morphogenesis (EGFR, MMPs) and such changes fa

74 These creative ways to develop CDK inhibitors are presented along with crystal structur

75 ations in substrate affinities for different CDK-cyclin complexes and the opposing phosphatases [1-4]

76 strate that the phosphorylation of different CDK substrates can be temporally ordered during the cell

77 We propose that qualitatively different CDK complexes are not absolutely required for cell cycle

78 Disrupting CDK function by RNA interference or pharmacological inhi

79 nd unscheduled mitotic entry due to elevated CDK activity.

80 m the nucleus to the cytoplasm, and enhances CDK-5 activity during lytic or acute infection.

81 to S phase transition of cells by enhancing CDK inhibitor p21(Cip-1/Waf1) expression through p53.

82 regulates spindle assembly at mitotic entry: CDK phosphorylates the Alp7-Alp14 complex to localize it

83 at Sld3, previously shown to be an essential CDK and Rad53 substrate, is recruited to the inactive MC

84 iate conformations not yet characterized for CDK members other than CDK2, which will be useful for th

85 fine the structure-activity relationship for CDK kinase inhibition.

86 are orders of magnitude lower than those for CDK-phosphorylated substrates, suggesting a simple model

87 Further, CDK inhibition with palbociclib promoted autophagy-depen

88 Phosphorylation by G1-CDK of Whi5/Rb inhibitors of SBF/E2F transcription facto

89 ding problems observed with first generation CDK inhibitors.

90 The first-generation CDK inhibitors demonstrated broad activity upon several

91 es (CDKs) and auxiliary proteins that govern CDK activities.

92 HR is a biphasic process requiring both high-CDK and low-CDK periods.

93 17) and Krentz et al. (2017) demonstrate how CDK phosphorylation of Ngn3 governs the switch between t

94 Despite this, how CDK mediates cell cycle and developmental transitions in

95 Hence, in CDK-independent manner, endogenous p21 prevents a type o

96 Indeed, CDK inhibitors trigger rapid and massive downregulation

97 ot Y421 residue is required for MCP1-induced CDK-interacting protein 1 (p21Cip1) nuclear export and d

98 e low in S phase and insufficient to inhibit CDKs.

99 PALB2 binding at least in part by inhibiting CDKs.

100 Paradoxically, ATR inhibits CDKs during checkpoint responses, but CDK activity is re

101 s PCNA interacting region (PIR), and not its CDK binding domain, is needed to prevent the replication

102 ant with phosphomimetic mutations at two key CDK-phosphorylated residues (TICRR(TESE)) stimulates DNA

103 Here, we show that the mitotic kinase CDK-1 phosphorylates Suppressor of Par-Two 1 (SPAT-1)/Bo

104 anscriptase by host cyclin-dependent kinase (CDK) 2 at a highly conserved Threonine residue.

105 t and specific oral cyclin-dependent kinase (CDK) 4/6 inhibitor that has strong preclinical data to s

106 We identified cyclin-dependent kinase (CDK) 6 as an upstream regulator of CDK2 controlling SAMH

107 and two sequential cyclin dependent kinase (CDK) activities, and experimental results concur in show

108 in G1 when overall cyclin-dependent kinase (CDK) activity is low.

109 g the cell cycle by cyclin-dependent kinase (CDK) and Dbf4-dependent kinase (DDK), and in response to

110 eplication requires cyclin-dependent kinase (CDK) and Dbf4-dependent kinase (DDK).

111 promote loading of cyclin-dependent kinase (CDK) and proliferating cell nuclear antigen (PCNA) onto

112 ther substrates, as cyclin-dependent kinase (CDK) binding-defective mutants are capable of stimulatin

113 DK4/6 are the first cyclin-dependent kinase (CDK) complexes to be activated by mitogenic/oncogenic pa

114 T387 lies in a cyclin-dependent kinase (CDK) consensus sequence, and CDK inhibitors decrease T38

115 s phosphorylated by cyclin-dependent kinase (CDK) in vitro, and mutation of the CDK consensus sites i

116 ient deprivation or cyclin-dependent kinase (CDK) inactivation express HO in the first cell cycle, wh

117 cle control through cyclin-dependent kinase (CDK) inhibition has therefore emerged as an attractive o

118 nes involved in the cyclin-dependent kinase (CDK) inhibitor (CKI)-CDK-retinoblastoma protein (Rb) pat

119 on levels of p21, a Cyclin-dependent kinase (CDK) inhibitor (CKI).

120 The cyclin-dependent kinase (CDK) inhibitor 1A, p21/Cip1, is a vital cell cycle regul

121 Cyclin-dependent kinase (CDK) inhibitor drugs induce neutrophil apoptosis in vitr

122 egulation of p21, a cyclin-dependent kinase (CDK) inhibitor encoded by CDKN1A, in HCC.

123 ort that p57Kip2, a cyclin-dependent kinase (CDK) inhibitor implicated in the development of tumor-pr

124 The levels of the cyclin-dependent kinase (CDK) inhibitor p21 are low in S phase and insufficient t

125 eased levels of the cyclin-dependent kinase (CDK) inhibitor p21(Cip1).

126 m proteins, such as cyclin-dependent kinase (CDK) inhibitor p21, which promotes cell-cycle arrest at

127 The cyclin-dependent kinase (CDK) inhibitor p27(kip1) is a critical regulator of the

128 es the level of the cyclin-dependent kinase (CDK) inhibitor p27, which inhibits cell cycle progressio

129 ts the induction of cyclin-dependent kinase (CDK) inhibitors (CDKIs), including p16(INK4a), p21(CIP1)

130 Cyclin dependent kinase (CDK) inhibitors have been the topic of intense research

131 d expression of the cyclin-dependent kinase (CDK) inhibitors p16INK4A (CDKN2A) and p21CIP1 (CDKN1A),

132 s, up-regulation of cyclin-dependent kinase (CDK) inhibitors p21 and p27, and inhibition of correlate

133 icantly increased 2 cyclin-dependent kinase (CDK) inhibitors, CDKN1B and CDKN1C.

134 Since cyclin-dependent kinase (CDK) inhibitors, CDKN2A and CDKN2B, and RASSF1A (Ras-ass

135 d by treatment with cyclin-dependent kinase (CDK) inhibitors.

136 f the expression of cyclin-dependent kinase (CDK) inhibitors.

137 Cyclin-dependent kinase (CDK) inhibits MCM loading by phosphorylating the origin

138 AKT, retinoblastoma/cyclin-dependent kinase (CDK) N2A-p16(INK4A), and TP53/mouse double minute (MDM)

139 ontrolled by cyclin/cyclin-dependent kinase (CDK) pairs.

140 , of the 11 minimal cyclin-dependent kinase (CDK) phospho-consensus sites (S/T-P) in Sum1.

141 Cyclin-dependent kinase (CDK) plays a vital role in proliferation control across

142 tment to CENP-C and cyclin-dependent kinase (CDK) regulating KMN network recruitment to CENP-T.

143 ing the analysis of cyclin-dependent kinase (CDK) regulation in chromatin.

144 alyses identified a cyclin-dependent kinase (CDK) signaling node that, when targeted using the CDK4/6

145 Cdc7 kinase (DDK), cyclin-dependent kinase (CDK), and Mec1, the yeast Ataxia telangiectasia mutated/

146 essential target of Cyclin-Dependent Kinase (CDK), are targets of the checkpoint kinase Rad53 for inh

147 osphorylated by the cyclin-dependent kinase (CDK)-activating kinase (Cak1), and Y209 is autophosphory

148 osphorylated by the cyclin-dependent kinase (CDK)-activating kinase, Cak1.

149 Cellular cyclin-dependent kinase (CDK)-mediated Rb inactivation through phosphorylation di

150 Cyclin-dependent kinase (CDK)4 and CDK6 are frequently overexpressed or hyperacti

151 attenuates MYC and cyclin-dependent kinase (CDK)4/6, inhibits the nuclear RelA levels and the expres

152 y the TFIIH kinase, cyclin-dependent kinase (CDK)7.

153 nt kinase (DDK) and cyclin-dependent-kinase (CDK) direct with the help of a large number of helicase-

154 nsing factor), p21 (cyclin-dependent kinase [CDK] inhibitor), and Set8 (histone methyltransferase) in

155 e to inhibitors of cyclin-dependent kinases (CDK), especially THZ1, a covalent inhibitor of CDK7.

156 ecule inhibitor of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.

157 ecule inhibitor of cyclin-dependent kinases (CDKs) 4 and 6 with preclinical evidence of growth-inhibi

158 led by a number of cyclin-dependent kinases (CDKs) and CDK inhibitors (CKIs), the expression of which

159 in this group, the cyclin dependent kinases (CDKs) and mitogen activated protein kinases (MAPKs) requ

160 ferent proteins by cyclin-dependent kinases (CDKs) and other kinases.

161 Cyclin-dependent kinases (CDKs) and their associated regulatory cyclins are centra

162 le progression are cyclin-dependent kinases (CDKs) and their partners.

163 Cyclins and cyclin-dependent kinases (CDKs) are hyperactivated in numerous human tumors.

164 Cyclin-dependent kinases (CDKs) are involved in temporal control of the cell cycle

165 Upon DNA damage, cyclin-dependent kinases (CDKs) are typically inhibited to block cell division.

166 Cyclin-dependent kinases (CDKs) are vital in regulating cell cycle progression, an

167 Inhibition of cyclin-dependent kinases (CDKs) caused dramatic reduction of switching rate within

168 Cyclin-dependent kinases (CDKs) control cell division in eukaryotes by phosphoryla

169 Cyclin-dependent kinases (CDKs) coordinate cell cycle checkpoints with DNA repair

170 rant activation of cyclin-dependent kinases (CDKs) has been shown to contribute to tumor cell progres

171 Cyclin-dependent kinases (CDKs) have been considered promising drug targets for a

172 (RBR) proteins by cyclin-dependent kinases (CDKs) is well documented, but the counteracting phosphat

173 rolled by multiple cyclin-dependent kinases (CDKs) largely in tissue-specific manners.

174 more, we show that cyclin-dependent kinases (CDKs) phosphorylate PAH1 at serine 162, which reduces bo

175 Cyclin-dependent kinases (CDKs) play important roles in the development of many ty

176 Cyclin-dependent kinases (CDKs) play key roles in cell cycle regulation.

177 Transcriptional cyclin-dependent kinases (CDKs) regulate RNA polymerase II initiation and elongati

178 S-phase cyclin-dependent kinases (CDKs) stimulate replication initiation and accelerate pr

179 a large family of cyclin-dependent kinases (CDKs) that reflect the complex interplay between cell cy

180 e the cyclins, the cyclin-dependent kinases (CDKs), and the CDK inhibitors, are critical for the prop

181 ompounds targeting cyclin-dependent kinases (CDKs), as well as by dominant-negative forms of CDK1 and

182 ical inhibitors of cyclin-dependent kinases (CDKs), we applied a variety of '-omics' techniques to th

183 P binds to several cyclin-dependent kinases (CDKs), which may perturb the CDK-mediated phosphorylatio

184 ansition points by cyclin-dependent kinases (CDKs).

185 ision is driven by cyclin-dependent kinases (CDKs).

186 ncreased levels of cyclin-dependent kinases (CDKs).

187 esponses involving cyclin-dependent kinases (CDKs).

188 n association with cyclin-dependent kinases (CDKs).

189 network of cyclin-dependent protein kinases (CDKs) and auxiliary proteins that govern CDK activities.

190 ycle-periodic expression changes are largely CDK independent, but later regulation (induction and rep

191 O1,2 deletion delays START in cells with low CDK activity.

192 asic process requiring both high-CDK and low-CDK periods.

193 ich would otherwise prematurely reverse many CDK-driven phosphorylations.

194 s the view that the only identified metazoan CDK-activating kinase, cyclin H-CDK7-Mat1 (CAK), which i

195 e conserved nature of the inactive monomeric CDK fold and its ability to be remodelled by cyclin bind

196 drug targets for a number of years, but most CDK inhibitors have failed rigorous clinical testing.

197 4/6 inhibitors such as palbociclib and multi-CDK inhibitors such as dinaciclib have rejuvenated the f

198 Here we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits

199 phosphoproteomics-based systems analysis of CDK substrates in fission yeast and demonstrate that the

200 viding a means for modulating the balance of CDK and phosphatase activity.

201 distance and the functional consequences of CDK phosphorylation.

202 es and prompt further clinical evaluation of CDK inhibitors in AML patients harboring MLL fusion prot

203 ary glioblastoma cells enabled expression of CDK inhibitors and decreased p53 protein turnover, which

204 lial cells resulted in reduced expression of CDK inhibitors and the histone demethylase KDM5A.

205 e results determine an essential function of CDK in metazoa and identify a developmental role for reg

206 suggested that changes in the total level of CDK kinase activity, rather than substrate specificity,

207 levels, changes the primary localization of CDK-5 from the nucleus to the cytoplasm, and enhances CD

208 of CDKs and cyclins and by contrast loss of CDK inhibitors, are all linked to gastrointestinal cance

209 The order of CDK substrate phosphorylation depends on rising CDK acti

210 either p38 MAPK overexpression or removal of CDK-5, an antagonizing kinase.

211 The recent successes of CDK inhibitors in the clinic, combined with the potentia

212 cle progression is driven by a succession of CDK complexes with different substrate specificities.

213 all PPs are potentially critical targets of CDK-cyclins in melanoma.

214 ribed in a pulsatile pattern in a variety of CDK-APC/C arrests.

215 tions between loss of Men1 and activation of CDKs, we examined the impact of Cdk4 or Cdk2 disruption

216 Therefore, small molecule inhibitors of CDKs comprise a strategic option in cancer therapy.

217 Accordingly, overexpression of CDKs and cyclins and by contrast loss of CDK inhibitors,

218 These results provide a dynamic view of CDKs revealing intermediate conformations not yet charac

219 the phosphatase can refocus its attention on CDK-phosphorylated substrates.

220 One CDK-like activity of pUL97 is to phosphorylate nuclear l

221 rylation, and overexpression of wild-type or CDK binding-defective Cks2 prevents checkpoint-dependent

222 , much less structural information for other CDK/cyclin complexes, including CDK4/cyclin D1, which di

223 -negative forms of CDK1 and CDK2 and the pan-CDK inhibitor, p21(Cip1/Waf1) Although induced in in viv

224 ew insights into the interactions of peptide CDK inhibitors with key subsites of the cyclin binding g

225 OsPP2A B'' contains three predicted CDK phosphorylation sites: Ser95, Ser102 and Ser119.

226 in addition to drive cell cycle progression, CDK also targets RNF4, which is involved in the regulato

227 ach for selected 2,6,9-trisubstituted purine CDK inhibitor conjugates with folic acid as a drug-deliv

228 in cyclin D1 expression levels, and reduced CDK-driven PELP1 phosphorylation.

229 This is achieved by rising CDK activity and the differential sensitivity of substra

230 substrate phosphorylation depends on rising CDK activity, coupled with variations in substrate affin

231 (DDK) and S-phase cyclin-dependent kinase (S-CDK) are two S phase-specific kinases that phosphorylate

232 ors demonstrated broad activity upon several CDKs, which likely explains their considerable toxicitie

233 during mitosis or meiosis, and that a single CDK complex can drive both cell cycle programmes.

234 ission yeast it has been shown that a single CDK complex generated by the fusion of the Cdc13 cyclin

235 Recent studies revealed that some CDK substrates contain a novel docking motif that is spe

236 The meiosis-specific CDK-like kinase, Ime2, was previously shown to positivel

237 iclib, an orally bioavailable clinical stage CDK-selective inhibitor, potently blocks CDK9, the trans

238 EP290 and DNA replication stress and suggest CDK inhibition as a potential treatment strategy for a w

239 ndent on p53 and its transcriptional target, CDK inhibitor p21.

240 rug Administration approval demonstrate that CDK inhibitors with narrow selectivity profiles can have

241 ompetitive CDK inhibitors, and evidence that CDK inhibitors may have use in suppressing chromosomal i

242 4/6 inhibitors and determine the extent that CDK activity is reactivated during acquired resistance a

243 y organisms, however, it has been found that CDK activity is required for DNA repair, especially for

244 hese studies further support the notion that CDK inhibitors or p21(Cip1) activators might be useful i

245 thal drug combinations inspire optimism that CDK inhibitors will become important weapons in the figh

246 We propose that CDK-5 is activated by the DDR to protect infected neuron

247 Genetic analysis revealed that CDK-8 most likely promotes I4 neurogenesis by inhibiting

248 These results show that CDK can stimulate initiation and compress the replicatio

249 tion of the CDK sites in sld-2, we show that CDK phosphorylation of SLD-2 is essential in C. elegans.

250 Our results suggest that CDK-1 activates PLK-1 via SPAT-1 phosphorylation to prom

251 osphorylated DNMT1 in vitro, suggesting that CDK activity is required for its stabilization.

252 Thus our results reveal one way that CDK regulates spindle assembly at mitotic entry: CDK pho

253 ering on p21(Cip1) and support the idea that CDKs can complement some activities of pUL97.

254 Here we show that CDKs 1/2 phosphorylate the long-range resection nuclease

255 The CDK inhibitor p57(Kip2) is a major target of miR-92a tha

256 uce variable expression of cyclin D1 and the CDK inhibitor p21 that almost exclusively determines cel

257 the cyclin-dependent kinases (CDKs), and the CDK inhibitors, are critical for the proper temporal and

258 regulates cyclin-CDK complexes, as does the CDK inhibitor p16, but acts as a master regulator of the

259 n3, indicating that FgSsn3 and Cid1 form the CDK-cyclin pair as a component of the mediator complex i

260 cal models of stochastic fluctuations in the CDK control system.

261 y promotes I4 neurogenesis by inhibiting the CDK-7/CYH-1 (CDK7/cyclin H) kinase module of the transcr

262 lack of FBL17 increases the stability of the CDK (CYCLIN-DEPENDENT KINASE) inhibitor KIP-RELATED PROT

263 t kinase (CDK) in vitro, and mutation of the CDK consensus sites in REC-1 compromises meiotic crossov

264 It is the founding member of the CDK family and is conserved across all eukaryotes.

265 cycle arrest and increased expression of the CDK inhibitor 1B (p27Kip1) and of proinflammatory and pr

266 is a known transcriptional repressor of the CDK inhibitor p21/WAF1, and knockdown of JLP resulted in

267 ates cell cycle arrest via expression of the CDK inhibitor, p21.

268 By mutation of the CDK sites in sld-2, we show that CDK phosphorylation of

269 axon specification through activation of the CDK-5 pathway in a calcium-dependent manner, involving a

270 ese are under the centralized control of the CDK-APC/C proteins or can be driven by a de-centralized

271 endent kinases (CDKs), which may perturb the CDK-mediated phosphorylation and cell cycle progression.

272 ssor gene (RB1) or components regulating the CDK-RB-E2F pathway have been identified in nearly every

273 relieves CDK2 inhibition by suppressing the CDK inhibitory activity of p27.

274 ase-associated protein 2), which targets the CDK inhibitor p27 for degradation, reduces neuroblast pr

275 We found that the CDK inhibitor dinaciclib and HDAC inhibitor panobinostat

276 We discovered that the CDK-8 Mediator kinase module acts together with a second

277 Multiple studies have demonstrated that the CDK-RB-E2F pathway is critical for the control of cell p

278 loss of p16 function is mediated through the CDK-cyclin pathway via its influence on the pocket prote

279 nd p8 is competent for DNA repair, while the CDK-activating kinase subcomplex, which includes the kin

280 d by the fusion of the Cdc13 cyclin with the CDK protein Cdc2 can drive the mitotic cell cycle.

281 S1/SUC1 and can physically interact with the CDK protein Cdc28, and Som1, a downstream regulator of t

282 In contrast to CDK hyperactivation, the acceleration of S-phase progres

283 o the inactive promoter during arrest due to CDK inactivation, and these bound factors allow the cell

284 rimary murine kidney cells after exposure to CDK inhibitors.

285 ) position of the cyclin partner relative to CDK, contrasting with the closed CDK2/cyclin A conformat

286 he differential sensitivity of substrates to CDK activity over a wide dynamic range.

287 in their dependence on this transcriptional CDK and suffer apoptotic cell death upon CDK7 inhibition

288 A catalytic subunit subtype II, PSTAIRE-type CDK and OsRBR1 were in the same protein complex, indicat

289 We identify the plant-specific B1-type CDKs (CDKB1s) and the class of B1-type cyclins (CYCB1s)

290 A majority of Men1(+/-) mice with wild-type CDKs developed pituitary and islet tumors by 15 months o

291 E1 inhibition degrades RRM2 through untimely CDK activation.

292 nd defines a mechanism by which this unusual CDK orchestrates migration-proliferation dichotomy durin

293 Using CDK inhibitors to reverse the constitutive inhibitory ph

294 ovirus (HCMV) UL97 protein is a viral CDK (v-CDK) that phosphorylates Rb.

295 MV)-encoded viral cyclin-dependent kinase (v-CDK) UL97 phosphorylates the retinoblastoma (Rb) tumor s

296 High p21 levels mediate G1 arrest via CDK inhibition, yet lower levels have no impact on G1 pr

297 tomegalovirus (HCMV) UL97 protein is a viral CDK (v-CDK) that phosphorylates Rb.

298 47 is required to promote resection, whereas CDK-dependent phosphorylation of CtIP-S327 is required f

299 tion timing program, but it is unknown which CDK substrates are responsible for these effects.

300 Treatment of Cep290-deficient cells with CDK inhibitors rescued DNA damage and centriole number.