ライフサイエンスコーパス: CDK

1 CDK phosphorylation in mitosis is compromised for approx

2 can be mono-phosphorylated on any one of 14 CDK phosphorylation sites.

3 s compounds against human kinases GSK-3beta, CDK-2, and CDK-4 were leveraged to try to improve the se

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

5 a Bcl-2 family inhibitor and Purvalanol A, a CDK inhibitor, as a potential targeted therapy for AML p

6 motif A, which we previously identified as a CDK-binding motif.

7 ate that p38 MAPK gamma (p38gamma) acts as a CDK-like kinase and thus cooperates with CDKs, regulatin

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

9 ells with high p27pT157pT198 or expressing a CDK-binding defective p27pT157pT198 phosphomimetic (p27C

10 We identified the LGO gene, a CDK inhibitor, as a key cell cycle regulatory factor inf

11 n by the interaction of TRAPP with hnRNPK, a CDK substrate that associates with SGs when phosphorylat

12 Here we identify a CDK phosphorylation site in the shelterin subunit at Ser

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

14 of MAPK pathway signalling, which restores a CDK-dependent suppression of RB.

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

16 Such a CDK/PP4-based regulation of cohesin loader activity coul

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

18 rogression, cyclin F does not partner with a CDK, but instead forms via its F-box domain an SCF (Skp1

19 en for negative regulators of Mis4 yielded a CDK called Pef1, whose closest human homologue is CDK5.

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

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

22 lysis, we unexpectedly found that cyclin E/A-CDK activity can only maintain Rb hyperphosphorylation s

23 ion until S phase, at which point cyclin E/A-CDK activity takes over.

24 and that CDK4/6 activity, but not cyclin E/A-CDK activity, is required to hyperphosphorylate Rb throu

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

26 tivity of >60 kinases, including ABLs, AKTs, CDKs and MAPKs.

27 against human kinases GSK-3beta, CDK-2, and CDK-4 were leveraged to try to improve the selectivity o

28 d that pharmacological inhibition of ATR and CDK activities attenuates SMARCAL1 degradation.

29 d S173 early during infection in an ATR- and CDK-dependent manner, and that pharmacological inhibitio

30 Therefore, inhibiting Brd4 and CDK concurrently with AZD5153 and dinaciclib would be mo

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

32 re we discover that in mouse ESCs FBXL19 and CDK-Mediator support long-range interactions between sil

33 ts a model whereby MPK-1/ERK, GSK-3/GSK3 and CDK-2/CDK2, along with SEL-10/FBXW7, constitute a regula

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

35 arget LA, including TNF, NFkappaB, MAPK, and CDK inhibitors.

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

37 protein components (cyclins D1, E2, B1, and CDKs 1, 2, and 4) in melanomas with a hyperactive BRAF o

38 cate that adenovirus utilizes ATR kinase and CDKs during infection to promote the degradation of SMAR

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

40 in one or more key components of this axis (CDKs, cyclins, CDK inhibitors and the RB family of prote

41 We show that Plasmodium berghei CDK-related kinase 5 (CRK5), is a critical regulator of

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

43 Together these contributions by CDK inherently link correct SPB morphogenesis, age and f

44 ough the cell cycle is tightly controlled by CDK inhibitors such as p27(Kip1).

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

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

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

48 SYP-1 phosphorylation by CDK-1 occurs just before meiotic onset.

49 K-2 is targeted to crossover sites primed by CDK-1 and spreads along the SC by reinforcing SYP-1 phos

50 It phosphorylates canonical CDK motifs of components in the pre-replicative complex

51 e species, and the presence of the canonical CDK motif, CDKB emerged as a likely candidate for a Sacc

52 ction by directing the localization of Cdc13-CDK to centrosomes and that this localization of CDK con

53 nd pharmacologic inhibition of the p38, CK2, CDK, AXL, and PIKFYVE kinases to possess antiviral effic

54 than via direct phosphorylation of classical CDK targets.

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

56 y inhibits both CDKA;1- and CDKB1-containing CDK complexes in vivo, thus promoting endoreplication in

57 kely have a multivalent interaction with CYC/CDK complexes.

58 iptional CDKs (CDK7 and CDK9) and cell cycle CDKs (CDK4 and CDK6) as well.

59 activating phosphorylation of all cell cycle CDKs.

60 p27 binds and inhibits cyclin-CDK to arrest the cell cycle.

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

62 d by the activity of a single mitotic cyclin-CDK complex [6, 7].

63 aryotic cells, which contain multiple cyclin-CDK forms that have poorly defined and partially overlap

64 ls, suggesting that this mechanism of cyclin-CDK spatial regulation may be conserved across eukaryote

65 onical model of RB regulation is that cyclin-CDKs phosphorylate and render RB inactive in late G1/S,

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

67 odium male gametogony, this divergent cyclin/CDK pair fills the functional space of other eukaryotic

68 ing evidence regarding which specific cyclin/CDK complexes are inhibited by SIM in vivo.

69 gnals, regulating the stoichiometric cyclin: CDK inhibitor ratio for ultrasensitive control of CDK4/6

70 key components of this axis (CDKs, cyclins, CDK inhibitors and the RB family of proteins) occur in v

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

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

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

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

75 Disrupting CDK function by RNA interference or pharmacological inhi

76 -specific groups which comprised 11 distinct CDK groups (CDKA-J) with CDKB being the most widely dist

77 with CDKB being the most widely distributed CDK protein.

78 vision cycles, and a repertoire of divergent CDKs and cyclins of poorly understood function and inter

79 arrest and interference with the downstream CDK-Rb (retinoblastoma protein)-E2F signaling pathway.

80 nd unscheduled mitotic entry due to elevated CDK activity.

81 ociated complications are very important for CDK diagnosis and treatment.

82 Patients with TNBC have been excluded from CDK 4/6 inhibitor clinical trials due to the perceived h

83 ein-protein interactions and shifts p27 from CDK inhibitor to oncogene.

84 p27 shifts from CDK inhibitor to oncogene when phosphorylated by PI3K ef

85 Furthermore, CDK-imposed order in the construction of the new SPB pro

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

87 ze the LP docking motif, which determines G1-CDK substrate specificity in fungi.

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

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

90 -finger protein MAT1 form the heterotrimeric CDK-activating kinase (CAK) complex which is vital for t

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

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

93 These data help explain how CDK activity controls replication initiation and suggest

94 The human CDK-activating kinase (CAK), a complex composed of cycli

95 o quantify target occupancy for all 21 human CDKs in live cells, and present a comprehensive evaluati

96 We identified CDKs and cyclins in different Symbiodiniaceae species an

97 This increased CDK activity is confirmed at the level of mRNA and prote

98 s to the cytoplasm in response to increasing CDK activity and consequent sensor phosphorylation.

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

100 PALB2 binding at least in part by inhibiting CDKs.

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

102 e drugs and chemical probes of intracellular CDK function.

103 finity and selectivity against intracellular CDKs is lacking.

104 CITe-Id analysis of our irreversible CDK inhibitor THZ1 identified dose-dependent covalent mo

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

106 demonstrate that the cyclin-dependent kinase CDK-1 primes the recruitment of PLK-2 to the synaptonema

107 ent and approval of cyclin-dependent kinase (CDK) 4 and 6 inhibitors for hormone receptor-positive an

108 oma (RB) protein by cyclin-dependent kinase (CDK) 4/6 and increased G1-S progression.

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

110 wnstream target for cyclin-dependent kinase (CDK) 4/6 inhibitors that are in clinical use.

111 lectively inhibited cyclin-dependent kinase (CDK) 5 over CDK2 in cancer cell lines.

112 Cyclin-dependent kinase (CDK) 7 has a unique functional repertoire by virtue of i

113 complex composed of cyclin-dependent kinase (CDK) 7, cyclin H, and MAT1, is a critical regulator of t

114 Although cyclin-dependent kinase (CDK) 9 has an established pathogenic role in various can

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

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

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

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

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

120 inhibit cyclin and cyclin-dependent kinase (CDK) complex that promotes fibrosis and hypertrophy.

121 sor inhibits cyclin/cyclin-dependent kinase (CDK) complexes and halts cell cycle progression.

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

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

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

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

126 thaliana) encodes a cyclin-dependent kinase (CDK) inhibitor that plays a central role in establishing

127 , we identify CR8-a cyclin-dependent kinase (CDK) inhibitor(6)-as a compound that acts as a molecular

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

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

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

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

132 hat transcriptional cyclin-dependent kinase (CDK) inhibitors targeting CDK7/12/13 and CDK9 potently s

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

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

135 independent of its cyclin-dependent kinase (CDK) inhibitory action.

136 se the HCMV-encoded cyclin-dependent kinase (CDK) ortholog pUL97 extensively phosphorylates the check

137 mediated by mitotic cyclin-dependent kinase (CDK) phosphorylation of the GTPase's downstream kinases.

138 Here, we adapt a cyclin-dependent kinase (CDK) sensor to uncouple these key events of the cell cyc

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

140 ylation networks of cyclin-dependent kinase (CDK) targets have opened a new level of signaling comple

141 of the cell cycle, cyclin-dependent kinase (CDK), temporally coordinates an array of complex molecul

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

143 ed by the conserved cyclin-dependent kinase (CDK)-cyclin protein complex(1).

144 The cyclin-dependent kinase (CDK)-RB-E2F axis forms the core transcriptional machiner

145 nder the control of cyclin-dependent kinase (CDK).

146 Cyclin-dependent kinase (CDK)/cyclin complexes drive most processes in cellular p

147 Cyclin-dependent kinase (CDK)6 is a member of the CDK family of cell cycle-relate

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

149 Brd4 and cyclin-dependent kinases (CDK) had critical regulatory roles in the expression and

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

151 The cyclin-dependent kinases (CDKs) 12 and 13 phosphorylate the C-terminal domain of R

152 ity of 4.35 toward cyclin-dependent kinases (CDKs) 2, 5, and 9, and the cocrystal with CDK2/cyclin A2

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

154 , proper levels of cyclin dependent kinases (CDKs) and cyclins, including D-type cyclins critical for

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

156 CKS) proteins bind cyclin-dependent kinases (CDKs) and play important roles in cell division control

157 onserved family of cyclin-dependent kinases (CDKs) and their partner cyclins.

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

159 Cyclin-dependent kinases (CDKs) are frequently deregulated in cancer and represent

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

161 The cyclin-dependent kinases (CDKs) are the major cell-cycle regulators that phosphory

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

163 gy, and identified cyclin-dependent kinases (CDKs) as overactivated kinases in specimens derived from

164 in the activity of cyclin-dependent kinases (CDKs) bound to cyclins.

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

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

167 ocking motifs help cyclin-dependent kinases (CDKs) phosphorylate different substrates at different st

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

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

170 Cyclin-dependent kinases (CDKs) regulate cell cycle progression and transcriptiona

171 ts the activity of cyclin-dependent kinases (CDKs) that promote cell division.

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

173 n conjunction with cyclin-dependent kinases (CDKs).

174 rily by inhibiting cyclin-dependent kinases (CDKs).

175 esponses involving cyclin-dependent kinases (CDKs).

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

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

178 activating cyclin dependent protein kinases (CDKs) via phosphorylation.

179 oblastoma tumour suppressor protein at known CDK target residues.

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

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

182 e phenotype of sae2 mutants lacking the main CDK (sae2-S267A) or Mec1 and Tel1 phosphorylation sites

183 fficient to cause resistance to combined MEK/CDK inhibition and to replace genetic depletion of oncog

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

185 A comparison of Breviolum minutum CDK and cyclin gene expression between free-living and s

186 omised for approximately half of all mitotic CDK substrates, with substrates affected generally being

187 When mitotic CDK (Cyclin B1-CDK1) is used to drive interphase egg ext

188 ed or altered in metastases, including mTOR, CDK/RB, cAMP/PKA, WNT, HKMT, and focal adhesion.

189 Dinaciclib is a small molecule multi-CDK inhibitor targeting CDK 2/5/9.

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

191 functional role of RB phosphorylation at non-CDK sites has remained elusive.

192 This review focuses on noncanonical, CDK-independent functions of p27 in migration, invasion,

193 reated with 4.35 showed dephosphorylation of CDK substrates, cleavage of PARP-1, downregulation of XI

194 t K19 may be used to predict the efficacy of CDK inhibitors for treatments of breast cancer.

195 The largest expansion of CDK groups was, however, in alveolate-specific groups wh

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

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

198 ecular brakes that determine the kinetics of CDK activation.

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

200 ing those that require the highest levels of CDK activity to become phosphorylated and those that are

201 to centrosomes and that this localization of CDK contributes to the CDK substrate phosphorylation nec

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

203 In fission yeast, the correct ordering of CDK substrate phosphorylation can be established by the

204 We investigated the potential of CDK inhibitors, Palbociclib and RO-3306, on neuroblastom

205 The present study examined the role of CDK blockers, p21(Cip1) /p27(Kip1) in the progression of

206 ble method for evaluating the selectivity of CDK inhibitors in living cells, and present a refined se

207 ehavior in C. elegans based on a snapshot of CDK activity in newly born cells.

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

209 e third larval stage relies on activation of CDKs.

210 of regulation, from the inferred ancestor of CDKs and MAPKs, to modern ERKs.

211 ity probes designed to bind to the family of CDKs.

212 These results demonstrate that inhibition of CDKs by palbociclib may be a therapeutic strategy in PAH

213 d it phosphorylates the regulatory T-loop of CDKs that control cell cycle progression.

214 rimeric complex phosphorylates the T-loop of CDKs that control cell-cycle progression.

215 studies of combinatorial treatment based on CDK inhibitors.

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

217 Epigenetically targeting Brd4 or CDKs with their respective inhibitors suppressed the exp

218 as a potential mechanism to correctly order CDK substrate phosphorylation.

219 define the global effects of THZ1 and other CDK inhibitors on RNA polymerase II dynamics.

220 ity probe-based competition assay to profile CDK inhibitors.

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

222 ing protein, through its capacity to recruit CDK-Mediator.

223 that it is solely responsible for regulating CDK functions in meiosis.

224 atients with nephropathic cystinosis-related CDK and 97 with CKD from other causes.

225 ins related to eumetazoan cell-cycle-related CDKs (CDK1) were identified as well as transcription-rel

226 identified as well as transcription-related CDKs.

227 ffects involving cGMP/cGK axis by repressing CDK blockers p21(Cip1) and p27(Kip1) .

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

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

230 to sequentially integrate both the G1- and S-CDK activities while keeping S-CDK inhibited towards oth

231 the G1- and S-CDK activities while keeping S-CDK inhibited towards other targets.

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

233 ersional phosphorylation routes within the S-CDK-Sic1 inhibitory complex.

234 But how can the same CDK induce different events when activated at different

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

236 rns of certain protein kinases, with several CDKs/MAPKs immediately active upon the infection, and ba

237 However, a single CDK can drive all events of cell division in both mammal

238 Specific CDK inhibition by dinaciclib and palbociclib decreases P

239 AMESE-RELATED (SMR) family of plant-specific CDK inhibitor genes.

240 tates showed that several alveolate-specific CDKs and two P/U-type cyclins exhibited altered expressi

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

242 ent a refined set of tool molecules to study CDK function.

243 3B1) are phosphorylated by the three-subunit CDK-activating kinase (CAK; CCNH, MAT1, and CDK7).

244 DK sensor consists of a fluorescently tagged CDK substrate that steadily translocates from the nucleu

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

246 small molecule multi-CDK inhibitor targeting CDK 2/5/9.

247 4/6 inhibitors and determine the extent that CDK activity is reactivated during acquired resistance a

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

249 We show that CDK enforces Spc72 asymmetric docking by phosphorylating

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

251 The CDK family plays a crucial role in the control of the ce

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

253 The CDK phosphorylates Rad21 on Threonine 262.

254 The CDK sensor consists of a fluorescently tagged CDK substr

255 The CDK-bound form of CR8 has a solvent-exposed pyridyl moie

256 CAK holds a special position among the CDK branch due to this dual activity and the dependence

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

258 ells, CDC25 phosphatase dephosphorylates the CDK releasing cells into mitosis, but in plants, its rol

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

260 The core elements of the CDK control system are conserved in eukaryotic cells, wh

261 well as its ability to enrich members of the CDK family from cell lysates, was investigated.

262 n-dependent kinase (CDK)6 is a member of the CDK family of cell cycle-related proteins and plays an i

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

264 ycle-arrest is mediated by expression of the CDK inhibitor p21WAF1/Cip1, which prevents phosphorylati

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

266 ase 7 (CDK7) is the catalytic subunit of the CDK-activating kinase complex.

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

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

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

270 A model target, the CDK inhibitor Sic1, contains linear phosphorylation moti

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

272 seq and ChIP-qPCR provided evidence that the CDK inhibitor directly inhibited Brd4 recruitment to act

273 Several studies reported that the CDK inhibitor p27(Kip1) promotes starvation-induced auto

274 We show that the CDK sensor can distinguish cycling cells in G1 from quie

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

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

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

278 this localization of CDK contributes to the CDK substrate phosphorylation necessary to ensure proper

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

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

281 e CDKs has been implicated in cancer and the CDKs have been investigated extensively as potential the

282 Dysregulation and mutation of the CDKs has been implicated in cancer and the CDKs have bee

283 ctive inhibition of specific isoforms of the CDKs is crucial to achieve therapeutic effect while mini

284 obic patch of mitotic cyclins contributes to CDK substrate selection by directing the localization of

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

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

287 f cyclin D3 and sensitivity of cells towards CDK inhibitor-induced cell death.

288 Notably, transcriptional CDK inhibition leads to preferential and concentration-d

289 In other cancer types, transcriptional CDK inhibitors have been observed to downregulate highly

290 CDK5 over not only CDK1, but transcriptional CDKs (CDK7 and CDK9) and cell cycle CDKs (CDK4 and CDK6)

291 Similar to cyclins, two CDK-groups found in Symbiodiniaceae species were solely

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

293 Using CDK inhibitors to reverse the constitutive inhibitory ph

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

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

296 These results support a model whereby CDK-catalyzed phosphorylation of Sae2 activates resectio

297 tency can advance or delay the time at which CDK substrate phosphorylation occurs, and thereby contro

298 n sensitivity and substrate specificity with CDK family members.

299 s a CDK-like kinase and thus cooperates with CDKs, regulating entry into the cell cycle.

300 In budding yeast, CDK substrates with Leu/Pro-rich (LP) docking motifs are