ライフサイエンスコーパス: CDK2

1 ansition related proteins (p21, cyclin E and Cdk2).

2 tes by activating cyclin-dependent kinase 2 (CDK2).

3 rogression by binding cyclin A- and cyclin E-CDK2.

4 d be partially reversed by overexpression of CDK2.

5 inhibitors that distinguish between CDK1 and CDK2.

6 ls treated with insulin or overexpression of CDK2.

7 he expression of cell cycle proteins p21 and CDK2.

8 able crossover differentiation by regulating CDK2.

9 ification could be resensitized by targeting CDK2.

10 .3% systems on SEQ17, and 76.9% vs. 61.5% on CDK2.

11 plex to promote binding of SIRT2 to cyclin A-Cdk2.

12 regulatory genes, including SKP2, CUL1, and CDK2.

13 y compensated its function in the absence of Cdk2.

14 tio for ultrasensitive control of CDK4/6 and CDK2.

15 S phase entry and progression by activating Cdk2.

16 mechanism depends on the activation state of CDK2.

17 , which functions as a regulatory subunit of CDK2.

18 Based on similarities with Cdk2 3D structure, the Cdk9 peptide cross-linked by Hexi

19 ppressed expression of its molecular targets CDK2/5/9, and anti-apoptotic BCL-XL and BCL2 proteins.

20 ring CDKN2A/p16 genomic deletions alleviated CDK2 activation and replication stress, attenuating CHKi

21 inase (FAK) axis leads to CDK4/6-independent CDK2 activation, involving as critical mechanistic event

22 ciation between CDKN2A/p16 copy number loss, CDK2 activation, replication stress, and hypersensitivit

23 exhibit higher p27 levels but have increased CDK2 activities and higher proliferation rates in the S-

24 system to simultaneously monitor CDK4/6 and CDK2 activities in single cells and found that CDK4/6 ac

25 some cell lines fail to restrain their high CDK2 activity and hence succumb to CHK1i in S phase.

26 ss through a noncycling period marked by low CDK2 activity and high p21 levels.

27 sted, the activation of RB and inhibition of CDK2 activity emerged as determinants of sensitivity.

28 hat CDK4/6 activity increases rapidly before CDK2 activity gradually increases, and that CDK4/6 activ

29 cycle with a slowed and fluctuating cyclin E-CDK2 activity increase.

30 CDK2 activity is largely dispensable for normal developm

31 In contrast, high CDK2 activity is required for sensitivity to CHK1i as mo

32 asis tests demonstrate that ectopic Cyclin E/Cdk2 activity is responsible for the extra cell cycles c

33 In contrast, reduced CDK2 activity leads to the complete absence of CO format

34 ion of Dap reduces the threshold of Cyclin E-Cdk2 activity necessary to trigger the subsequent G-S tr

35 Thus, increasing cyclin E/Cdk2 activity over the course of G1 is not only critical

36 Reduced Cdk2 activity results in smaller HLBs and the appearance

37 This high CDK2 activity threshold usually occurs late in the cell

38 Elevated CDK2 activity was associated with increased numbers of L

39 ng tissues with compromised PP2A retain high Cdk2 activity when they should be quiescent, and genetic

40 c cyclin E degradation and maintain cyclin E-CDK2 activity while also enabling cyclin E destruction i

41 plication stress, but the dependence on high CDK2 activity, as well as MRE11, contradicts this hypoth

42 Second, HKL decreased CDK2 activity, leading to G1 cell cycle arrest.

43 puts, and generate outputs including altered Cdk2 activity, p27 stability, and, ultimately, cell cycl

44 We found that in the absence of cyclin E/Cdk2 activity, there was a 10-fold decrease in chromatin

45 ncoupling cyclin E degradation from cyclin E-CDK2 activity.

46 uiescence through the regulation of Cyclin E/Cdk2 activity.

47 pse microscopy of Cyclin-Dependent Kinase 2 (CDK2) activity followed by endpoint immunofluorescence a

48 rylation of three known regulators of Pol I, CDK2, AKT and AMPK, is altered during ribosomal stress a

49 odel whereby MPK-1/ERK, GSK-3/GSK3 and CDK-2/CDK2, along with SEL-10/FBXW7, constitute a regulatory n

50 nted downregulation of the pro-growth signal CDK2 and ablated TGFbeta-induced EMT.

51 Together, our study links Cdk2 and Akt pathways to the control of DNA replication

52 K2 degrader with degradation selectivity for CDK2 and CDK5 over not only CDK1, but transcriptional CD

53 herapeutic targets in NB and that abrogating CDK2 and CDK9 activity by small molecules like dinacicli

54 ndidate 4ab with a nanomolar potency against CDK2 and CDK9 and potent antiproliferative activities ag

55 Taken together, this study suggests that CDK2 and CDK9 are potential therapeutic targets in NB an

56 rmatics strategy as cyclin-dependent kinases CDK2 and CDK9 inhibitors, which play critical roles in t

57 of NB cell lines by blocking the activity of CDK2 and CDK9.

58 nd validated the general prognostic index of CDK2 and CDKN3 compared with CDKN2D and CDKN1B.

59 ding subsequently to selective inhibition of CDK2 and cyclin A expression and G2-M cell-cycle arrest.

60 nus of p17 is necessary for interaction with CDK2 and for induction of autophagy.

61 ed signaling crosstalk between the oncogenic CDK2 and HER2 pathways.

62 ivates the cyclin-dependent kinases Cdk1 and Cdk2 and is expressed at elevated levels from S phase un

63 gmentation in Cdk1(AF) MEFs does not rely on CDK2 and is partly caused by premature activation of MUS

64 ore the start of DNA replication by cyclin E/Cdk2 and made irreversible by Emi1.

65 of CDK2 suggesting a regulatory loop between CDK2 and PDK1.

66 e, inhibition of pERK both reduced levels of CDK2 and prevented EMT independent of exogenous TGFbeta,

67 o trigger a bistable switch whereby cyclin E-CDK2 and Rb mutually reinforce each other to induce Rb h

68 ll as by dominant-negative forms of CDK1 and CDK2 and the pan-CDK inhibitor, p21(Cip1/Waf1) Although

69 also attenuates p27's inhibitory activity on CDK2 and thereby contributes to increased G1-S phase tra

70 in Spy1 that ablate its ability to activate Cdk2 and to proliferate cells.

71 ry subunit of the cyclin-dependent kinase 2 (Cdk2) and controls cell cycle re-entry.

72 expression of the cyclin-dependent kinase 2 (CDK2) and cyclin D1 proteins.

73 inhibited phospho-cyclin-dependent kinase 2 (CDK2) and cyclin-A expression, arresting cell cycle prog

74 ernary complex with cyclin-dependent kinase (Cdk2) and cyclins (e.g., Cdk2/Cyclin A).

75 on of Cylin E and Cyclin-dependent kinase 2 (CDK2) and downregulation of p21, p27 and p57.

76 cence by inducing cyclin-dependent kinase 2 (CDK2) and reducing p21(CIP1) and NEUROG3 protein levels

77 l known proteins such as actin, tropomyosin, CDK2, and alpha-synuclein (alphaSyn).

78 the ternary complex between p27(Kip1) (p27), Cdk2, and cyclin A to study these questions using enhanc

79 eview the core pharmacophores used to target CDK2, and outline strategies for the rational design of

80 n of cyclins A, E, and D1, activated phospho-CDK2, and phospho-S477/T479 AKT.

81 ssion activates the cyclin-dependent kinase, Cdk2, and this directly promotes invasion by increasing

82 uces CDK1-dependent RIF1 phosphorylation and CDK2- and CDC7-dependent activation of the replicative h

83 Mice with pancreas-specific deletion of Cdk2 are glucose-intolerant, primarily due to defects in

84 Both CDK1 and CDK2 are potential cancer targets for which selective co

85 ar weight cyclin E or LMW-E) in complex with CDK2 are preferentially mislocalized to the cytoplasm.

86 is, cytoplasmic cyclin E plus phosphorylated CDK2 (as one variable) predicted breast cancer recurrenc

87 rom apoptosis and that reduced expression of CDK2 associates with the development of DN.

88 identify RingoA as an important activator of Cdk2 at meiotic telomeres, and provide genetic evidence

89 Hence, both pathways require CDK2 but appear to depend on different CDK2 substrates.

90 Here we show that not only Cdk2 but Cdk1 phosphorylates p27 at the Thr-187.

91 bose binding pocket and that is preferred in CDK2 but has not been observed in CDK1.

92 Preventing downregulation of CDK2 by blocking the TLR pathway with GIT27 may provide

93 ibition of PI3K and MEK in combination or of CDK2 by their respective small-molecule inhibitors reduc

94 at prevents aberrant DNA replication and the Cdk2-c-Myc-miR-571 axis as a new pathway for regulating

95 ults suggest that cytoplasmic cyclin E and p-CDK2 can be readily detected with immunohistochemistry a

96 We demonstrate that cyclin-dependent kinase (CDK2) can bind to the promoters of a number of genes in

97 diated by this pathway can be antagonized by Cdk2/Cdc2 inhibitors in vitro and in vivo.

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

99 th treatment arms, whereas CNAs in MYC, ATM, CDK2, CDK4, and MDM2 had no prognostic value.

100 nhibitor of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.

101 to increased expression of EGFR, MAPK, CDK4, CDK2, CDK7, CCNE1 and CCNE2.

102 ycle promotion and cancer progression (CDK1, CDK2, CDK8, CHEK1, CHEK2, GSK-3 beta, NPM, PAK1, PP2C-al

103 y exhibited 10-80-fold greater inhibition of CDK2 compared to CDK1.

104 HX enhances Sirt1 and Sirt1/Cdk2 complex formation through HIF1alpha activation.

105 dk2 (Thr14), led to inactivation of Cyclin A/Cdk2 complex, arrested cell cycle at S phase.

106 Furthermore, we show that correctly docked CDK2 complexes re-create on average 79.8% of all pairwis

107 1 is able to interact with the cyclin A-CDK1-CDK2 complexin monocytic THP-1 cells and primary monocyt

108 cycle regulator, cyclin-dependent kinase 2 (CDK2), couples primary beta-cell dysfunction to the prog

109 e-specific measurements of Pin1-catalysis of CDK2/CycA-phosphorylated full-length tau reveal a number

110 to predict progression of DN, downregulated CDK2 (cyclin-dependent kinase 2).

111 , upon binding to cyclin-dependent kinase 2 (Cdk2)/cyclin A.

112 Relative to CDK2-cyclin A, CDK1-cyclin B is less thermally stable, h

113 The cdk2-cyclin E inhibitor roscovitine did not prevent the

114 D1 initiates binding, (ii) p27 wraps around Cdk2/Cyclin A and D2 binds, and (iii) the fully-formed f

115 integrative study of p27 and its binding to Cdk2/Cyclin A complex by performing single-molecule mult

116 Binding of p27 to the Cdk2/cyclin A complex is accompanied by partial folding

117 osed conformation is the most stable for the CDK2/cyclin A complex, in agreement with their experimen

118 changes in D1 facilitate initial binding to Cdk2/Cyclin A complex.

119 rt that RRM1 is phosphorylated at Ser 559 by CDK2/cyclin A during S/G2 phase.

120 Structural studies of CDK2/cyclin A have provided a wealth of information conc

121 th the N- and C-termini of p27 interact with Cdk2/cyclin A in multiple, closely associated states.

122 R signals during p27 folding upon binding to Cdk2/cyclin A on a time scale of several seconds.

123 7 underpins its functional interactions with Cdk2/Cyclin A provides insight into the complex binding

124 pendent kinase (Cdk)/cyclin complexes (e.g., Cdk2/cyclin A), causing cell cycle arrest.

125 n-dependent kinase (Cdk2) and cyclins (e.g., Cdk2/Cyclin A).

126 Even when tightly bound to Cdk2/cyclin A, intrinsic flexibility enables p27 to inte

127 Cell division progresses when stably Cdk2/cyclin A-bound p27 is phosphorylated on one or two

128 ntegrated biophysical approach, we show that Cdk2/cyclin A-bound p27 samples lowly-populated conforma

129 olation and within the trimeric complex with Cdk2/cyclin A.

130 d conformations resembling that captured for CDK2/cyclin A.

131 eflecting a multi-step mechanism for binding Cdk2/Cyclin A.

132 ificant structural heterogeneity compared to Cdk2/cyclin A.

133 The trimeric Cdk2/cyclin A/p27-KID complex possesses significant stru

134 kt by downregulating complexes of mTORC2 and CDK2/cyclin A2 and upregulating PSMB6, which together in

135 iscovered that p17 binds to and inhibits the CDK2/cyclin A2 complex, further inhibiting phosphorylati

136 s (CDKs) 2, 5, and 9, and the cocrystal with CDK2/cyclin A2 revealed its binding in the active site.

137 carries out its function after GSK3beta- and CDK2/cyclin A2-dependent phosphorylation events on Thr17

138 reveals an interaction between ASPM and the Cdk2/Cyclin E complex, regulating the Cyclin activity by

139 s (through a pathway involving AKT, ROCK and CDK2/Cyclin E-nucleophosmin) and in mouse tissues, and i

140 n Cycle 6 (CDC6), Cyclin-dependent kinase 2 (CDK2), Cyclins D1 and D3, indicating that key cell cycle

141 in ovarian cancer cells (OVCAR8) depends on CDK2 degradation and correlates with high expression of

142 ents a lead for further development and that CDK2 degradation is a potentially valuable therapeutic s

143 evelopment of TMX-2172, a heterobifunctional CDK2 degrader with degradation selectivity for CDK2 and

144 cle 7 (CDC7)- and cyclin-dependent kinase 2 (CDK2)-dependent reactivation of the replicative helicase

145 In conclusion, DOX exposure induces CDK2-dependent FOXO1 activation, resulting in cardiomyoc

146 nts demonstrated that loss of MCPH1 caused a CDK2-dependent increase in STIL levels at the centrosome

147 sed mechanisms activate this novel KAP/ROCK2/Cdk2-dependent invasion pathway in glioblastoma.

148 , but not in HIV-1-infected CD4 T cells, via CDK2-dependent mechanisms.

149 We identify CDK2-dependent phosphorylation of RB as an effector of M

150 ere we demonstrate that DOX exposure induces CDK2-dependent phosphorylation of the transcription fact

151 m the C-terminus of BRCA2, prevents cyclin A-CDK2-dependent Ser3291 phosphorylation and facilitates R

152 AD repressed the p27/CDKN1B gene, activating CDK2-dependent SMAD3 phosphorylation to induce p50 NFkap

153 Cdk2-dependent TopBP1-treslin interaction is critical fo

154 ging showed that depletion of SKP2, CUL1, or CDK2 did not rescue the Wee1 inhibition-induced karyokin

155 Interestingly, CDK2 directly phosphorylates ELK4 at Thr194 and Ser387 a

156 d that S19 site phosphorylation of PTPN12 by CDK2 discharged its antitumor activity by down-regulatio

157 n of CDKs, we examined the impact of Cdk4 or Cdk2 disruption on tumorigenesis in Men1(+/-) mice.

158 but become dependent upon an ATR/CHK1/CDC25A/CDK2 DNA damage response axis.

159 Cyclin-dependent kinase 2 (CDK2) drives the progression of cells into the S- and M-

160 1 by I-BET151 in both monocytic and T cells, CDK2 enhanced HIV-1 transcription in monocytic cells but

161 In this study, we found that ectopic CDK2 enhances Ras (G12V)-induced foci formation and knoc

162 2V)-induced foci formation and knocking down CDK2 expression markedly decreases epidermal growth fact

163 ed in melanoma and knocking down the ELK4 or CDK2 expression significantly attenuated the malignant p

164 smic scoring systems for both cyclin E and p-CDK2 expression to demonstrate altered cellular accumula

165 LPS-treatment of mice also reduced CDK2 expression.

166 selectively in BLBC tumors, indicating that CDK2 hyperactivity is a genome integrity vulnerability e

167 Furthermore, in CDK2 hypomorphic cells there was reduced nuclear AID acc

168 mide (73) that exhibited high potency toward CDK2 (IC50 0.044 muM) but was approximately 2000-fold le

169 vealed that the phosphorylation of PTPN12 by CDK2 impaired recruitment of the serine/threonine-protei

170 o evaluated the expression of cyclin E and p-CDK2 in 1676 breast carcinoma patients by immunohistoche

171 hibited cyclin-dependent kinase (CDK) 5 over CDK2 in cancer cell lines.

172 Our findings reveal a role for CDK2 in differential modulation of HIV-1 gene expression

173 ether, our study reveals a novel function of CDK2 in EGF-induced cell transformation and the associat

174 s in mice has revealed an essential role for Cdk2 in meiosis, which renders Cdk2 knockout (KO) mice s

175 uss the latest understandings of the role of CDK2 in normal and cancer cells, review the core pharmac

176 Our data suggest an important role for CDK2 in regulating MLH1 focus numbers and that the activ

177 Phosphorylation of NBS1 serine 432 by CDK2 in S/G2 dissociates NBS1 from TRF2, promoting TRF2-

178 Furthermore, induced deletion of Cdk2 in spermatocytes results in increased expression of

179 Further, we identified a requirement for CDK2 in the compensatory increases in beta-cell mass tha

180 Although the role of CDK2 in tumorigenesis has been controversial, emerging e

181 However, the role of CDK2 in tumorigenesis is controversial.

182 inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putativ

183 the oncogene c-Myc and the neural ESC marker CDK2 in vitro, which was accompanied by altered expressi

184 report that poleta is also phosphorylated by CDK2, in the absence of damage, in a cell cycle-dependen

185 ll-cycle proteins in actively proliferating (CDK2-increasing) versus spontaneously quiescent (CDK2-lo

186 AS mutations sensitized lung cancer cells to CDK2 inhibition by deregulating CP110 expression.

187 gression, we hypothesized that PIN1 relieves CDK2 inhibition by suppressing the CDK inhibitory activi

188 We previously discovered that CDK2 inhibition causes lung cancer cells with more than

189 l, emerging evidence proposes that selective CDK2 inhibition may provide a therapeutic benefit agains

190 depletion of SKP2, CUL1, or CDK2 or chemical Cdk2 inhibition rescued the gamma-H2AX induction and abr

191 tic role in response of lung cancer cells to CDK2 inhibition, especially in the presence of activated

192 ging provided direct evidence that following CDK2 inhibition, lung cancer cells develop multipolar an

193 Thus, CP110 is a critical mediator of CDK2 inhibition-driven anaphase catastrophe.

194 KRAS mutations were especially sensitive to CDK2 inhibition.

195 t, sensitizing cells for apoptosis following CDK2 inhibition.

196 s, a direct link was found between CP110 and CDK2 inhibitor antineoplastic response.

197 Treatment with GSK2334470 or the CDK2 inhibitor dinaciclib was sufficient to reverse thes

198 upregulation of TGF-beta and nuclear p27, a CDK2 inhibitor, in samples from PTC.

199 te DNA replication despite the presence of a Cdk2 inhibitor.

200 ld be targeted using a clinically applicable CDK2 inhibitor.

201 P1 in cancer cells restores sensitivity to a Cdk2 inhibitor.

202 d was prevented by lower concentrations of a CDK2 inhibitor.

203 HCC cells to the cyclin-dependent kinase 2 (CDK2) inhibitor, roscovitine.

204 Development of CDK2 inhibitors has been extremely challenging as its AT

205 Several small-molecule CDK2 inhibitors have progressed to the clinical trials.

206 cation have been reported to be sensitive to CDK2 inhibitors).

207 utline strategies for the rational design of CDK2 inhibitors.

208 This indicates that CDK2 is a useful molecular target for the chemopreventio

209 ll as colon cancer cell lines indicated that CDK2 is dispensable for cell proliferation.

210 We also observed that CDK2 is downregulated in the glomeruli of obese Zucker r

211 Cyclin-dependent kinase 2 (CDK2) is a known regulator in the cell cycle control of

212 Cyclin-dependent kinase 2 (CDK2) is a potential therapeutic target for the treatmen

213 are reduced, and cyclin-dependent kinase 2 (CDK2) is activated upon SIRT1 reduction.

214 Cyclin-dependent kinase 2 (CDK2) is known to localize to so-called "late recombinat

215 Whereas cyclin-dependent kinase 2 (Cdk2) is not necessary for mouse viability or gametogene

216 umbers of LRN-associated proteins, including CDK2 itself and the MutL homolog 1 (MLH1) component of t

217 Expression of the cyclin-dependent kinase 2 (CDK2), itself a downstream target of PI3K/MAPK signaling

218 WEE1 suppresses CDK1 and CDK2 kinase activities to regulate the G1/S transition a

219 sults demonstrate that precise regulation of CDK2 kinase activity in male germ cell development is cr

220 However, the role of CDK2 kinase activity in the process of CO formation rema

221 in A- or cyclin E-CDK2, leading to increased CDK2 kinase activity.

222 ated replication protein CDC6 binds Cyclin E-CDK2 kinase and in a feedback loop removes RB from ORC1,

223 PP1 dephosphorylates key CDC7 and CDK2 kinase substrates to inhibit the assembly and activ

224 CDK2 knockdown also reduced expression of PDK1, an activ

225 CDK2 knockdown had minimum effects on RB phosphorylation

226 tial role for Cdk2 in meiosis, which renders Cdk2 knockout (KO) mice sterile.

227 cts virtually identical to those observed in Cdk2 KO mice including non-homologous chromosome pairing

228 p27's interaction with cyclin A- or cyclin E-CDK2, leading to increased CDK2 kinase activity.

229 ression mediated by elevated levels of CCNE1-CDK2 led to the loss of functional HSPCs in vivo.

230 -increasing) versus spontaneously quiescent (CDK2-low) cells, including Cyclin D1, the levels of whic

231 gulation of NRF1 transcriptional activity by CDK2 may allow the modulation of Ehmt1 expression, there

232 Mechanisms of CDK2-mediated anaphase catastrophe and how activated KRA

233 This interaction is abrogated by cyclin A-CDK2-mediated phosphorylation of BRCA2 at serine 3291 (S

234 Our data indicate that CDK2-mediated phosphorylation of NRF1 can occur at two d

235 ostasis, in part, via noncanonical cyclin D1-CDK2-mediated S-phase entry.

236 Low level activation of CDK2 mediates helicase activation, cell cycle progressio

237 reas tumors in Men1(+/-) mice and Men1(+/-); Cdk2(-/-) mice exhibited LOH.

238 In contrast, Men1(+/-); Cdk2(-/-) mice showed pituitary and islet tumorigenesis

239 Stable depletion of SKP2, CUL1, or CDK2 or chemical Cdk2 inhibition rescued the gamma-H2AX

240 Pharmacological inhibition of CDK2 or EZH2 allows re-expression of ERalpha and convert

241 Furthermore, the combination of either CDK2 or EZH2 inhibitor with tamoxifen effectively suppre

242 Knockdown of CDK2, or inhibiting its activity with roscovitine in pod

243 e aim of achieving selectivity of binding to CDK2 over CDK1.

244 fication induced by DNA damage or by PLK4 or CDK2 overexpression was markedly reduced in the absence

245 lin E correlated strongly with cytoplasmic p-CDK2 (P < 0.0001), high tumor grade, negative estrogen/p

246 In the absence of Cdk2, p27 phosphorylation at Thr-187 was mainly carried

247 with p28 was facilitated through the p53/p21/CDK2 pathway.

248 At the beginning of S-phase, Cdk2 phosphorylated c-Myc at Serine 62, promoting its as

249 ort that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2)

250 -loop harboring a cyclin-dependent kinase 2 (CDK2) phosphorylation site.

251 Here, we describe the phenotype of 2 Cdk2 point mutants with elevated or decreased activity,

252 Collectively, our data show that CDK2 protects podocytes from apoptosis and that reduced

253 ivator, phospho-cyclin-dependent kinase 2 (p-CDK2), regulate G1 to S phase transition and their dereg

254 -linked Ig class switching is in part due to CDK2-regulated AID nuclear access at the G1/S border.

255 This suggests that CDK2 regulates the activity of the cell survival pathway

256 catalytic partner cyclin-dependent kinase 2 (CDK2), regulates cell cycle progression as cells exit qu

257 identify the histone deacetylase Sirt1 as a Cdk2 regulator in OPC proliferation and response to HX.

258 -3 (an ortholog of human GSK3B) and cdk-2 (a CDK2-related kinase) as required for LIN-45 degron-media

259 owever, when CDK4/6 is activated relative to CDK2 remained incompletely understood.

260 However, the signaling pathway downstream of CDK2 remains to be characterized, and it is also unclear

261 er TGFbeta-induced pSMAD2 phosphorylation or CDK2 repression, but was required for upregulation of p2

262 not conformational) mutp53s can override the Cdk2 requirement to promote replication by facilitating

263 However, a CDK2-selective inhibitor is yet to be discovered.

264 We attempt to provide an outlook on how CDK2-selective inhibitors may open new avenues for cance

265 draciclib), a clinical inhibitor of CDK9 and CDK2, selectively targeted MYCN-amplified neuroblastoma

266 Thus, CDK2 serves as an important nexus linking primary beta-c

267 TGF-beta/SMAD-dependent p27 repression, and CDK2/SMAD3 phosphorylation, leading to p65 NFkappaB upre

268 X2, FGF9, and WNT2), and hypoxia adaptation (CDK2, SOCS2, NOXA1, and ENPEP) were identified.

269 We have determined crystal structures of the Cdk2-Spy1 and p27-Cdk2-Spy1 complexes that reveal how Sp

270 crystal structures of the Cdk2-Spy1 and p27-Cdk2-Spy1 complexes that reveal how Spy1 activates Cdk.

271 teins with greatest functional similarity to CDK2 substrates, particularly proteins involved in the o

272 quire CDK2 but appear to depend on different CDK2 substrates.

273 re, PDK1 knockdown reduced the expression of CDK2 suggesting a regulatory loop between CDK2 and PDK1.

274 The siRNA-mediated repression of the CDK2 target and centrosome protein CP110 induced anaphas

275 Interestingly, RingoA is required for Cdk2 targeting to telomeres and RingoA KO spermatocytes

276 in RingoA, an atypical activator of Cdk1 and Cdk2 that has no amino acid sequence homology to cyclins

277 ce for a physiological function of mammalian Cdk2 that is not dependent on cyclins.

278 find that Spy1 confers structural changes to Cdk2 that obviate the requirement of Cdk activation loop

279 function requires phosphorylation by Cdk1 or Cdk2 that primes FoxM1b for phosphorylation by Plk1, whi

280 n, p53 induces p21, leading to inhibition of CDK2, the main kinase substituting for CDK4/6 and a key

281 Cyclin A-Cdk2 then phosphorylates SIRT2 at Ser331.

282 sting MYBL2 as a putative biomarker for anti-CDK2-therapy.

283 factor E2F1 and cycling-dependent kinase 2 (CDK2), thereby reversing the malignant phenotype.

284 Because S384 is autophosphorylated by bound CDK2, this presents a paradox as to how cyclin E can eva

285 and p-Cdk2 (Thr160) expression, increased p-Cdk2 (Thr14), led to inactivation of Cyclin A/Cdk2 compl

286 1-48 significantly suppressed Cyclin A and p-Cdk2 (Thr160) expression, increased p-Cdk2 (Thr14), led

287 xpressed in cancer and can bypass control by Cdk2 to interact with treslin, leading to enhanced DNA r

288 CKS proteins greatly enhance the ability of Cdk2 to phosphorylate the key replication initiation pro

289 promote centriole duplication by recruiting CDK2 to the centrosome.

290 LPS-induced downregulation of CDK2 was prevented in vitro and in vivo by inhibiting th

291 Previously, Cdk2 was thought to be essential for the G1/S transition

292 titive inhibition at the ATP binding site of CDK2 were identified and typically exhibited 10-80-fold

293 D1 interacts with a cyclin-dependent kinase, CDK2, which also accumulates in crossover-specific recom

294 omes may be mediated directly by the loss of CDK2, which binds to and phosphorylates the transcriptio

295 ycle regulatory proteins cyclin A, CDK1, and CDK2, which mediates phosphorylation of SAMHD1 at threon

296 substrate recognition mechanism of PTPN12 by CDK2, which orchestrated signaling crosstalk between the

297 in this context was the activation status of CDK2, which was suppressed with CDK4/6 inhibition in an

298 ophase I, mice bearing a deregulated allele (Cdk2(Y15S) ) are severely deficient in spermatogonial di

299 ochemical and genetic data demonstrated that Cdk2(Y15S) is a gain-of-function allele causing elevated

300 Remarkably, Cdk2(Y15S/Y15S) mice possess abnormal clusters of mitoti