ライフサイエンスコーパス: CDK2

1 ification could be resensitized by targeting CDK2.

2 .3% systems on SEQ17, and 76.9% vs. 61.5% on CDK2.

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

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

5 y compensated its function in the absence of Cdk2.

6 S phase entry and progression by activating Cdk2.

7 itotic G1-like checkpoint in the presence of Cdk2.

8 eracted with cyclin A2, cyclin B1, CDK1, and CDK2.

9 ts with cyclin-dependent kinase 1 (Cdk1) and Cdk2.

10 ows over 80-fold selectivity for CDK9 versus CDK2.

11 he active state, as is the case for Cdk1 and Cdk2.

12 d be partially reversed by overexpression of CDK2.

13 inhibitors that distinguish between CDK1 and CDK2.

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

15 ls treated with insulin or overexpression of CDK2.

16 he expression of cell cycle proteins p21 and CDK2.

17 oint mutation of miR-29b binding site in the cdk2 3'-UTR prevents miR-29b-induced repression of CDK2

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

19 ning 17 pairs of apo-holo structures; and 2) CDK2 -a ligand diversity set composed of one CDK2 apo st

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

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

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

23 bited proliferation and subsequent decreased CDK2 activities, indicating an endogenous, non-ligand-de

24 Here, we introduce a live-cell sensor for CDK2 activity and unexpectedly found that proliferating

25 ms that drive these oscillations of Cyclin E-Cdk2 activity are not fully understood.

26 odel, we demonstrate that constitutive CCND1/CDK2 activity effectively confers anchorage independent

27 In normal cells, cyclin E/Cdk2 activity is associated with DNA replication-related

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

29 at targeted inhibition of constitutive CCND1/CDK2 activity may enhance the effectiveness of current t

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

31 e next cell cycle by immediately building up CDK2 activity or to enter a transient G0-like state by s

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

33 By contrast, Cdk2 activity promotes lysosomal degradation of HIF-1alp

34 In contrast, cyclin E/Cdk2 activity was required for maximal loading of Mcm2-7

35 of Mcm2-7 loaded in the absence of cyclin E/Cdk2 activity were strictly localized to ORC binding sit

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

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

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

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

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

41 ip1) or p27(Kip1) responsible for regulating CDK2 activity.

42 ter a transient G0-like state by suppressing CDK2 activity.

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

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

45 ition of G1-phase cyclin-dependent kinase 2 (CDK2) activity.

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

47 Only a Cdk2 allele mimicking SNP rs3087335, which alters an inh

48 We demonstrate that conditional deletion of Cdk2 alone in hepatocytes resulted in accelerated induct

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

50 phthisis, and DNA damage control by cyclin A/Cdk2 and ATR-Chk1, providing new ideas for targeted ther

51 Concomitant ablation of Cdk2 and CcnE1 in hepatocytes caused a defect in pre-RC

52 Thus, combined inactivation of Cdk2 and CcnE1 is the minimal requirement for blocking S

53 e-specific RNAi sensitivity mutations in the CDK2 and CDK1 genes resulted in a >85% site-specific rec

54 its associated cell cycle-promoting kinases, CDK2 and CDK4.

55 gh selectivity for CDKs, with preference for CDK2 and CDK5 over CDK9, CDK1, CDK4, and CDK6.

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

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

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

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

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

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

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

63 tivity, this did not occur with loss of both Cdk2 and cyclin A2.

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

65 d high selectivity over the off-target human CDK2 and good selectivity over human GSK3beta enzyme, ha

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

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

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

69 proaches are tested on crystal structures of CDK2 and other CMGC protein kinases and a simulation of

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

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

72 horylation of replication protein A (RPA) by Cdk2 and the checkpoint kinase ATR (ATM and Rad3 related

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

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

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

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

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

78 n SAMHD1, namely, cyclin-dependent kinase 2 (CDK2) and S-phase kinase-associated protein 2 (SKP2).

79 ted in ovarian cancer such as AURKA1, ERBB3, CDK2, and mTOR, as well as several novel candidates incl

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 CDK2 -a ligand diversity set composed of one CDK2 apo structure and 52 known bound inhibitors.

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 , before the G1/S transition) revealed a p21-CDK2 axis that determines quiescent and cycling cell sta

90 tion of CTD-host interactions indicated that CDK2 binding by CTD may mediate its inhibitory effect on

91 a model in which estrogen-activated cyclin E-CDK2 binds and phosphorylates ERalphaS341, to prime ERal

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

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

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

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

96 -terminal repressor domain, and we show that CDK2 can partner with cyclin E to phosphorylate Foxp3 at

97 In the absence of Cdk2, CcnE1 performs crucial kinase-independent function

98 mbined loss of CcnE1 and CcnE2, but also the Cdk2/CcnE1/CcnE2 triple KO in liver, significantly inhib

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

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

101 association with cyclin-dependent kinase 2 (CDK2), CDK4 and proliferating cell nuclear antigen.

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

103 BRAF(V600E) induced elevated expression of CDK2, CDK4, MITF and EST1/2 protein in hNCPCs, and also

104 Inhibition of CDK2/CDK4 activity disrupted Olig2-CDK2/CDK4 interaction

105 bition of CDK2/CDK4 activity disrupted Olig2-CDK2/CDK4 interactions and attenuated Olig2 protein stab

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

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

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

109 cal for human neurodevelopment that promotes CDK2 centrosomal localization and centriole duplication.

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

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

112 The LMW-E/CDK2 complex phosphorylated Hbo1 at T88 without affectin

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

114 ND1 leads to accumulation of activated CCND1/CDK2 complexes in breast cancer cells.

115 here the role of constitutively active CCND1/CDK2 complexes in human mammary epithelial cell (HMEC) t

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

117 1 is able to interact with the cyclin A-CDK1-CDK2 complexin monocytic THP-1 cells and primary monocyt

118 t kinase (CDK) 6 as an upstream regulator of CDK2 controlling SAMHD1 phosphorylation in primary T cel

119 Here we reported that CDK2 could phosphorylate RNF4 on T26 and T112 and enhanc

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

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

122 The expression levels of bMSTN-mut, P21 and CDK2 (cyclin dependent kinase 2) were examined with qPCR

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

124 rboxy terminus by cyclin-dependent kinase 2 (Cdk2)/cyclin A or mTORC2, under distinct physiological c

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

126 three previously unknown cellular proteins (CDK2, cyclin B1, and SKP2).

127 Cdk4 and Cdk2, cyclin-dependent kinases required for myocardial d

128 mparison between Pho85-Pcl10, phosphorylated CDK2-cyclin A, and CDK5-p25 complexes reveals the conver

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

130 ent features like those observed for the p27/Cdk2/cyclin A complex to directly suggest the ability of

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

132 relative to CDK, contrasting with the closed CDK2/cyclin A conformation.

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

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

135 to tyrosine phosphorylation and altered p21:Cdk2/cyclin A stoichiometry.

136 ers the regulatory interplay between p21 and Cdk2/cyclin A, as well as its responses to tyrosine phos

137 crystal structures bound to CDK9/cyclin T or CDK2/cyclin A, we conclude that selective inhibition of

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

139 e series that bind to both CDK9/cyclin T and CDK2/cyclin A.

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

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

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

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

144 Treslin is phosphorylated by CDK2/cyclin E in a cell cycle-dependent manner, and its

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

146 In genetic mosaics, CycE- and Cdk2-deficient GSCs are rapidly lost from the niche, rem

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

148 CDK2-dependent phosphorylation increased the efficacy an

149 from "elite controllers," potently inhibited CDK2-dependent phosphorylation of HIV-1 reverse transcri

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

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

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

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

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

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

156 ingle genetic ablation of either E-cyclin or Cdk2 does not affect overall liver regeneration.

157 l cycle, we explored a hypothesized role for Cdk2 dysregulation in this effect through conditional de

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

159 hibited, resulting in the changes of P21 and CDK2 expression levels which are related to the regulati

160 f P21 expression levels and up-regulation of CDK2 expression levels.

161 2V)-induced foci formation and knocking down CDK2 expression markedly decreases epidermal growth fact

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

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

164 LPS-treatment of mice also reduced CDK2 expression.

165 ctly regulate Cdk4 while only Tbx5 activates Cdk2 expression.

166 nases 1 and 2 phosphorylation, and increased CDK2 expression.

167 igated the contribution of CcnE1, CcnE2, and Cdk2 for liver regeneration after partial hepatectomy (P

168 H, whereas concomitant ablation of CcnE2 and Cdk2 had no effect.

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

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

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

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

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

174 ts show unequivocally that the roles of CycE/Cdk2 in GSC division cycle regulation and GSC maintenanc

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

176 Knock-down of CDK2 in proliferating control cells increased the CYP3A4

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

178 Because cyclin A2 acts in complex with Cdk2 in the cell cycle, we explored a hypothesized role

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

180 direct target of Gata4 and the regulation of Cdk2 in the developing heart has not been studied.

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

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

183 k1, which binds p21 with lower affinity than Cdk2, in abrogating the postmitotic checkpoint in E6-exp

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

185 At the late G1 Restriction Point, cyclin E:Cdk2 inactivates Rb by quantum hyper-phosphorylation.

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

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

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

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

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

196 Here, we show that the Drosophila Cyclin E-Cdk2 inhibitor Dacapo (Dap) is targeted for destruction

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 n contrast, CP110 overexpression antagonized CDK2 inhibitor-mediated anaphase catastrophe.

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

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

202 ationale to explore combinations of Cdk1 and Cdk2 inhibitors as a general approach in cancer therapy.

203 type from which we have designed more potent CDK2 inhibitors using, in the first instance, quantum me

204 uring mitosis are well described, studies of Cdk2 inhibitory phosphorylation during S phrase have lar

205 s reveal the specific and essential roles of Cdk2 inhibitory phosphorylation in the successful execut

206 To specifically study the functions of Cdk2 inhibitory phosphorylation, we used gene targeting

207 l)-purine derivative exhibited submicromolar CDK2-inhibitory activity by virtue of engineered additio

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 the pituitary and pancreatic islet, whereas CDK2 is dispensable for tumorigenesis in these neuroendo

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

212 transient but druggable allosteric pocket in CDK2 is predicted to occur under the CMGC insert.

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

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

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

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

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

218 A key S phase regulator is the Cyclin E-Cdk2 kinase, which must alternate between periods of hig

219 CDK2 knockdown also reduced expression of PDK1, an activ

220 CDK2 knockdown had minimum effects on RB phosphorylation

221 we used gene targeting to make an endogenous Cdk2 knockin allele in human cells, termed Cdk2AF, which

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

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

224 ty to inhibit the cyclin-dependent kinase 2 (Cdk2), leading to shortening of G1 and S phases.

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

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

227 d in subconfluent control cells, whereas the CDK2 levels increased.

228 s performed using 35 cocrystal structures of CDK2 liganded with distinct analogues of the parent comp

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

230 ctions with binding proteins such as LIMK-1, CDK2, Mash1, and Hes5 either by controlling their site o

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

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

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

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

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

236 nslation through direct interaction with the cdk2 mRNA via its 3'-untranslated region (3'-UTR), where

237 These results indicate that CDK2 negatively regulates the stability and activity of

238 ation by cyclin A-cyclin-dependent kinase 2 (CDK2) on a novel site, serine 595 (S595), directly regul

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

240 Knockdown of Skp2, CDK2, or cyclin E, three key elements within the network

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

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

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

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

245 ouble-negative feedback regulation involving CDK2, p21, and E3 ubiquitin ligases.

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

247 zygotic knockin cells resulted in the mutant Cdk2 phenotype cell cycle arrest, whereas allele specifi

248 est that, in addition to CDK1 and cyclin A2, CDK2 phosphorylates T592 of human SAMHD1 and thereby reg

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

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

251 crystal structures of 12u bound to CDK9 and CDK2 provide insights into the binding modes.

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

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

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

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

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

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

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

259 silico modeling of 6b in the active site of CDK2 revealed a high interaction energy, which we believ

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

261 roteins cyclin E, cyclin-dependent kinase 2 (CDK2), Skp2, and Cdt1.

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

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

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

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

266 yltransferase (HAT) Hbo1 as a novel cyclin E/CDK2 substrate.

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

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

269 n human cells, termed Cdk2AF, which prevents Cdk2 T14 and Y15 phosphorylation.

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

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

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

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

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

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

276 dduct of the phosphorylated, fully activated CDK2, the prototypic cell cycle CDK, complexed with cycl

277 Cyclin A-Cdk2 then phosphorylates SIRT2 at Ser331.

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

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

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

281 1-48 significantly suppressed Cyclin A and p-Cdk2 (Thr160) expression, increased p-Cdk2 (Thr14), led

282 al structures of these agents complexed with CDK2 to highlight differences in their binding sites and

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

284 promote centriole duplication by recruiting CDK2 to the centrosome.

285 miR-29b represses CDK2 translation through direct interaction with the cdk

286 '-UTR prevents miR-29b-induced repression of CDK2 translation.

287 bits intestinal mucosal growth by repressing CDK2 translation.

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

289 In turn, CDK2 was strongly linked to cell cycle progression and c

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

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

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

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

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

295 he PI3K/AKT pathway is necessary to activate CDK2, which phosphorylates ERalphaSer294, and mediates t

296 yet characterized for CDK members other than CDK2, which will be useful for the design of inhibitors

297 When coexpressed with LMW-E/CDK2, wild-type Hbo1 promoted enrichment of cancer stem-

298 whereas allele specific knockdown of mutant CDK2 with siSN resulted in a wild type phenotype.

299 RNAi knockdown of wild type (WT) Cdk2 with siWT in heterozygotic knockin cells resulted i

300 d by complexes of cyclin-dependent kinase 2 (Cdk2) with E-type cyclins (CcnE1 or CcnE2).