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1 edict progression of DN, downregulated CDK2 (cyclin-dependent kinase 2).
2 RK2 and the cell cycle control enzyme, Cdk2 (cyclin-dependent kinase 2).
3 (1) phase and thereby prevents activation of cyclin-dependent kinase 2.
4 entry of quiescent T cells is dependent upon cyclin-dependent kinase 2.
5 he G(1)/S transition through inactivation of cyclin-dependent kinase 2.
6  and decreased levels of cyclins A and D and cyclin-dependent kinase 2.
7 and p21(WAF1), and had decreased activity of cyclin-dependent kinase 2.
8 ression of cyclins A and E but a decrease in cyclin-dependent kinase 2.
9 1 reverse transcriptase, p38 MAP kinase, and cyclin-dependent kinase 2.
10 evels and binding of p21cip1 to cyclin A and cyclin-dependent kinase-2.
11 A and protein levels of cyclins (D1, E1) and cyclin-dependent kinases (2, 4, and 6).
12 ecting expression of cyclin D2, cyclin E, or cyclin-dependent kinases 2, 4 or 6.
13                                 Furthermore, cyclin-dependent kinases 2, 4, and 6 showed an opposite
14                             Cyclin D1/D3 and cyclin-dependent kinase 2/4 (cdc2/cdc4) were downregulat
15                                              Cyclin-dependent kinase 2 activated by cyclin E is invol
16 y in FADDdd T cells, cyclin E expression and cyclin-dependent kinase 2 activation were markedly impai
17 ataset of 17 550 compounds and corresponding cyclin-dependent kinase-2 activities showed that informa
18 ly significant as evidenced by inhibition of cyclin-dependent kinase 2 activity and decreased cell pr
19    UCN-01 prevented the increase of cyclin A/cyclin-dependent kinase 2 activity induced by CPT and en
20 tor p27(kip1) was decreased in TR cells, and cyclin-dependent kinase 2 activity was increased.
21 ger-term progression through the cell cycle (cyclin-dependent kinase 2 activity).
22 tive PLK4 following deregulation of cyclin E/cyclin-dependent kinase 2 activity, as is frequently obs
23 sion prevented the PTEN-induced reduction of cyclin-dependent kinase 2 activity, indicating that p27K
24 ence of PTTG were associated with suppressed cyclin-dependent kinase 2 activity, Rb phosphorylation,
25  imposed by p27(kip1)-mediated inhibition of cyclin-dependent kinase 2 activity.
26 reased p27, reduced cyclin A1 and attenuated cyclin-dependent kinase 2 activity.
27 n of cyclin A-associated kinase activity and cyclin-dependent kinase 2 activity.
28 endent kinase-I p21(Waf-1) and inhibition of cyclin-dependent kinase 2 activity.
29 into DNA was significantly inhibited, as was cyclin-dependent kinase 2 activity.
30 egulation, leading to inhibition of cyclin E/cyclin-dependent kinase 2 activity.
31 , CPT increased cyclin A levels and cyclin A/cyclin-dependent kinase 2 activity.
32 ated with lack of p21 induction and enhanced cyclin-dependent kinase 2 activity.
33 n-dependent kinase inhibitor p21 and reduced cyclin-dependent kinase 2 activity.
34 oma tumor suppressor pRb and is dependent on cyclin-dependent kinase 2 activity.
35  to the G1 restriction point, which inhibits cyclin-dependent kinase-2 activity and phosphorylation o
36 er members of the growth regulatory complex, cyclin dependent kinase 2 and cyclin A, but not prolifer
37 clear receptors and transcription factors to cyclin-dependent kinase 2 and Bcl2 family members.
38 50 and 55 and phosphorylation of vimentin by cyclin-dependent kinase 2 and cAMP-dependent protein kin
39 hich subsequently enhanced the expression of cyclin-dependent kinase 2 and cyclin E.
40 howed that silibinin decreases the levels of cyclin-dependent kinase 2 and cyclin-dependent kinase 4
41 reas ultraviolet-B exposure had no effect on cyclin-dependent kinase 2 and cyclin-dependent kinase 6
42                                              Cyclin-dependent kinase 2 and other kinases associated w
43 n was dependent on dissociation of p130 from cyclin-dependent kinase 2 and p130 dephosphorylation.
44  increases the levels and phosphorylation of cyclin-dependent kinase 2 and the retinoblastoma protein
45 ation was not associated with suppression of cyclin-dependent kinases 2 and 4 activity but rather wit
46  phosphorylation is driven by the actions of cyclin-dependent kinases 2 and 4/6 at G1/S cell-cycle ch
47                    The protein expression of cyclin-dependent kinases 2 and 6 and Cdc2 was also decre
48 ting cell nuclear antigen (PCNA), Ki-67, and cyclin-dependent kinases-2 and -4.
49 tains Skp2 itself, p27(kip1) (p27), cyclin E-cyclin dependent kinase 2, and the retinoblastoma protei
50 clear p27kip1 is an established inhibitor of cyclin-dependent kinase-2, and it now appears that cytop
51  p53-activating peptide (DV3-TATp53C') and a cyclin-dependent kinase 2 antagonist peptide (DV3-TAT-Rx
52 ter at maternal centrioles requires cyclin E/cyclin-dependent kinase 2 as well as Polo-like kinase 4
53 Kinases known to phosphorylate BRCA1 include cyclin-dependent kinase 2, as well as ataxia telangiecta
54 y still increases the amount of cyclin A and cyclin-dependent kinase 2-associated kinase activity in
55 f p21 and p27 with a concomitant decrease in cyclin-dependent kinase 2-associated kinase activity.
56                                 We show that cyclin-dependent kinase 2-associated protein 1 (CDK2AP1)
57                                              Cyclin-dependent Kinase 2-associated Protein 1 (CDK2AP1)
58                                     CDK2AP1 (cyclin-dependent kinase 2-associated protein 1), corresp
59 l experimental data indicating that Cdk2ap1 (cyclin-dependent kinase 2-associating protein 1), an inh
60                                Inhibition of cyclin-dependent kinase 2 by p27(Kip1) is believed to be
61 f Cdc25A, and decreased activity of cyclin E-cyclin-dependent kinase 2; by 4 h, a continued delay at
62                               An increase in cyclin-dependent kinase 2 (cdk-2) protein expression occ
63 SK-3beta and an enhanced selectivity against cyclin-dependent kinase 2 (CDK-2).
64 crease in the p27(Kip1) level, inhibition of cyclin-dependent kinase-2 (CDK-2) activity, dephosphoryl
65 ted retinoblastoma protein by inhibiting the cyclin-dependent kinase-2 (CDK-2) activity.
66   IFN alpha treatment of DU145 cells reduced cyclin dependent kinase 2 (cdk2) activity.
67 se of very large sets of X-ray structures of cyclin dependent kinase 2 (CDK2) and heat shock protein
68 on of fragment-based screening techniques to cyclin dependent kinase 2 (CDK2) identified multiple (>3
69                                          The cyclin dependent kinase 2 (Cdk2) is required for initiat
70                                              Cyclin dependent kinase 2 (CDK2) is the major kinase tha
71 res of trisubstituted purines complexed with cyclin dependent kinase 2 (cdk2), a protein important in
72                                        Since cyclin dependent kinase 2 (CDK2)/cyclin E triggers DNA s
73 sphates from threonine-14 and tyrosine-15 of cyclin dependent kinase-2 (cdk2) in vitro, and it is the
74 ted cells were characterized by a decline in cyclin-dependent kinase 2 (CDK2) activities, loss of hyp
75                  1,25-VD treatment inhibited cyclin-dependent kinase 2 (cdk2) activity and induced G0
76 ed S-phase entry is accompanied by increased cyclin-dependent kinase 2 (CDK2) activity as well as dec
77 revious studies concluded that FB1 repressed cyclin-dependent kinase 2 (CDK2) activity but induced CD
78  G1 arrest brought about by an inhibition of cyclin-dependent kinase 2 (Cdk2) activity by p27(kip1).
79  we use single-cell time-lapse microscopy of Cyclin-Dependent Kinase 2 (CDK2) activity followed by en
80 sent study, we report that downregulation of cyclin-dependent kinase 2 (cdk2) activity in serum-depri
81 imulated HUVEC caused a decrease in cyclin E-cyclin-dependent kinase 2 (cdk2) activity with resulting
82  expression of p27Kip1, inhibition of cyclin/cyclin-dependent kinase 2 (cdk2) activity, accumulation
83                                     Cyclin A-cyclin-dependent kinase 2 (CDK2) activity, but not cycli
84  is partially required for the inhibition of cyclin-dependent kinase 2 (Cdk2) activity, cyclin A expr
85 nase inhibitor p27Kip1 levels, inhibition of cyclin-dependent kinase 2 (Cdk2) activity, hypophosphory
86 est was attributed to inhibition of G1-phase cyclin-dependent kinase 2 (CDK2) activity.
87 d levels of cyclin E protein and deregulated cyclin-dependent kinase 2 (CDK2) activity.
88 fect on the G(1)-S transition and stimulated cyclin-dependent kinase 2 (Cdk2) activity.
89 vent model to study the interactions between cyclin-dependent kinase 2 (CDK2) and analogues of the cl
90 xpression of cell cycle genes that stimulate cyclin-dependent kinase 2 (Cdk2) and Cdk1 activity.
91  cycle arrest is attributed to inhibition of cyclin-dependent kinase 2 (CDK2) and concomitant dephosp
92  E1 (CcnE1) is the regulatory subunit of the cyclin-dependent kinase 2 (Cdk2) and controls cell cycle
93 structural conservation in interactions with cyclin-dependent kinase 2 (Cdk2) and cyclin A.
94 l activation due to impaired accumulation of cyclin-dependent kinase 2 (Cdk2) and cyclin E.
95                                Activation of cyclin-dependent kinase 2 (cdk2) and cyclin-dependent ki
96 trosome duplication requires the activity of cyclin-dependent kinase 2 (Cdk2) and cyclins E and A [7-
97 hase of cell cycle, elevation of Cylin E and Cyclin-dependent kinase 2 (CDK2) and downregulation of p
98 saccharomyces pombe and are similar to human cyclin-dependent kinase 2 (CDK2) and extracellular signa
99 nteracting proteins controls the activity of cyclin-dependent kinase 2 (Cdk2) and governs the entry o
100 on of p21(Waf1/Cip1); p21, in turn, binds to cyclin-dependent kinase 2 (cdk2) and inhibits its functi
101                        This aptamer binds to cyclin-dependent kinase 2 (Cdk2) and inhibits its kinase
102 tion of EGFR and Neu signaling, reduction of cyclin-dependent kinase 2 (Cdk2) and mitogen-activated p
103 teins interacting with human SAMHD1, namely, cyclin-dependent kinase 2 (CDK2) and S-phase kinase-asso
104 Here we report that changes in the levels of cyclin-dependent kinase 2 (CDK2) and the cell cycle inhi
105      Cyclic strain increased the activity of cyclin-dependent kinase 2 (cdk2) and the cellular level
106 could disrupt the interaction between cyclin/cyclin-dependent kinase 2 (cdk2) and the E2F repressor c
107 o]-6,7-dimethoxyquinazoline) in complex with cyclin-dependent kinase 2 (CDK2) and the other (4-[3-met
108 53, was cloned by expression cloning through cyclin-dependent kinase 2 (CDK2) association.
109 rsion of p21 was capable of interacting with cyclin-dependent kinase 2 (Cdk2) but failed to inhibit i
110 e phosphorylation of pRb, activates cyclin E-cyclin-dependent kinase 2 (cdk2) by titrating Cip/Kip cd
111                                 The cyclin E-cyclin-dependent kinase 2 (CDK2) complex accelerates ent
112  domain bound to the phosphorylated cyclin A-cyclin-dependent kinase 2 (Cdk2) complex has been determ
113 is likely that it downregulates the cyclin A-cyclin-dependent kinase 2 (CDK2) complex, which is requi
114  on binding with the phosphorylated cyclin A-cyclin-dependent kinase 2 (Cdk2) complex.
115 c-Myc may stimulate the activity of cyclin E/cyclin-dependent kinase 2 (Cdk2) complexes and antagoniz
116                                    Cyclin D1/cyclin-dependent kinase 2 (Cdk2) complexes are present a
117 sically associates with E- and A-type cyclin/cyclin-dependent kinase 2 (Cdk2) complexes through a cyc
118                   Expression of cyclin E and cyclin-dependent kinase 2 (cdk2) correlated with the pro
119          The arrested cells contain inactive cyclin-dependent kinase 2 (cdk2) despite the presence of
120 llagen promoter, whereas a dominant-negative cyclin-dependent kinase 2 (cdk2) enhanced repression by
121 pression is correlated with higher levels of cyclin-dependent kinase 2 (Cdk2) enzymatic activity in v
122 els in the small intestinal mucosa increases cyclin-dependent kinase 2 (CDK2) expression and stimulat
123 as evidenced by increased histone 3 mRNA and cyclin-dependent kinase 2 (cdk2) expression, and this is
124     Here we show that the G1/S phase-related cyclin-dependent kinase 2 (CDK2) gene is a novel prolife
125                                              Cyclin-dependent kinase 2 (CDK2) has been proposed to fu
126 the cell cycle control proteins cyclin E and cyclin-dependent kinase 2 (CDK2) in carotids of apolipop
127 -dependent colocalization of MEQ protein and cyclin-dependent kinase 2 (CDK2) in coiled bodies and th
128 e late G1/S cell-cycle proteins cyclin E and cyclin-dependent kinase 2 (cdk2) in human islets.
129 has been implicated as a target for cyclin E/cyclin-dependent kinase 2 (CDK2) in modulating centrosom
130              We investigated the function of cyclin-dependent kinase 2 (Cdk2) in neural progenitor ce
131 hibition of NF90 sensitized HCC cells to the cyclin-dependent kinase 2 (CDK2) inhibitor, roscovitine.
132                                              Cyclin-dependent kinase 2 (CDK2) is a known regulator in
133                                              Cyclin-dependent kinase 2 (cdk2) is a small serine/threo
134 eracetylated, levels of p27 are reduced, and cyclin-dependent kinase 2 (CDK2) is activated upon SIRT1
135                                              Cyclin-dependent kinase 2 (Cdk2) is essential for initia
136                              The activity of cyclin-dependent kinase 2 (CDK2) is essential for progre
137                              The function of cyclin-dependent kinase 2 (CDK2) is often abolished afte
138                                              Cyclin-dependent kinase 2 (Cdk2) is required for multipl
139 horylation of p27 on threonine 187 (T187) by cyclin-dependent kinase 2 (Cdk2) is thought to initiate
140 lizes NPAT/p220, a substrate of the cyclin E/cyclin-dependent kinase 2 (CDK2) kinase complex, as a ke
141                                              Cyclin-dependent kinase 2 (Cdk2) mediates this suppressi
142 nd show that its phosphorylation by cyclin A-cyclin-dependent kinase 2 (CDK2) on a novel site, serine
143  the human NPM's phosphorylation by cyclin E-cyclin-dependent kinase 2 (cdk2) on threonine (Thr) 199
144 ading does not result from downregulation of cyclin-dependent kinase 2 (Cdk2) or Cdc7 activity and is
145               Cyclin E-associated kinase and cyclin-dependent kinase 2 (cdk2) phosphorylation are inh
146             Human UHRF1 contains a conserved cyclin-dependent kinase 2 (CDK2) phosphorylation site at
147 ed a specific PTPN12-insert-loop harboring a cyclin-dependent kinase 2 (CDK2) phosphorylation site.
148                                              Cyclin-dependent kinase 2 (cdk2) plays a critical role i
149 by modulating the activities of cyclin E and cyclin-dependent kinase 2 (cdk2) proteins and their comp
150            Kinetic analysis establishes that Cyclin-dependent kinase 2 (CDK2) requires simultaneous b
151 -P; gene symbol HINFP) bound to its cyclin E/cyclin-dependent kinase 2 (CDK2) responsive coactivator
152 his was achieved for compounds targeting the cyclin-dependent kinase 2 (CDK2) substrate recruitment s
153                                        Since cyclin-dependent kinase 2 (CDK2) triggers initiation of
154 essed by plasmids encoding human cyclins and cyclin-dependent kinase 2 (CDK2) were used as antigens i
155 med hepatocytes is regulated by complexes of cyclin-dependent kinase 2 (Cdk2) with E-type cyclins (Cc
156 ght to determine if reducing the activity of cyclin-dependent kinase 2 (CDK2) with the purine analogu
157                                              Cyclin-dependent kinase 2 (CDK2), a known modulator of t
158        To support drug discovery efforts for cyclin-dependent kinase 2 (CDK2), a moderate-throughput
159                                Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator o
160 ect on pol-alpha:primase or by its effect on cyclin-dependent kinase 2 (CDK2), a recently identified
161 The two E-cyclins share a catalytic partner, cyclin-dependent kinase 2 (CDK2), and activate their ass
162 decreased expression of cyclin D1, cyclin E, cyclin-dependent kinase 2 (cdk2), and cdk4.
163 where they bind the cyclin E kinase partner, cyclin-dependent kinase 2 (Cdk2), and have associated ki
164  showed that CycE and its canonical partner, Cyclin-dependent kinase 2 (Cdk2), are required not only
165 ncreased p21 expression and association with cyclin-dependent kinase 2 (CDK2), CDK4 and proliferating
166 anied by acquisition of new partners such as cyclin-dependent kinase 2 (cdk2), cdk4, and cdk6 in infe
167 companied by cell cycle arrest, with reduced cyclin-dependent kinase 2 (Cdk2), Cdk4, Aurora kinase A,
168 Here, we show that the cell cycle regulator, cyclin-dependent kinase 2 (CDK2), couples primary beta-c
169  In vitro, LSF is phosphorylated by cyclin E/cyclin-dependent kinase 2 (CDK2), cyclin C/CDK2, and cyc
170            Cyclin E, a regulatory subunit of cyclin-dependent kinase 2 (Cdk2), is an important regula
171                    Cyclin E, an activator of cyclin-dependent kinase 2 (Cdk2), is targeted for protea
172                            Expression of the cyclin-dependent kinase 2 (CDK2), itself a downstream ta
173 7Xic1 and reduces its ability to inhibit the cyclin-dependent kinase 2 (Cdk2), leading to shortening
174 y eight inhibitors of three protein kinases, cyclin-dependent kinase 2 (CDK2), lymphocyte-specific ki
175 E, in conjunction with its catalytic partner cyclin-dependent kinase 2 (CDK2), regulates cell cycle p
176 tion of the pro-oncogenic proteins cyclin E, cyclin-dependent kinase 2 (CDK2), Skp2, and Cdt1.
177  to both DNA polymerase alpha/primase and to cyclin-dependent kinase 2 (CDK2), thereby inhibiting the
178                  Importantly, restoration of cyclin-dependent kinase 2 (CDK2)-cyclin A and thus PCNA
179 matography indicated that LRP interacts with cyclin-dependent kinase 2 (cdk2)-cyclin complexes or cdc
180                                Activation of cyclin-dependent kinase 2 (CDK2)-cyclin E in the late G(
181                       The kinase activity of cyclin-dependent kinase 2 (CDK2)-cyclin E is required fo
182  by the late G1 phase-specific activation of cyclin-dependent kinase 2 (CDK2)-cyclin E, which trigger
183 d degradation, a process directed in part by cyclin-dependent kinase 2 (CDK2)-mediated phosphorylatio
184 and this correlates with changes in cyclin E-cyclin-dependent kinase 2 (CDK2)-specific activity, cycl
185 t in S-phase that involved the inhibition of cyclin-dependent kinase 2 (Cdk2).
186 azolylthio acetic ester 1 as an inhibitor of cyclin-dependent kinase 2 (CDK2).
187 DNA synthesis, we investigated its effect on cyclin-dependent kinase 2 (CDK2).
188 indol-2-ones, were shown to potently inhibit cyclin-dependent kinase 2 (CDK2).
189 h, and activating its catalytic partner, the cyclin-dependent kinase 2 (Cdk2).
190 osine triphosphate-binding site of the human cyclin-dependent kinase 2 (CDK2).
191 re co-expressed with their catalytic partner cyclin-dependent kinase 2 (Cdk2).
192 on of p27Kip1 (p27), a negative regulator of cyclin-dependent kinase 2 (Cdk2).
193 f phosphorylation sites on recombinant human cyclin-dependent kinase 2 (CDK2).
194  T479 at the Akt extreme carboxy terminus by cyclin-dependent kinase 2 (Cdk2)/cyclin A or mTORC2, und
195  an alpha-helical structure, upon binding to cyclin-dependent kinase 2 (Cdk2)/cyclin A.
196  and the LR protein (LRP) is associated with cyclin-dependent kinase 2 (Cdk2)/cyclin complexes during
197         First, tetrandrine inhibits purified cyclin-dependent kinase 2 (CDK2)/cyclin E and CDK4 witho
198          Upon phosphorylation on Thr(199) by cyclin-dependent kinase 2 (CDK2)/cyclin E, the majority
199 of p21WAF1/CIP1 in complexes of p21WAF1/CIP1/cyclin-dependent kinase 2 (cdk2)/cyclin showed that the
200     p27 functions in the nucleus to suppress cyclin-dependent kinase-2 (Cdk2) activity and has been r
201 in TCDD-treated mice correlated with reduced cyclin-dependent kinase-2 (CDK2) activity, a pivotal reg
202 profoundly inhibited cyclin E expression and cyclin-dependent kinase-2 (CDK2) activity, but not D-typ
203 n between OP proliferation rate and cyclin E/cyclin-dependent kinase-2 (cdk2) activity.
204 ssion and attenuated pRb phosphorylation and cyclin-dependent kinase-2 (CDK2) activity.
205 e show that activation of the human E2F1 and cyclin-dependent kinase-2 (CDK2) promoters requires elem
206           Here we describe regulation of the cyclin-dependent kinase-2 (CDK2) protein, an enzyme that
207 -ylamines as moderately potent inhibitors of cyclin-dependent kinase-2 (CDK2), a CDK inhibitor analog
208 p-1 binding and decrease p27kip-1 binding to cyclin-dependent kinase-2 (cdk2), an enzyme required for
209 ic, cicaprost, selectively inhibits cyclin E-cyclin-dependent kinase-2 (Cdk2), and now we show that i
210 esponds to the increased binding of p21 with cyclin-dependent kinase-2 (Cdk2), and the decreased Cdk2
211 le inhibitors-p16, p21, or dominant-negative cyclin-dependent kinase-2 (Cdk2).
212 rrest, caused primarily by the inhibition of cyclin-dependent-kinase 2 (cdk2), is a critical step in
213 ramatic up-regulation of cyclin A-associated cyclin-dependent kinase 2(cdk2) activity.
214 The 2.6 Angstrom crystal structure for human cyclin-dependent kinase 2(CDK2) in complex with CksHs1,
215 1- and p27-mediated inactivation of cyclin E-cyclin-dependent kinase 2 complex kinase activity.
216 S phase block cannot fully saturate cyclin A-cyclin-dependent kinase 2 complexes and does not interac
217                                     Cyclin E/cyclin-dependent kinase 2 complexes are essential during
218 ivate the cyclin A promoter, induce cyclin A-cyclin-dependent kinase 2 complexes, and promote cycling
219 its S phase entry by binding to cyclin-cdk2 (cyclin-dependent kinase-2) complexes.
220     Specifically, binding of Cks1 or Cks2 to cyclin-dependent kinase 2 confers partial resistance to
221 en (OHT) leads to the activation of Cyclin E/Cyclin-dependent kinase 2 (CycE/Cdk2) complexes followed
222 2 and DACAPO (DAP), an inhibitor of Cyclin E/cyclin-dependent kinase 2 (CycE/cdk2).
223 OH-terminal region of p300 binds to cyclin E-cyclin-dependent kinase 2 (cyclin E-Cdk2) and TFIIB, as
224 on were blocked by selective inactivation of cyclin-dependent kinase 2-cyclin E (Cdk2-E) and were res
225 ll plates, to measure direct binding between cyclin-dependent kinase 2/cyclin E complex (CDK2/E) and
226  with Src family kinases and an inhibitor of cyclin dependent kinase 2, demonstrating that high-throu
227 kinase inhibitor, expression of cyclin A and cyclin-dependent kinase 2, DNA replication, MCE, and, su
228 hthalmia-associated transcription factor and cyclin dependent kinase 2 expression.
229 p2 targets beta-TrCP for degradation via the cyclin-dependent kinase 2-facilitated recognition of the
230 sphatidylinositol 3-kinase, calcineurin, and cyclin-dependent kinase 2 has facilitated the elucidatio
231 ndicating that p27Kip1 functions upstream of cyclin-dependent kinase 2 in the PTEN regulatory cascade
232                              Addition of the cyclin-dependent kinase 2 inhibitor p21(cip1) specifical
233                                              Cyclin-dependent kinase 2 is a serine/threonine protein
234                              The activity of cyclin-dependent kinase 2 is required for G(1)-S-phase p
235 ncreased expression of p21 and inhibition of cyclin-dependent kinase 2 kinase activity by FP was also
236 e G1/S transition, and the activity of cdk2 (cyclin-dependent kinase 2) kinase is impaired by the con
237 r selectivity were investigated by producing cyclin-dependent kinase 2 mutants bearing equivalent cyc
238 orylation of Rb and the activity of cyclin E-cyclin-dependent kinase 2 on IL-2 signaling.
239       Cyclin E and its co-activator, phospho-cyclin-dependent kinase 2 (p-CDK2), regulate G1 to S pha
240 icity of protein tyrosine phosphatase N12 by cyclin-dependent kinase 2 phosphorylation orchestrating
241 ened cyclin-dependent kinase inhibitor (CKI)-cyclin-dependent kinase 2 positive-feedback loop, normal
242 ression of transforming growth factor beta1, cyclin-dependent kinase 2, protein kinase C betaII and e
243            Kinase activities of cyclin E and cyclin-dependent kinase 2 responsible for the G(1)-S tra
244                                   Use of the cyclin-dependent kinase 2-selective 6-cyclohexylmethoxy-
245 ation inhibits the phosphorylation of pRB at cyclin-dependent kinase 2-specific, but not cyclin-depen
246 pus laevis Tipin as a substrate for cyclin E/cyclin-dependent kinases 2 that is phosphorylated in int
247 decreased steady-state levels and binding of cyclin-dependent kinase-2 to cyclin A and increased stea
248 ad, and annexin I were induced; cyclin E and cyclin-dependent kinase 2 were repressed; and bcl-2 and
249 g Cip1 and Kip1 genes encoding inhibitors of cyclin-dependent kinase-2 were used to further explore t
250 xpression levels of bMSTN-mut, P21 and CDK2 (cyclin dependent kinase 2) were examined with qPCR and W
251 crucial role in the cell cycle by activating cyclin-dependent kinase 2, which phosphorylates Rb, lead
252 y dephosphorylation of pRb and inhibition of cyclin-dependent kinase 2, which results in part from in
253 on, only the generic CCRK phosphorylates the cyclin-dependent kinase 2, which was accompanied by a do

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