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   1  fingerprint analysis identified it as cdc2 (cyclin-dependent kinase 1).                             
     2 mulation of Tyr-15-phosphorylated (inactive) cyclin-dependent kinase 1.                              
     3 ed to uninfected cells, have lower levels of cyclin-dependent kinase 1.                              
     4 he drug Roscovitine, a specific inhibitor of cyclin-dependent kinases 1, 2, 5, 7, and 9, we have show
  
     6 bers, seven are pro-proliferation molecules: cyclin-dependent kinase-1, -2, -4, and -6 and cyclins A,
     7 tein kinase kinase, ribosomal S6 kinase, and cyclin-dependent kinase 1/2 in combination with Bcl-XL i
     8  phosphorylation and inhibition of cdc25B, a cyclin dependent kinase 1-activating phosphatase, and is
     9 tus begins before M phase, is independent of cyclin-dependent kinase 1 activation, and requires MEK s
  
    11 cle arrest in association with inhibition of cyclin-dependent kinase 1 activity and hyperphosphorylat
    12 were competent for actin cable assembly, and cyclin-dependent kinase 1 activity was indispensible.   
  
  
  
    16 G(2)/M transition due to the decreased CDK1 (cyclin-dependent kinase 1) activity and upregulated p21,
    17 hase; reduced levels of cyclin B1, cyclin A, cyclin dependent kinases 1 and 2; and increased p21(Cip1
    18 uration promoting factor (MPF), a complex of cyclin-dependent kinase 1 and cyclin B, drives oocyte ma
    19 s G(2) arrest and represses the synthesis of cyclin-dependent kinase 1 and cyclin B1, two proteins re
  
    21  cycle regulators and proliferation markers (cyclin-dependent kinase 1 and proliferating cell nuclear
  
    23 d in all tissues by combined treatment where cyclin-dependent kinase 1 and proliferating cell nuclear
    24  of retinoblastoma protein and activation of cyclin-dependent kinases 1 and 2 and promoted cell cycle
  
    26 activity of several kinases, including CDK1 (cyclin-dependent kinase 1) and protein kinase C (PKC), h
    27 and repression of G2/M regulators cyclin B1, cyclin-dependent kinase 1, and cyclin A indicated a G2/e
    28 o on serine 368 by the cell-cycle regulator, cyclin-dependent kinase 1, and dephosphorylated by the p
    29 c regulatory proteins reveals that cyclin B, cyclin-dependent kinase 1, and the Ancdc14 phosphatase f
    30 n a pool of inactive "pre-MPF" consisting of cyclin-dependent kinase 1 bound to B-type cyclins, of wh
  
    32 on of human CaP cells via an inactivation of cyclin-dependent kinase 1 (Cdc2)/cyclin B 1-mediated mit
    33 ed with increased Tyr(15) phosphorylation of cyclin-dependent kinase 1 (Cdk 1) and inhibition of Cdk 
  
    35 inds to a phosphoepitope generated by either cyclin dependent kinase 1 (Cdk1) (non-self-priming) or P
    36 mportant in cell proliferation and survival: cyclin dependent kinase 1 (CDK1), inhibitor of growth 4 
    37 yclin A2, cyclin E, cyclin B1, cyclin F, and cyclin dependent kinase-1 (Cdk1) genes and diminished pr
  
  
    40  under physiological conditions, we show how cyclin-dependent kinase 1 (CDK1) activates the APC/C thr
  
    42 it, which is regulated by degradation of the cyclin-dependent kinase 1 (Cdk1) activator, cyclin B.   
  
    44 725) demonstrate that the down-regulation of cyclin-dependent kinase 1 (Cdk1) activity triggers the o
    45 effect of ATR ablation is not due to altered cyclin-dependent kinase 1 (CDK1) activity, DNA damage re
  
  
  
  
    50 n of human SAMHD1 at threonine 592 (T592) by cyclin-dependent kinase 1 (CDK1) and cyclin A2 impairs i
    51 iven by the activities of two major kinases, cyclin-dependent kinase 1 (Cdk1) and mitogen-activated p
    52 rodimer undergoes mitotic phosphorylation by cyclin-dependent kinase 1 (Cdk1) at a single site, p27 T
  
    54 ba is phosphorylated in vitro and in vivo by cyclin-dependent kinase 1 (CDK1) at Ser(119) and Ser(175
  
  
    57 sister chromatid disjunction and inactivates cyclin-dependent kinase 1 (Cdk1) causing mitotic exit.  
    58  Mitotic entry is controlled by the cyclin B-cyclin-dependent kinase 1 (Cdk1) complex, and the inhibi
  
    60 e show that the mitotic kinases Aurora B and Cyclin-dependent kinase 1 (Cdk1) destabilize interaction
    61 l4 is phosphorylated in vitro and in vivo by cyclin-dependent kinase 1 (CDK1) during antimitotic drug
  
  
    64 t study sheds light on two distinct roles of cyclin-dependent kinase 1 (CDK1) in promoting polarized 
  
    66 nd the hydrophobic side chain, are selective cyclin-dependent kinase 1 (CDK1) inhibitors with an IC(5
  
    68 tase promotes entry into mitosis by removing cyclin-dependent kinase 1 (Cdk1) inhibitory phosphorylat
  
  
  
  
  
  
  
    76 promote checkpoint recovery independently of cyclin-dependent kinase 1 (Cdk1) or Plx1 (Xenopus polo-l
  
  
  
    80  failure to remove inhibitory phosphate from cyclin-dependent kinase 1 (Cdk1) prevents entry into mit
  
  
  
  
    85 osphorylated at T341 most likely by Cyclin B/Cyclin-dependent kinase 1 (Cdk1), and then dephosphoryla
  
    87 (Rosco) is a purine derivative that inhibits cyclin-dependent kinase 1 (cdk1), cdk2, cdk5, cdk7, and 
    88 s involved in mitotic progression, including cyclin-dependent kinase 1 (Cdk1), cyclin B2, and their t
  
    90  The Wee1 kinase phosphorylates and inhibits cyclin-dependent kinase 1 (Cdk1), thereby delaying entry
  
  
  
  
    95 s inhibited during prophase and metaphase by cyclin-dependent kinase 1 (CDK1)-mediated phosphorylatio
    96 -box domain (PBD) of Plk1 and is enhanced by cyclin-dependent kinase 1 (Cdk1)-mediated phosphorylatio
  
  
  
  
  
  
  
  
  
  
   107 CDC25C activity and, consequentially, higher cyclin-dependent kinase 1 (CDK1)/cyclin B activity, and 
   108   In this report, evidence is presented that cyclin-dependent kinase 1 (CDK1)/cyclin B catalyzes mito
   109 orylated at Ser 29 (S29) specifically by the cyclin-dependent kinase 1 (cdk1)/cyclinB complex, primar
   110 osphorylation of hundreds of proteins by the cyclin-dependent kinase 1 (Cdk1):cyclin B (CycB) complex
   111  that Ser1232 in eIF4G1 is phosphorylated by cyclin-dependent kinase 1 (Cdk1):cyclin B during mitosis
  
  
   114 Resumption of meiosis requires activation of cyclin-dependent kinase-1 (CDK1, p34cdc2), one component
   115  Rad53, was required to both maintain active cyclin-dependent kinase 1, Cdk1(Cdc28), and prevent anap
   116  urchin zygotes arrested in S phase, whether cyclin-dependent kinase 1-cyclin B (Cdk1-B) activity rem
  
  
  
  
   121 an cells by signaling that is independent of cyclin-dependent kinase 1/cyclin B1 down-regulation.    
   122 osphorylation of ADD1 at Ser12 and Ser355 by cyclin-dependent kinase 1 enables ADD1 to bind to myosin
  
   124 ,3 -b] pyridine), which were shown to act as cyclin-dependent kinase 1 inhibitors, consistently reduc
  
   126 NSC 649890, L86-8275), a potent inhibitor of cyclin-dependent kinase 1/p34cdc2 phosphorylation and ki
  
   128 Hamartin with alanine mutations in the three cyclin-dependent kinase 1 phosphorylation sites increase
  
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