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1                                              Chk1 kinase inhibitors are currently under clinical inve
2 lay only briefly in CPT medium by activating Chk1 kinase, cdc2.1w cells bypass Chk1 to enter an exten
3                                   The active Chk1 kinase was essential for both the accurate focal co
4  46d, with potent enzymatic activity against Chk1 kinase.
5 inding interactions between compound 46b and Chk1 kinase, revealed by X-ray cocrystal structure, were
6  gamma-H2AX, replication protein A foci, and Chk1 kinase phosphorylation, a readout for activation of
7 examined the respective roles of the ATR and Chk1 kinases in ovarian cancer cells using genetic and p
8 n abrogates IR-induced activation of ATR and Chk1 kinases, as well as phosphorylation of Cdc2-Tyr15,
9  RS response (RSR) is coordinated by ATR and Chk1 kinases.
10 licon initiation is dependent on the ATR and Chk1 kinases.
11 giectecia-mutated and Rad3-related (ATR) and Chk1 kinases and inhibition of Cdc2/Cyclin B activity.
12  elements in the signaling network (Myt1 and Chk1 kinases), and fits a large and diverse body of data
13 (ataxia telangiectasia and Rad3 related) and Chk1 kinases.
14 t activation involves activation of Wee1 and Chk1 kinases and inhibition of Cdc25A and Cdc25C phospha
15 Cdc25C expression and activation of Wee1 and Chk1 kinases.
16  site previously identified for Chk2 (or/and Chk1) kinase.
17                             Although the ATR-Chk1 kinase cascade was associated with hypoxia-induced
18  transmit DNA damage signals through the ATR-Chk1 kinase cascade, whether post-translational modifica
19 473 can be phosphorylated by ATM-Chk2 or ATR-Chk1 kinases.
20 egulation in BER-depleted cells requires ATR/Chk1 kinase activities, demonstrating that PD-L1 upregul
21           This upregulation requires ATM/ATR/Chk1 kinases.
22          One is the previously characterized Chk1 kinase.
23 SUMOylation occurs in cells with compromised Chk1 kinase activity, necessary for known posttranslatio
24 rgeted phospho-Ser 345, leading to decreased Chk1 kinase activity.
25 system in which the phosphorylation of human Chk1 kinase by ATR (ataxia telangiectasia mutated and Ra
26 A resolution crystal structures of the human Chk1 kinase domain and its binary complex with an ATP an
27              Structural studies of the human Chk1 kinase domain show an open conformation; the activi
28 nserved C-terminal region negatively impacts Chk1 kinase activity.
29          These phenotypes reflect defects in Chk1 kinase induction, as the mutants are either partial
30 rest was also associated with an increase in Chk1 kinase activity.
31 ive indolocarbazole inhibitor (SB-218078) of Chk1 kinase activity and used this compound to assess ce
32                                Activation of Chk1 kinase also requires its association with Claspin,
33 is suggests the expression and activation of Chk1 kinase is associated with cells undergoing active D
34           Here, we report that inhibition of Chk1 kinase activity paradoxically leads to the accumula
35  in solution, which results in inhibition of Chk1 kinase activity.
36                                Inhibition of Chk1 kinase with 7-hydroxystaurosporine (UCN-01) abrogat
37                              An inhibitor of Chk1 kinase activity, UCN-01, overcomes the HuCdc6 media
38 lues of 3-10 nM) and selective inhibitors of Chk1 kinase was described.
39  excision repair leads to phosphorylation of Chk1 kinase in both G1 and S phase of the cell cycle, su
40  might serve as substrates for hCds1/Chk2 or Chk1 kinase activity.
41 s a homolog of the Schizosaccharomyces pombe Chk1 kinase, provides a cell-cycle checkpoint that delay
42                          Separately purified Chk1 kinase and KA1 domains are intimately associated in
43                            In other systems, Chk1 kinase phosphorylates and suppresses the activity o
44                           Here, we show that Chk1 kinase activity is rapidly stimulated in a cell-cyc
45                                          The Chk1 kinase is a major effector of S phase checkpoint si
46                                          The Chk1 kinase, an effector of the DNA-damage checkpoint, p
47 w that BRCA1 is essential for activating the Chk1 kinase that regulates DNA damage-induced G2/M arres
48 o demonstrate that serine 83 of Mcd1 and the Chk1 kinase are critical determinants for DSB-induced co
49 ved in the structures between UCN-01 and the Chk1 kinase domain.
50 se TMZ-induced effects were inhibited by the Chk1 kinase inhibitor UCN-01.
51      Taken together our results identify the Chk1 kinase and the Cdc25C pathway as potential targets
52 role of Cdc2 tyrosine phosphorylation in the Chk1 kinase-mediated DNA damage checkpoint has remained
53  partner ATR-interacting protein but not the Chk1 kinase.
54 ivation typically leads to activation of the Chk1 kinase among other substrates.
55 cation checkpoint and phosphorylation of the Chk1 kinase are dependent on RNA primer synthesis by DNA
56 tion specifically destroys regulation of the Chk1 kinase but not the Chk2 kinase, suggesting involvem
57 , we determined the crystal structure of the Chk1 kinase domain in complex with UCN-01.
58                          The addition of the Chk1 kinase inhibitor 7-hydroxystaurosporine (UCN-01) to
59 14/Y15 and activating phosphorylation of the Chk1 kinase no longer occur.
60 dine and pyrrolopyrimidine inhibitors of the Chk1 kinase, an oncology target.
61 is intimately linked to the integrity of the Chk1 kinase-Cdc25A phosphatase pathway.
62 TM and ATR kinase inhibitor caffeine, or the Chk1 kinase inhibitor UCN-01.
63            In Schizosaccharomyces pombe, the Chk1 kinase is essential for mitotic arrest and is phosp
64 ve in DNA replication initiation require the Chk1 kinase.
65 he Chk1 catalytic cleft were consistent with Chk1 kinase assays defining substrate suitability.