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1 checkpoint arrest due to phosphorylation of checkpoint kinase 1.
2 CX-5461 is associated with activation of the checkpoint kinases 1/2, an aberrant G2/M cell-cycle prog
6 mber of downstream substrates, such as Chk1 (checkpoint kinase 1) and H2AX (histone 2A variant X).
9 elangiectasia-mutated (ATM) and Rad3-related-checkpoint kinase 1 (ATR-CHK1)) is not activated in hTER
10 n of a number of cell cycle genes, including checkpoint kinase 1 (Chek1), which we identified as a hi
11 Zeneca compound collection was performed for checkpoint kinase-1 (Chk-1 kinase) using a knowledge-bas
13 ) cell signalling network is activated, with checkpoint kinase 1 (Chk1) activation indicating prolong
14 cells expressing apoptin with inhibitors of checkpoint kinase 1 (Chk1) and Chk2 causes apoptin to lo
15 sponses (DDRs) through its interactions with checkpoint kinase 1 (CHK1) and microcephalin (MCPH1).
18 elangiectasia mutated and Rad3-related (ATR)-checkpoint kinase 1 (Chk1) axis is the major signaling p
19 d through regulated degradation of activated checkpoint kinase 1 (Chk1) by this pathway after the gen
20 d on the crystallographic analysis of a urea-checkpoint kinase 1 (Chk1) complex and molecular modelin
22 vealed that human Chk2 and a closely related checkpoint kinase 1 (Chk1) directly phosphorylate human
23 lated (ATR) kinase and its downstream target checkpoint kinase 1 (Chk1) facilitate survival of cells
24 eplication stress triggers the activation of Checkpoint Kinase 1 (Chk1) in a pathway that requires th
27 of MK-8776 (SCH 900776), a potent, selective checkpoint kinase 1 (Chk1) inhibitor, as monotherapy and
28 The present studies sought to define whether checkpoint kinase 1 (CHK1) inhibitors and poly(ADP-ribos
30 ave been synthesized as potent and selective checkpoint kinase 1 (Chk1) inhibitors via structure-base
40 us work indicates that the checkpoint kinase Checkpoint kinase 1 (Chk1) is capable of phosphorylating
41 report that depletion or acute inhibition of checkpoint kinase 1 (Chk1) is sufficient to restore gamm
42 diated by the ATM and Rad3-related (ATR) and checkpoint kinase 1 (CHK1) kinases to transiently suppre
45 rogates for the LRRK2 kinase domain based on checkpoint kinase 1 (CHK1) mutants were designed, expres
46 ia telangiectasia and Rad3-related (ATR) and checkpoint kinase 1 (Chk1) pathway in p53-deficient cell
49 owing that hydrogen peroxide (H2O2) triggers checkpoint kinase 1 (Chk1) phosphorylation in an ATR [at
52 in loss of the G1 checkpoint and reliance on checkpoint kinase 1 (Chk1) to arrest cells in response t
56 actor intimately involved in this process is checkpoint kinase 1 (Chk1), a DNA damage repair inducing
59 teins including ATM, ATR (ATM-Rad3-related), checkpoint kinase 1 (CHK1), BRCA1, NBS1, and RAD51 by We
60 otein kinase, ataxia-telangiectasia mutated, checkpoint kinase 1 (CHK1), checkpoint kinase 2 (CHK2) a
61 ia mutated and Rad3-related kinase (ATR) and checkpoint kinase 1 (Chk1), leading to changes that bloc
62 Suppression of ATR, or its downstream target checkpoint kinase 1 (Chk1), selectively sensitizes DNA-d
65 y when depleted, with loss of the cell cycle checkpoint kinase 1 (CHK1/CHEK1) being the most potent.
66 activity of virally induced AID resulted in checkpoint kinase-1 (chk1) phosphorylation and ultimatel
67 that, in the absence of induced DNA damage, checkpoint kinase-1 (CHK1), an enzyme essential for prev
68 inding motif of Rad18 is phosphorylated in a checkpoint kinase 1-dependent manner in genotoxin-treate
69 of the present study suggest existence of a checkpoint kinase 1-dependent mechanism for diallyl tris
71 nown to phosphorylate Cdc25C on Ser216, both checkpoint kinase 1 (hChk1) and Cdc25C-associated protei
72 1 mutant that was proficient for ATR-induced checkpoint kinase 1 phosphorylation nevertheless conferr
74 n of gemcitabine metabolites, and diminished checkpoint kinase 1, thereby sensitizing cells in the SN
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