PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16151644-3 2005 Etoposide activated p38, inhibited the G2/M transition with the persistent inhibitory phosphorylation of Cdc2 on Tyr15, and caused apoptosis of Daudi cells. Etoposide 0-9 cyclin dependent kinase 1 Homo sapiens 105-109 17636382-0 2007 New alternative phosphorylation sites on the cyclin dependent kinase 1/cyclin a complex in p53-deficient human cells treated with etoposide: possible association with etoposide-induced apoptosis. Etoposide 130-139 cyclin dependent kinase 1 Homo sapiens 45-70 17636382-0 2007 New alternative phosphorylation sites on the cyclin dependent kinase 1/cyclin a complex in p53-deficient human cells treated with etoposide: possible association with etoposide-induced apoptosis. Etoposide 167-176 cyclin dependent kinase 1 Homo sapiens 45-70 17636382-6 2007 The p53-negative myeloid leukemia cell lines K562 and HL-60 were used to determine Cdk1 phosphorylation status during etoposide treatment. Etoposide 118-127 cyclin dependent kinase 1 Homo sapiens 83-87 17636382-13 2007 These findings suggest novel Cdk1 phosphorylation sites, which appear to be associated with p53-independent cell death following etoposide treatment. Etoposide 129-138 cyclin dependent kinase 1 Homo sapiens 29-33 16151644-5 2005 SB203580, a specific inhibitor of p38alpha and p38beta, similarly reduced the inhibitory phosphorylation of Cdc2 as well as G2/M arrest and augmented apoptosis of Daudi cells treated with etoposide. Etoposide 188-197 cyclin dependent kinase 1 Homo sapiens 108-112 16151644-6 2005 These results suggest that p38 plays a role in G2/M checkpoint activation through induction of the persistent inhibitory phosphorylation of Cdc2 and, thereby, inhibits apoptosis of Daudi cells treated with etoposide. Etoposide 206-215 cyclin dependent kinase 1 Homo sapiens 140-144 15674326-4 2005 Erythropoietin or IL-3 significantly enhanced etoposide-induced activation-specific phosphorylation of Chk1, a checkpoint kinase that inhibits Cdc2 activation by Cdc25 phosphatases, and led to the inhibition of Cdc2 kinase activity with the persistent inhibitory phosphorylation on Tyr15. Etoposide 46-55 cyclin dependent kinase 1 Homo sapiens 143-147 15790566-6 2005 Furthermore, we found that Cdk1 activity was required for etoposide-induced apoptosis of HeLa cells. Etoposide 58-67 cyclin dependent kinase 1 Homo sapiens 27-31 15674326-4 2005 Erythropoietin or IL-3 significantly enhanced etoposide-induced activation-specific phosphorylation of Chk1, a checkpoint kinase that inhibits Cdc2 activation by Cdc25 phosphatases, and led to the inhibition of Cdc2 kinase activity with the persistent inhibitory phosphorylation on Tyr15. Etoposide 46-55 cyclin dependent kinase 1 Homo sapiens 162-166 15674326-5 2005 The inhibitory Cdc2 phosphorylation and G2/M block by etoposide were enhanced or inhibited by overexpression of Chk1 or by the specific Chk1 inhibitor SB218078, respectively. Etoposide 54-63 cyclin dependent kinase 1 Homo sapiens 15-19 15674326-8 2005 These results indicate that hematopoietic cytokines protect etoposide-treated cells from DNA damage-induced apoptosis by promoting, through the PI3K/Akt/GSK3 signaling pathway, G2/M checkpoint that is dependent on Chk1-mediated inhibition of Cdc2. Etoposide 60-69 cyclin dependent kinase 1 Homo sapiens 242-246 12569391-4 2003 The increased sensitivity to etoposide-induced G(2)-M arrest was associated with disruption of cell cycle-related events, including hyperphosphorylation of p34(cdc2) kinase, change in cdc25C expression and phosphorylation, and alteration in cyclin B1 expression. Etoposide 29-38 cyclin dependent kinase 1 Homo sapiens 160-164 9230211-2 1997 Abnormal activation of cyclin B-associated CDC 2 kinase has been implicated in apoptosis induced by cancer chemotherapeutic agents such as paclitaxel (Taxol) and etoposide (VP-16). Etoposide 162-171 cyclin dependent kinase 1 Homo sapiens 43-48 11841447-7 2002 We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15). Etoposide 90-99 cyclin dependent kinase 1 Homo sapiens 230-234 11841447-7 2002 We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15). Etoposide 193-202 cyclin dependent kinase 1 Homo sapiens 230-234 10368682-0 1999 Use of CDC2 from etoposide-treated cells as substrate to assay CDC25 phosphatase activity. Etoposide 17-26 cyclin dependent kinase 1 Homo sapiens 7-11 10368682-2 1999 In response to Etoposide (VP-16) induced DNA damage, cells undergo a G2-phase arrest resulting in the accumulation of inactive CDK1 (CDC2) kinase complexes. Etoposide 15-24 cyclin dependent kinase 1 Homo sapiens 127-131 10368682-2 1999 In response to Etoposide (VP-16) induced DNA damage, cells undergo a G2-phase arrest resulting in the accumulation of inactive CDK1 (CDC2) kinase complexes. Etoposide 15-24 cyclin dependent kinase 1 Homo sapiens 133-137 10368682-3 1999 Here we report that upon Etoposide treatment CDC2 is phosphorylated on tyrosine 15 and is dephosphorylated and activated in vitro by recombinant CDC25 phosphatase. Etoposide 25-34 cyclin dependent kinase 1 Homo sapiens 45-49 10368682-4 1999 We also show that inactive CDC2 kinase from Etoposide-treated cells can be used as a substrate in a sensitive two-step assay of CDC25 phosphatase. Etoposide 44-53 cyclin dependent kinase 1 Homo sapiens 27-31 9635591-3 1998 In this study, we have demonstrated the existence of an additional pathway, independent of the p34cdc2 kinase activation pathway, that leads to a G2 arrest in etoposide-treated cells. Etoposide 159-168 cyclin dependent kinase 1 Homo sapiens 95-102 9635591-4 1998 Both the X-ray-induced and the etoposide-induced G2 arrest were associated with inhibition of the p34cdc2 H1 kinase activation pathway as judged by p34cdc2 H1 kinase activity and phosphorylation of cdc25C. Etoposide 31-40 cyclin dependent kinase 1 Homo sapiens 98-105 9635591-4 1998 Both the X-ray-induced and the etoposide-induced G2 arrest were associated with inhibition of the p34cdc2 H1 kinase activation pathway as judged by p34cdc2 H1 kinase activity and phosphorylation of cdc25C. Etoposide 31-40 cyclin dependent kinase 1 Homo sapiens 148-155 7812949-6 1995 The same transient activation and subsequent inactivation of cyclin B1/Cdc2 kinase were observed after DNA damage by etoposide or bis-(2-chloroethyl)methylamine hydrochloride. Etoposide 117-126 cyclin dependent kinase 1 Homo sapiens 71-75 1933864-8 1991 In contrast to senescent and low serum-arrested cells, cdc2 mRNA was expressed at normal levels in cells partially growth arrested by isoleucine deficiency in G1, by aphidicolin at G1-S, by etoposide in G2, or by Colcemid in the M phase of the cell cycle, indicating that cdc2 down-regulation does not always occur upon growth arrest. Etoposide 190-199 cyclin dependent kinase 1 Homo sapiens 55-59 8069859-4 1994 Brief caffeine exposures (5 or 10 mM for 1-2 h) caused specific tyrosine dephosphorylation and activation of p34cdc2 kinase, and mitotic progression to a limited extent, in cells which were arrested in G2 following etoposide treatment. Etoposide 215-224 cyclin dependent kinase 1 Homo sapiens 109-116 21573322-5 1993 A brief exposure to etoposide causes both cell lines to arrest in G2, with a concomittant increase in cyclin-B levels and accumulation of hyperphosphorylated p34cdc2. Etoposide 20-29 cyclin dependent kinase 1 Homo sapiens 158-165 21573322-6 1993 Failure to activate the p34cdc2 kinase following etoposide treatment to levels comparable with synchronous G2/M-phase cells is not due to inhibition of p34cdc2/cyclin-B complex formation, but relies more on an inability to tyrosine dephosphorylate p34cdc2. Etoposide 49-58 cyclin dependent kinase 1 Homo sapiens 24-31 1551112-0 1992 Inhibition of p34cdc2 kinase activation, p34cdc2 tyrosine dephosphorylation, and mitotic progression in Chinese hamster ovary cells exposed to etoposide. Etoposide 143-152 cyclin dependent kinase 1 Homo sapiens 14-21 1551112-0 1992 Inhibition of p34cdc2 kinase activation, p34cdc2 tyrosine dephosphorylation, and mitotic progression in Chinese hamster ovary cells exposed to etoposide. Etoposide 143-152 cyclin dependent kinase 1 Homo sapiens 41-48 1551112-1 1992 p34cdc2 kinase, an enzyme essential for mitosis in mammalian cells, may play a role in etoposide-induced G2 phase arrest of Chinese hamster ovary cells. Etoposide 87-96 cyclin dependent kinase 1 Homo sapiens 0-7 1551112-2 1992 In this study, etoposide is shown to cause inhibition of a specific p34cdc2 kinase activation pathway, that of tyrosine dephosphorylation. Etoposide 15-24 cyclin dependent kinase 1 Homo sapiens 68-75 1551112-3 1992 Exposure of asynchronously dividing cells to etoposide caused a simultaneous rapid decline of both mitotic index and p34cdc2 kinase activity, suggesting that the kinase was not activated and that the arrest point was in late G2 phase. Etoposide 45-54 cyclin dependent kinase 1 Homo sapiens 117-124 1551112-6 1992 A 1-h exposure to etoposide during early G2 phase inhibited p34cdc2 kinase activation, its shift in electrophoretic mobility, and its tyrosine dephosphorylation, all of which correlated with a delay in mitotic progression. Etoposide 18-27 cyclin dependent kinase 1 Homo sapiens 60-67 2187601-0 1990 Inhibition of p34cdc2 kinase activity by etoposide or irradiation as a mechanism of G2 arrest in Chinese hamster ovary cells. Etoposide 41-50 cyclin dependent kinase 1 Homo sapiens 14-21 2187601-7 1990 Treatment of either asynchronous CHO cells or an enriched G2 population with the antitumor agent, etoposide, results in rapid inhibition of immunoprecipitated p34cdc2 kinase activity, which is not due to a direct effect of drug upon the enzyme. Etoposide 98-107 cyclin dependent kinase 1 Homo sapiens 159-166 2187601-8 1990 p34cdc2 kinase activity recovers as cells arrest in G2 and a second etoposide treatment further inhibits p34cdc2 kinase activity and prolongs G2 arrest. Etoposide 68-77 cyclin dependent kinase 1 Homo sapiens 0-7 2187601-8 1990 p34cdc2 kinase activity recovers as cells arrest in G2 and a second etoposide treatment further inhibits p34cdc2 kinase activity and prolongs G2 arrest. Etoposide 68-77 cyclin dependent kinase 1 Homo sapiens 105-112 25607114-5 2015 However, co-treatment with anti-VEGF significantly restored etoposide-induced cell apoptosis and cell cycle arrest, as indicated by the elimination of B-cell lymphoma 2 (Bcl-2), procaspase 3, cyclin B1 and Cdc2. Etoposide 60-69 cyclin dependent kinase 1 Homo sapiens 206-210