| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-102 |
Sentence |
denotes |
The Chk1 protein kinase and the Cdc25C regulatory pathways are targets of the anticancer agent UCN-01. |
| T1 |
0-102 |
Sentence |
denotes |
The Chk1 protein kinase and the Cdc25C regulatory pathways are targets of the anticancer agent UCN-01. |
| TextSentencer_T2 |
103-220 |
Sentence |
denotes |
A checkpoint operating in the G(2) phase of the cell cycle prevents entry into mitosis in the presence of DNA damage. |
| T2 |
103-220 |
Sentence |
denotes |
A checkpoint operating in the G(2) phase of the cell cycle prevents entry into mitosis in the presence of DNA damage. |
| TextSentencer_T3 |
221-415 |
Sentence |
denotes |
UCN-01, a protein kinase inhibitor currently undergoing clinical trials for cancer treatment, abrogates G(2) checkpoint function and sensitizes p53-defective cancer cells to DNA-damaging agents. |
| T3 |
221-415 |
Sentence |
denotes |
UCN-01, a protein kinase inhibitor currently undergoing clinical trials for cancer treatment, abrogates G(2) checkpoint function and sensitizes p53-defective cancer cells to DNA-damaging agents. |
| TextSentencer_T4 |
416-565 |
Sentence |
denotes |
In most species, the G(2) checkpoint prevents the Cdc25 phosphatase from removing inhibitory phosphate groups from the mitosis-promoting kinase Cdc2. |
| T4 |
416-565 |
Sentence |
denotes |
In most species, the G(2) checkpoint prevents the Cdc25 phosphatase from removing inhibitory phosphate groups from the mitosis-promoting kinase Cdc2. |
| TextSentencer_T5 |
566-660 |
Sentence |
denotes |
This is accomplished by maintaining Cdc25 in a phosphorylated form that binds 14-3-3 proteins. |
| T5 |
566-660 |
Sentence |
denotes |
This is accomplished by maintaining Cdc25 in a phosphorylated form that binds 14-3-3 proteins. |
| TextSentencer_T6 |
661-823 |
Sentence |
denotes |
The checkpoint kinases, Chk1 and Cds1, are proposed to regulate the interactions between human Cdc25C and 14-3-3 proteins by phosphorylating Cdc25C on serine 216. |
| T6 |
661-823 |
Sentence |
denotes |
The checkpoint kinases, Chk1 and Cds1, are proposed to regulate the interactions between human Cdc25C and 14-3-3 proteins by phosphorylating Cdc25C on serine 216. |
| TextSentencer_T7 |
824-893 |
Sentence |
denotes |
14-3-3 proteins, in turn, function to keep Cdc25C out of the nucleus. |
| T7 |
824-893 |
Sentence |
denotes |
14-3-3 proteins, in turn, function to keep Cdc25C out of the nucleus. |
| TextSentencer_T8 |
894-1018 |
Sentence |
denotes |
Here we report that UCN-01 caused loss of both serine 216 phosphorylation and 14-3-3 binding to Cdc25C in DNA-damaged cells. |
| T8 |
894-1018 |
Sentence |
denotes |
Here we report that UCN-01 caused loss of both serine 216 phosphorylation and 14-3-3 binding to Cdc25C in DNA-damaged cells. |
| TextSentencer_T9 |
1019-1111 |
Sentence |
denotes |
In addition, UCN-01 potently inhibited the ability of Chk1 to phosphorylate Cdc25C in vitro. |
| T9 |
1019-1111 |
Sentence |
denotes |
In addition, UCN-01 potently inhibited the ability of Chk1 to phosphorylate Cdc25C in vitro. |
| TextSentencer_T10 |
1112-1253 |
Sentence |
denotes |
In contrast, Cds1 was refractory to inhibition by UCN-01 in vitro, and Cds1 was still phosphorylated in irradiated cells treated with UCN-01. |
| T10 |
1112-1253 |
Sentence |
denotes |
In contrast, Cds1 was refractory to inhibition by UCN-01 in vitro, and Cds1 was still phosphorylated in irradiated cells treated with UCN-01. |
| TextSentencer_T11 |
1254-1379 |
Sentence |
denotes |
Thus, neither Cds1 nor kinases upstream of Cds1, such as ataxia telangiectasia-mutated, are targets of UCN-01 action in vivo. |
| T11 |
1254-1379 |
Sentence |
denotes |
Thus, neither Cds1 nor kinases upstream of Cds1, such as ataxia telangiectasia-mutated, are targets of UCN-01 action in vivo. |
| TextSentencer_T12 |
1380-1516 |
Sentence |
denotes |
Taken together our results identify the Chk1 kinase and the Cdc25C pathway as potential targets of G(2) checkpoint abrogation by UCN-01. |
| T12 |
1380-1516 |
Sentence |
denotes |
Taken together our results identify the Chk1 kinase and the Cdc25C pathway as potential targets of G(2) checkpoint abrogation by UCN-01. |