| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-105 |
Sentence |
denotes |
Extracellular signal-regulated kinase activity is sustained early during human cytomegalovirus infection. |
| TextSentencer_T2 |
106-236 |
Sentence |
denotes |
Expression of many early viral genes during human cytomegalovirus (HCMV) infection is dependent on cellular transcription factors. |
| TextSentencer_T3 |
237-541 |
Sentence |
denotes |
Several immediate-early and early viral promoters contain DNA binding sites for cellular factors such as CREB, AP-1, serum response factor, and Elk-1, and these transcription factors can be activated by phosphorylation via the cellular mitogen-activated protein kinase (MAPK) signal transduction cascade. |
| TextSentencer_T4 |
542-730 |
Sentence |
denotes |
To determine if the extracellular signal-regulated MAPKs, ERK1 and ERK2, play a role in transcription factor activation during infection, we tested for ERK activity during viral infection. |
| TextSentencer_T5 |
731-916 |
Sentence |
denotes |
We found that HCMV infection resulted in the maintenance of previously activated ERK1 and ERK2 by a mechanism which appears to involve the inhibition of a cellular phosphatase activity. |
| TextSentencer_T6 |
917-1083 |
Sentence |
denotes |
ERK phosphorylation and activity were sustained for at least 8 h after infection, whereas in mock-infected cells, ERK activity steadily declined by 1 h postinfection. |
| TextSentencer_T7 |
1084-1209 |
Sentence |
denotes |
The activity of at least one cellular substrate of the ERKs, the protein kinase RSK1, was also maintained during this period. |
| TextSentencer_T8 |
1210-1315 |
Sentence |
denotes |
UV inactivation experiments suggested that viral gene expression was required for sustained ERK activity. |
| TextSentencer_T9 |
1316-1563 |
Sentence |
denotes |
In turn, activation of the ERKs appeared to be important for viral gene expression, as evidenced by the observed decrease in the transcriptional activity of the HCMV UL112-113 promoter during infection in the presence of the MEK inhibitor PD98059. |
| TextSentencer_T10 |
1564-1767 |
Sentence |
denotes |
These data suggest that HCMV utilizes cellular signal transduction pathways to activate viral or cellular transcription factors involved in the control of early viral gene expression and DNA replication. |
| T1 |
0-105 |
Sentence |
denotes |
Extracellular signal-regulated kinase activity is sustained early during human cytomegalovirus infection. |
| T2 |
106-236 |
Sentence |
denotes |
Expression of many early viral genes during human cytomegalovirus (HCMV) infection is dependent on cellular transcription factors. |
| T3 |
237-541 |
Sentence |
denotes |
Several immediate-early and early viral promoters contain DNA binding sites for cellular factors such as CREB, AP-1, serum response factor, and Elk-1, and these transcription factors can be activated by phosphorylation via the cellular mitogen-activated protein kinase (MAPK) signal transduction cascade. |
| T4 |
542-730 |
Sentence |
denotes |
To determine if the extracellular signal-regulated MAPKs, ERK1 and ERK2, play a role in transcription factor activation during infection, we tested for ERK activity during viral infection. |
| T5 |
731-916 |
Sentence |
denotes |
We found that HCMV infection resulted in the maintenance of previously activated ERK1 and ERK2 by a mechanism which appears to involve the inhibition of a cellular phosphatase activity. |
| T6 |
917-1083 |
Sentence |
denotes |
ERK phosphorylation and activity were sustained for at least 8 h after infection, whereas in mock-infected cells, ERK activity steadily declined by 1 h postinfection. |
| T7 |
1084-1209 |
Sentence |
denotes |
The activity of at least one cellular substrate of the ERKs, the protein kinase RSK1, was also maintained during this period. |
| T8 |
1210-1315 |
Sentence |
denotes |
UV inactivation experiments suggested that viral gene expression was required for sustained ERK activity. |
| T9 |
1316-1563 |
Sentence |
denotes |
In turn, activation of the ERKs appeared to be important for viral gene expression, as evidenced by the observed decrease in the transcriptional activity of the HCMV UL112-113 promoter during infection in the presence of the MEK inhibitor PD98059. |
| T10 |
1564-1767 |
Sentence |
denotes |
These data suggest that HCMV utilizes cellular signal transduction pathways to activate viral or cellular transcription factors involved in the control of early viral gene expression and DNA replication. |