| Id |
Subject |
Object |
Predicate |
Lexical cue |
| S1 |
0-231 |
Sentence |
denotes |
Protein kinase B (c-Akt), phosphatidylinositol 3-kinase, and STAT5 are activated by erythropoietin (EPO) in HCD57 erythroid cells but are constitutively active in an EPO-independent, apoptosis-resistant subclone (HCD57-SREI cells). |
| S2 |
232-370 |
Sentence |
denotes |
We found that erythropoietin (EPO) and stem cell factor (SCF) activated protein kinase B (PKB/Akt) in EPO-dependent HCD57 erythroid cells. |
| S3 |
371-553 |
Sentence |
denotes |
To better understand signals controlling proliferation and viability, erythroid cells that resist apoptosis in the absence of EPO were subcloned and characterized (HCD57-SREI cells). |
| S4 |
554-652 |
Sentence |
denotes |
Constitutive activations of PKB/Akt, STAT5a, and STAT5b were noted in these EPO-independent cells. |
| S5 |
653-824 |
Sentence |
denotes |
PI3-kinase activity was an upstream activator of PKB/Akt because the PI3-kinase inhibitor LY294002 blocked both constitutive PKB/Akt and factor-dependent PKB/Akt activity. |
| S6 |
825-1035 |
Sentence |
denotes |
The LY294002 study showed that proliferation and viability of both HCD57-SREI and HCD57 cells correlated with the activity of PKB/Akt; however, PKB/Akt activity alone did not protect these cells from apoptosis. |
| S7 |
1036-1129 |
Sentence |
denotes |
Treatment of HCD57 cells with SCF also activated PKB/Akt, but did not protect from apoptosis. |
| S8 |
1130-1255 |
Sentence |
denotes |
This result suggested that PKB/PI3-kinase activity is necessary but not sufficient to promote viability and/or proliferation. |
| S9 |
1256-1515 |
Sentence |
denotes |
Constitutive STAT5 activity, activated through an unknown pathway not including JAK2 or EPOR, may act in concert with the constitutive PI3-kinase/PKB/Akt pathway to protect the EPO-independent HCD57-SREI cells from apoptosis and promote limited proliferation. |
