| First Author | Blagosklonny MV | Year | 1999 |
| Journal | Bioessays | Volume | 21 |
| Issue | 8 | Pages | 704-9 |
| PubMed ID | 10440867 | Mgi Jnum | J:56662 |
| Mgi Id | MGI:1342156 | Doi | 10.1002/(SICI)1521-1878(199908)21:8<704::AID-BIES10>3.0.CO;2-5 |
| Citation | Blagosklonny MV (1999) A node between proliferation, apoptosis, and growth arrest. Bioessays 21(8):704-9 |
| abstractText | Paradoxically, oncogenes and growth factors can induce proliferation and promote cellular survival but can also cause apoptosis and growth arrest. What determines whether a cell decides to proliferate, arrest growth, or die? Mitogens and activators of mitogen-activated pathways initiate the simultaneous production of proliferative (cyclins) and anti-proliferative (CDK inhibitors such as p21WAF1/CIP1) signals. Quiescent cells may respond to these signals by proliferation whereas proliferating cells may respond by growth arrest. Although pro-apoptotic oncoproteins, which constitute the downstream pathway (cyclin D, E2F, c-myc) directly induce proliferation, the activation of the upstream steps (growth factor receptors, Ras, cytoplasmic kinases) is required to prevent apoptosis. Copyright 1999 John Wiley Sons, Inc. |
