| First Author | Fox CJ | Year | 2003 |
| Journal | Genes Dev | Volume | 17 |
| Issue | 15 | Pages | 1841-54 |
| PubMed ID | 12869584 | Mgi Jnum | J:84700 |
| Mgi Id | MGI:2669068 | Doi | 10.1101/gad.1105003 |
| Citation | Fox CJ, et al. (2003) The serine/threonine kinase Pim-2 is a transcriptionally regulated apoptotic inhibitor. Genes Dev 17(15):1841-54 |
| abstractText | Growth factor withdrawal results in the termination of factor-dependent transcription. One transcript that declines rapidly following growth factor deprivation of hematopoietic cells is the serine/threonine kinase pim-2. When constitutively expressed, Pim-2 conferred long-term resistance to a variety of apoptotic stimuli including growth factor withdrawal and endogenous levels of Pim-2 contributed to growth factor-mediated apoptotic resistance. Pim-2 expression maintained cell size and mitochondrial potential independently of the PI3K/Akt/TOR pathway. Pim-2-dependent maintenance of cell size and survival correlated with its ability to maintain rapamycin-resistant phosphorylation of the translational repressor 4E-BP1 and phosphorylation of the BH3 protein BAD. These results establish Pim-2 as a direct link between growth factor-induced transcription and a novel, kinase-dependent pathway that promotes cell-autonomous survival. |
