First Author | Aho TL | Year | 2004 |
Journal | FEBS Lett | Volume | 571 |
Issue | 1-3 | Pages | 43-9 |
PubMed ID | 15280015 | Mgi Jnum | J:91967 |
Mgi Id | MGI:3051205 | Doi | 10.1016/j.febslet.2004.06.050 |
Citation | Aho TL, et al. (2004) Pim-1 kinase promotes inactivation of the pro-apoptotic Bad protein by phosphorylating it on the Ser112 gatekeeper site. FEBS Lett 571(1-3):43-9 |
abstractText | Constitutive expression of the Pim-1 kinase prolongs survival of cytokine-deprived FDCP1 cells, partly via maintenance of Bcl-2 expression. Here, we show that Pim-1 colocalizes and physically interacts with the pro-apoptotic Bad protein and phosphorylates it in vitro on serine 112, which is a gatekeeper site for its inactivation. Furthermore, wild-type Pim-1, but not a kinase-deficient mutant, enhances phosphorylation of this site in FDCP1 cells and protects cells from the pro-apoptotic effects of Bad. Our results suggest that phosphorylation of Bad by Pim-1 is one of several mechanisms via which the Pim-1 kinase can enhance Bcl-2 activity and promote cell survival. |