| Background | Promotes cell survival in response to a variety of proliferative signals via positive regulation of the I-kappaB kinase/NF-kappaB cascade | this process requires phosphorylation of MAP3K8/COT. Prevents apoptosis induced by growth factor withdrawal via inhibition of caspase-3 activation, and via phosphorylation of pro-apoptotic proteins. Inhibits BAD-induced cell death via phosphorylation of BAD. PIM2-mediated cell survival is glucose-dependent but independent of several AKT regulators such as PI3K, HSP-90 and TOR, indicating that PIM2 and PI3K/AKT/TOR function via distinct pathways. Involved in the positive regulation of chondrocyte survival and autophagy in the epiphyseal growth plate. |