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.
Highly expressed in hematopoietic tissues, in leukemic and lymphoma cell lines, testis, small intestine, colon and colorectal adenocarcinoma cells. Weakly expressed in normal liver, but highly expressed in hepatocellular carcinoma tissues.
Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. PIM subfamily. Contains 1 protein kinase domain.