|Other Names||Serine/threonine-protein kinase pim-2, Pim2, Pim-2|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression, the regulation of cap-dependent protein translation and through survival signaling by phosphorylation of a pro-apoptotic protein, BAD. Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM2 might explain partly the strong synergism between these 2 oncogenes in tumorigenesis. Regulates cap-dependent protein translation in a mammalian target of rapamycin complex 1 (mTORC1)-independent manner and in parallel to the PI3K-Akt pathway. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti- apoptotic protein Bcl-X(L)/BCL2L1. Promotes cell survival in response to a variety of proliferative signals via positive regulation of the I-kappa-B kinase/NF-kappa-B cascade; this process requires phosphorylation of MAP3K8/COT. Promotes growth factor-independent proliferation by phosphorylation of cell cycle factors such as CDKN1A and CDKN1B. Involved in the positive regulation of chondrocyte survival and autophagy in the epiphyseal growth plate.|
|Tissue Location||Widely expressed, with highest expression in spleen, thymus and brain. Expressed in epiphyseal chondrocytes|
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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; isoform 1 is less active in this respect. 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.
Agrawal-Singh, S., et al. Blood 115(22):4507-4516(2010)Lin, Y.W., et al. Blood 115(4):824-833(2010)Narayana, Y., et al. Mol. Immunol. 46(15):2947-2954(2009)Grundler, R., et al. J. Exp. Med. 206(9):1957-1970(2009)Derudder, E., et al. Nat. Immunol. 10(6):647-654(2009)
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