|Application ||WB, IHC|
|Calculated MW||45412 Da|
|Other Names||Serine/threonine-protein kinase pim-1, PIM1|
|Target/Specificity||A synthetic peptide corresponding to residues in human Pim1 was used as an immunogen.|
|Format||PBS 49%,Sodium azide 0.01%,Glycerol 50%,BSA 0.05%|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Pim1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl- X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post- translational levels. Phosphorylation of CDKN1B,induces 14-3-3- proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.|
|Cellular Location||Isoform 2: Cytoplasm. Nucleus.|
|Tissue Location||Expressed primarily in cells of the hematopoietic and germline lineages. Isoform 1 and isoform 2 are both expressed in prostate cancer cell lines|
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Provided below are standard protocols that you may find useful for product applications.
Protein kinase Pim-1 is a serine/threonine kinase that has been implicated in the development of hematopoietic and prostatic malignancies. Two isoforms, the 44 and 33 kDa Pim-1, are expressed in all human prostate cancer cell lines examined. The subcellular localization of human 44 kDa Pim-1 is primarily on the plasma membrane, while the 33 kDa isoform is present in both the cytosol and nucleus in PCA cells (1). The nuclear location of Pim-1 is essential for its regulation of the levels of HDM2 protein, and possibly for additional biological activities of this protein kinase. Studies imply a physiological role of the Pim-1 protooncogene during hematopoietic development and a deregulation in various leukemias. Pim-1 is capable of enhancing the rate of occurrence of c-Myc-induced lymphomas, and functions to block factor-withdrawal and genotoxic stress-induced apoptosis. During human fetal hematopoiesis Pim-1 is highly expressed in the liver and spleen. In contrast, at the adult stage it is only slightly expressed in circulating granulocytes (2-3).
1. Xie Y, et al. Oncogene 25(1):70-8, 2006
2. Ionov, Y, et al. FEBS Lett 467(1):17-21, 2000
3. Amson R, et al. Proc Natl Acad Sci 86(22):2257-61, 1989
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