Pim-3 (D17C9) Rabbit mAb #4165
- WB
Supporting Data
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 35 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Pim-3 (D17C9) Rabbit mAb detects endogenous levels of total Pim-3 protein. It does not cross-react with other Pim family members.
Species Reactivity:
Human, Mouse, Rat
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser275 of human Pim-3.
Background
Pim proteins (Pim-1, Pim-2 and Pim-3) are oncogene-encoded serine/threonine kinases (1). Pim-1, a serine/threonine kinase highly expressed in hematopoietic cells, plays a critical role in the transduction of mitogenic signals and is rapidly induced by a variety of growth factors and cytokines (1-4). Pim-1 cooperates with c-Myc in lymphoid cell transformation and protects cells from growth factor withdrawal and genotoxic stress-induced apoptosis (5,6). Pim-1 also enhances the transcriptional activity of c-Myb through direct phosphorylation within the c-Myb DNA binding domain as well as phosphorylation of the transcriptional coactivator p100 (7,8). Hypermutations of the Pim-1 gene are found in B-cell diffuse large cell lymphomas (9). Phosphorylation of Pim-1 at Tyr218 by Etk occurs following IL-6 stimulation and correlates with an increase in Pim-1 activity (10). Various Pim substrates have been identified; Bad is phosphorylated by both Pim-1 and Pim-2 at Ser112 and this phosphorylation reverses Bad-induced cell apoptosis (11,12).
Pim-3, originally named Kid-1, was identified as a protein induced by depolarization in PC-12 cells (13). Like other family members, Pim-3 can phosphorylate Bad to inhibit Bad-mediated apoptosis (14). Aberrant expression of Pim-3 has been observed in a number of types of cancer, including liver, pancreas, colon and gastric cancer (14-17).
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- Möröy, T. et al. (1993) Proc Natl Acad Sci USA 90, 10734-8.
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- Leverson, J.D. et al. (1998) Mol Cell 2, 417-25.
- Winn, L.M. et al. (2003) Cell Cycle 2, 258-62.
- Pasqualucci, L. et al. (2001) Nature 412, 341-6.
- Kim, O. et al. (2004) Oncogene 23, 1838-44.
- Aho, T.L. et al. (2004) FEBS Lett 571, 43-9.
- Yan, B. et al. (2003) J Biol Chem 278, 45358-67.
- Feldman, J.D. et al. (1998) J Biol Chem 273, 16535-43.
- Li, Y.Y. et al. (2006) Cancer Res 66, 6741-7.
- Fujii, C. et al. (2005) Int J Cancer 114, 209-18.
- Popivanova, B.K. et al. (2007) Cancer Sci 98, 321-8.
- Zheng, H.C. et al. (2008) J Cancer Res Clin Oncol 134, 481-8.
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