Render Target: STATIC
Render Timestamp: 2024-12-20T12:04:43.068Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-08-01 15:25:52.531
Product last modified at: 2024-12-17T18:55:40.749Z
Cell Signaling Technology Logo
1% for the planet logo
PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Pim-2 (D1D2) Rabbit mAb #4730

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 40, 38, 34
    Source/Isotype Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Pim-2 (D1D2) Rabbit mAb detects endogenous levels of total Pim-2 protein. The antibody does not cross-react with other Pim family members.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Cys266 of human Pim-2.

    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-2 is highly homologous to Pim-1 with similar oncogenic functions (13,14). Three isoforms of Pim-2 can be generated from alternative start sites which run at 34, 38, and 40 kDa (13). Pim-2 leads to resistance to a variety of apoptotic stimuli and its expression is negatively regulated by growth factor withdrawal (15,16). Increased levels of Pim-2 have also been observed in certain cancers (17,18).
    1. Mikkers, H. et al. (2004) Mol Cell Biol 24, 6104-15.
    2. Selten, G. et al. (1986) Cell 46, 603-11.
    3. Meeker, T.C. et al. (1987) J Cell Biochem 35, 105-12.
    4. Dautry, F. et al. (1988) J Biol Chem 263, 17615-20.
    5. Möröy, T. et al. (1993) Proc Natl Acad Sci USA 90, 10734-8.
    6. Lilly, M. and Kraft, A. (1997) Cancer Res 57, 5348-55.
    7. Leverson, J.D. et al. (1998) Mol Cell 2, 417-25.
    8. Winn, L.M. et al. (2003) Cell Cycle 2, 258-62.
    9. Pasqualucci, L. et al. (2001) Nature 412, 341-6.
    10. Kim, O. et al. (2004) Oncogene 23, 1838-44.
    11. Aho, T.L. et al. (2004) FEBS Lett 571, 43-9.
    12. Yan, B. et al. (2003) J Biol Chem 278, 45358-67.
    13. van der Lugt, N.M. et al. (1995) EMBO J 14, 2536-44.
    14. Breuer, M.L. et al. (1989) EMBO J 8, 743-8.
    15. Fox, C.J. et al. (2003) Genes Dev 17, 1841-54.
    16. White, E. (2003) Genes Dev 17, 1813-6.
    17. Cohen, A.M. et al. (2004) Leuk Lymphoma 45, 951-5.
    18. Dai, H. et al. (2005) Prostate 65, 276-86.
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.