Product Pathways - Lymphocyte Signaling
Pim-2 Antibody #4723
| Applications | Reactivity | MW (kDa) | Source |
|---|---|---|---|
| W | H (Mk) | 40, 38, 34 | Rabbit |
Applications Key:
W=Western Blotting
Reactivity Key:
H=Human
Mk=Monkey
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.
Specificity / Sensitivity
Pim-2 Antibody detects endogenous levels of total Pim-2 protein. The antibody does not cross-react with other Pim family members.
Source / Purification
Polyclonal antibodies were prepared by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to residues surrounding Gln287 of human Pim-2. Antibodies were purified by peptide affinity chromatography.
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 is correlated 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 has also been observed in certain cancers (17,18).
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Application References
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