PU.1 (E8I8L) Mouse mAb #89136
Filter:
- WB
- IP
- IF
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 42 |
| Source/Isotype | Mouse IgG1 kappa |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:10 - 1:50 |
| Immunoprecipitation | 1:50 |
| Immunofluorescence (Immunocytochemistry) | 1:100 - 1:200 |
| Flow Cytometry (Fixed/Permeabilized) | 1:50 - 1:200 |
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
PU.1 (E8I8L) Mouse mAb recognizes endogenous levels of total PU.1 protein. This antibody does not cross-react with other Ets family members.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp26 of human PU.1 protein.
Background
PU.1 is a member of the Ets family of transcription factors and activates target genes through the purine-rich PU-box (1). PU.1 plays a pivotal role in the differentiation of myeloid cells and lymphocytes and is expressed in several hematopoietic cells, including B lymphocytes, macrophages, neutrophils, mast cells, early erythroid cells, and megakaryocytes (1,2). The concentration of PU.1 is critical for both the determination of hematopoietic cell lineage and the regulation of differentiation versus stem cell proliferation (3,4). In addition, PU.1 activity is influenced by phosphorylation and interactions with other hematopoietic transcription factors. Phosphorylation of PU.1 at Ser146 by CK2 promotes binding to IRF-4 and synergistic activation through the immunoglobulin κ 3' enhancer (5). Treatment of pro-B cells with IL-3 leads to phosphorylation of PU.1 at Ser140, resulting in increased PU.1 activity and activation of the anti-apoptotic gene MCL-1 (6). GATA1 binding blocks PU.1 activity during erythroid cell development (7). Overexpression of PU.1 resulting from proviral insertion during Friend virus infection can induce erythroleukemia, while reduced expression has been associated with acute myeloid leukemia (8).
- Lloberas, J. et al. (1999) Immunol Today 20, 184-9.
- Klemsz, M.J. et al. (1990) Cell 61, 113-24.
- Dahl, R. and Simon, M.C. (2003) Blood Cells Mol Dis 31, 229-33.
- DeKoter, R.P. and Singh, H. (2000) Science 288, 1439-41.
- Pongubala, J.M. et al. (1993) Science 259, 1622-5.
- Wang, J.M. et al. (2003) Mol Cell Biol 23, 1896-909.
- Zhang, P. et al. (1999) Proc Natl Acad Sci U S A 96, 8705-10.
- Moreau-Gachelin, F. et al. (1988) Nature 331, 277-80.
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