DLL4 Antibody #2589
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 75-80 |
| SOURCE | 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 | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
DLL4 Antibody detects endogenous levels of total DLL4 protein.
Species Reactivity:
Human
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to a region surrounding residue Leu617 of human DLL4. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Notch signaling is activated upon engagement of the Notch receptor with its ligands, the DSL (Delta, Serrate, Lag2) proteins of single-pass type I membrane proteins. The DSL proteins contain multiple EGF-like repeats and a DSL domain that is required for binding to Notch (1,2). Five DSL proteins have been identified in mammals: Jagged1, Jagged2, Delta-like (DLL) 1, 3 and 4 (3). Ligand binding to the Notch receptor results in two sequential proteolytic cleavages of the receptor by the ADAM protease and the γ-secretase complex. The intracellular domain of Notch is released and then translocates to the nucleus where it activates transcription. Notch ligands may also be processed in a way similar to Notch, suggesting a bi-directional signaling through receptor-ligand interactions (4-6).
DLL4 expression is highly restricted to the vascular endothelium (7), and haploinsufficiency of DLL4 results in major defects in vascular systems in mouse (8-11). Blockade of DLL4 inhibits tumor growth in model systems (12-14).
DLL4 expression is highly restricted to the vascular endothelium (7), and haploinsufficiency of DLL4 results in major defects in vascular systems in mouse (8-11). Blockade of DLL4 inhibits tumor growth in model systems (12-14).
- Wilson, A. and Radtke, F. (2006) FEBS Lett. 580, 2860-2868.
- Hansson, E.M. et al. (2004) Semin. Cancer Biol. 14, 320-328.
- Chiba, S. (2006) Stem Cells 24, 2437-2447.
- Bland, C.E. et al. (2003) J. Biol. Chem. 278, 13607-13610.
- Six, E. et al. (2003) Proc. Natl. Acad. Sci. USA 100, 7638-7643.
- LaVoie, M.J. and Selkoe, D.J. (2003) J. Biol. Chem. 278, 34427-34437.
- Shutter, J.R. et al. (2000) Genes Dev. 14, 1313-1318.
- Gale, N.W. et al. (2004) Proc. Natl. Acad. Sci. USA 101, 15949-15954.
- Krebs, L.T. et al. (2004) Genes Dev. 18, 2469-2473.
- Duarte, A. et al. (2004) Genes Dev. 18, 2474-2478.
- Hellström, M. et al. (2007) Nature 445, 776-780.
- Noguera-Troise, I. et al. (2006) Nature 444, 1032-1037.
- Lobov, I.B. et al. (2007) Proc. Natl. Acad. Sci. USA 104, 3219-3224.
- Scehnet, J.S. et al. (2007) Blood 109, 4753-4760.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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