R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
DLL4 (D7N3H) Rabbit mAb #96406
Filter:
- WB
- IP
- IF
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 75-80 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:200 |
| Immunofluorescence (Immunocytochemistry) | 1:400 |
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
DLL4 (D7N3H) Rabbit mAb recognizes endogenous levels of total DLL4 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the carboxy terminus of human DLL4 protein.
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, 1313-8.
- Gale, N.W. et al. (2004) Proc Natl Acad Sci U S A 101, 15949-54.
- Krebs, L.T. et al. (2004) Genes Dev 18, 2469-73.
- Duarte, A. et al. (2004) Genes Dev 18, 2474-8.
- Hellström, M. et al. (2007) Nature 445, 776-80.
- Noguera-Troise, I. et al. (2006) Nature 444, 1032-7.
- Lobov, I.B. et al. (2007) Proc Natl Acad Sci U S A 104, 3219-24.
- Scehnet, J.S. et al. (2007) Blood 109, 4753-60.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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