R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
DLL3 (E3J5R) Rabbit mAb #71804
Filter:
- WB
- IP
- IHC
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 65 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Immunohistochemistry (Paraffin) | 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.
For a carrier free (BSA and azide free) version of this product see product #88260.
For a carrier free (BSA and azide free) version of this product see product #88260.
Protocol
Specificity / Sensitivity
DLL3 (E3J5R) Rabbit mAb recognizes endogenous levels of total DLL3 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro566 of human DLL3 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).
Mutations in DLL3 cause spondylocostal dysostoses (SCD), a diverse group of disorders of axial skeletal malformation (7-10).
Mutations in DLL3 cause spondylocostal dysostoses (SCD), a diverse group of disorders of axial skeletal malformation (7-10).
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- 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.
- Whittock, N.V. et al. (2004) Clin Genet 66, 67-72.
- Turnpenny, P.D. et al. (2003) J Med Genet 40, 333-9.
- Bulman, M.P. et al. (2000) Nat Genet 24, 438-41.
- Bonafé, L. et al. (2003) Clin Genet 64, 28-35.
限制使用
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