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DLL4/Delta-like 4  Protein, Antibody, ELISA Kit, cDNA Clone

Description: Active  
Expression host: Human Cells  
  • Slide 1
10171-H02H-50
10171-H02H-100
50 µg 
100 µg 
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Description: Active  
Expression host: Human Cells  
  • Slide 1
10171-H08H-50
10171-H08H-100
50 µg 
100 µg 
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Expression host: Human Cells  
  • Slide 1
10171-HCCH-50
10171-HCCH-200
50 µg 
200 µg 
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Description: Active  
Expression host: Human Cells  
  • Slide 1
50640-M08H-50
50640-M08H-100
50 µg 
100 µg 
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DLL4/Delta-like 4 Related Area

DLL4/Delta-like 4 Related Pathways

    DLL4/Delta-like 4 Summary & Protein Information

    DLL4/Delta-like 4 Background

    Gene Summary: This DLL4 gene is a homolog of the Drosophila delta gene. The delta gene family encodes Notch ligands that are characterized by a DSL domain, EGF repeats, and a transmembrane domain. [provided by RefSeq, Jul 2008]
    General information above from NCBI
    Subunit structure: Binds to Notch-1 and Notch-4 (By similarity).
    Domain: The Delta-Serrate-Lag2 (DSL) domain is required for binding to the Notch receptor.
    Subcellular location: Membrane; Single-pass type I membrane protein (Probable).
    Tissue specificity: Expressed in vascular endothelium.
    Post-translational: Ubiquitinated by MIB (MIB1 or MIB2), leading to its endocytosis and subsequent degradation (By similarity).
    Sequence similarity: Contains 1 DSL domain.
    Contains 8 EGF-like domains.C
    General information above from UniProt

    Delta-like protein 4 (DLL4, Delta4), a type I membrane-bound Notch ligand, is one of five known Notch ligands in mammals and interacts predominantly with Notch 1, which has a key role in vascular development. Recent studies yield substantial insights into the role of DLL4 in angiogenesis. DLL4 is induced by vascular endothelial growth factor (VEGF) and acts downstream of VEGF as a 'brake' on VEGF-induced vessel growth, forming an autoregulatory negative feedback loop inactivating VEGF. DLL4 is downstream of VEGF signaling and its activation triggers a negative feedback that restrains the effects of VEGF. Attenuation of DLL4/Notch signaling results in chaotic vascular network with excessive branching and sprouting. DLL4 is widely distributed in tissues other than vessels including many malignancies. Furthermore, the molecule is internalized on binding its receptor and often transported to the nucleus. In pathological conditions, such as cancer, DLL4 is up-regulated strongly in the tumour vasculature. Blockade of DLL4-mediated Notch signaling strikingly increases nonproductive angiogenesis, but significantly inhibits tumor growth in preclinical mouse models. In preclinical studies, blocking of DLL4/Notch signaling is associated with a paradoxical increase in tumor vessel density, yet causes marked growth inhibition due to functionally defective vasculature. Thus, DLL4 blockade holds promise as an additional strategy for angiogenesis-based cancer therapy.

    DLL4/Delta-like 4 Alternative Name

    hdelta2, [homo-sapiens]
    delta 4,delta ligand 4,DLL4,hdelta2,MGC126344, [human]
    Delta4,Dll4,RP23-46P4.8, [mouse]
    Delta4, [mus-musculus]

    DLL4/Delta-like 4 Related Studies

  • Yan M, et al. (2007) Delta-like 4/Notch signaling and its therapeutic implications. Clin Cancer Res. 13(24): 7243-6.
  • Sainson RC, et al. (2007) Anti-Dll4 therapy: can we block tumour growth by increasing angiogenesis? Trends Mol Med. 13(9): 389-95.
  • Martinez JC, et al. (2009) Nuclear and membrane expression of the angiogenesis regulator delta-like ligand 4 (DLL4) in normal and malignant human tissues. Histopathology. 54(5): 598-606.
  • Li JL, et al. (2010) Targeting DLL4 in tumors shows preclinical activity but potentially significant toxicity. Future Oncol. 6(7): 1099-103.
  • Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"