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Human DLL4 qPCR primer pairs

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Human DLL4 qPCR Product Information
Gene Synonym:DLL4, hdelta2, MGC126344
PCR_SIZE (bp):
QPCR Primer Description:Verified forward and reverse primers for analyzing the quantitative expression of gene
Quality Control:The primer mix has been verified to generate satisfactory qPCR data on Roche LightCycler480
Shipping_carrier:1 vial of lyophilized qPCR primer mix (1 nmol each primer, sufficient for 200 numbers of 25 μl reactions) is shipped at ambiente temperatura.
Storage:The lyophilized product is stable for one year from date of receipt when stored at -20℃.
The suspended product is stable for six months from date of receipt when stored at -20℃.
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Sino biological qEASY qPCR primer pairs are used for SYBR Green-based real-time RT-PCR, The primers are designed by using SBI's proprietary primer design algorithm. Our primer collection covers the entire human genomes. It can be widely applied in the quantitative analysis of gene expression.

Unique Primer Design

To avoid genomic DNA amplification, at least one primer is designed crosses the junction of exons according to the conserved region of a specific gene with all variants.

Strict Validation Process

Confirmed in positive organizations; screened the primer with high specificity and high sensitivity.

Uniform PCR conditions, Saving time and cost

~100% amplification curve, ensuring the accuracy of the RNA quantitative

DLL4/Delta-like 4 Background

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.

Human DLL4/Delta-like 4 References
  • 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.
  • Size / Price
    Catalog: HP100239
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    Availability5-8 Business daysShipping instructions
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