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pMD18-T Simple Vector is a high-efficiency TA cloning vector constructed from pUC18, of which the initial multiple cloning sites (MCS) were destroyed. Thus the cDNA should be amplified by PCR with primers containing a restriction site for subclone. Competent cells appropriate for pUC18 are also appropriated for the Vector, e.g. JM109, DH5α, TOP10. The pMD18-T Simple Vector is 2.6kb in size. Selection of the plasmid in E. coli is conferred by the ampicillin resistance gene. The coding sequence was inserted by TA cloning at site 425.
The coding sequence can be amplified by PCR with M13-47 and RV-M primers.
|Human DLL4 ORF mammalian expression plasmid, C-GFPSpark tag||HG10171-ACG|
|Human DLL4 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||HG10171-ACR|
|Human DLL4 ORF mammalian expression plasmid, C-Flag tag||HG10171-CF|
|Human DLL4 ORF mammalian expression plasmid, C-His tag||HG10171-CH|
|Human DLL4 ORF mammalian expression plasmid, C-Myc tag||HG10171-CM|
|Human DLL4 ORF mammalian expression plasmid, C-HA tag||HG10171-CY|
|Human DLL4 natural ORF mammalian expression plasmid||HG10171-M-N|
|Human DLL4 ORF mammalian expression plasmid, N-Flag tag||HG10171-NF|
|Human DLL4 ORF mammalian expression plasmid, N-His tag||HG10171-NH|
|Human DLL4 ORF mammalian expression plasmid, N-Myc tag||HG10171-NM|
|Human DLL4 ORF mammalian expression plasmid, N-HA tag||HG10171-NY|
|Human DLL4 natural ORF mammalian expression plasmid||HG10171-UT|
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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.