|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A myc tag can be used in many different assays that require recognition by an antibody. If there is no antibody against the studied protein, adding a myc-tag allows one to follow the protein with an antibody against the Myc epitope. Examples are cellular localization studies by immunofluorescence or detection by Western blotting.
The peptide sequence of the myc-tag is: N-EQKLISEEDL-C (1202 Da). It can be fused to the C-terminus and the N-terminus of a protein. It is advisable not to fuse the tag directly behind the signal peptide of a secretory protein, since it can interfere with translocation into the secretory pathway.
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), C-GFPSpark 标签||HG10171-ACG|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), C-OFPSpark 标签||HG10171-ACR|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), C-Flag 标签||HG10171-CF|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), C-His 标签||HG10171-CH|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), C-Myc 标签||HG10171-CM|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), C-HA 标签||HG10171-CY|
|人 DLL4/Delta-like 4 基因ORF全长cDNA(克隆载体)||HG10171-M|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体)||HG10171-M-N|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), N-Flag 标签||HG10171-NF|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), N-His 标签||HG10171-NH|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), N-Myc 标签||HG10171-NM|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体), N-HA 标签||HG10171-NY|
|人 DLL4/Delta-like 4 基因ORF全长cDNA克隆(表达载体)||HG10171-UT|
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.