
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Delta-4 CRISPR Activation Plasmid (h) | sc-401271-ACT | 20 µg | $397.00 |
Human DLL4 encodes Delta-4, a membrane-bound Notch ligand that mediates juxtacrine signaling to regulate arterial specification, tip–stalk cell decisions, and vascular branching morphogenesis. DLL4–NOTCH interactions coordinate transcriptional programs that couple angiogenic sprouting with endothelial quiescence, integrating cues from VEGF and other microenvironmental signals. Dysregulated DLL4 expression or signaling balance is linked to abnormal vascular remodeling and altered perfusion states observed across tumor angiogenesis and other vascular-associated pathologies. As a pathway node, DLL4 is frequently studied for its effects on endothelial differentiation, cell–cell communication, and context-dependent control of proliferation.
Delta-4 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DLL4 expression without altering the underlying DNA sequence.
Delta-4 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DLL4 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the DLL4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Delta-4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DLL4 locus and enabling the study of Delta-4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Delta-4 pathway restoration in tumor cells with silenced or reduced DLL4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.