Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
VEGF CRISPR Activation Plasmid (m): sc-423665-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VEGF CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- VEGF CRISPR Activation Plasmid (m) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by VEGF CRISPR Activation Plasmid (m) and VEGF CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Vegfa transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: VEGF Antibody (C-1): sc-7269
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VEGF CRISPR Activation Plasmid (m) | sc-423665-ACT | 20 µg | $397.00 | |||
VEGF CRISPR Activation Plasmid (m2) | sc-423665-ACT-2 | 20 µg | $397.00 |
Mouse Vegfa encodes vascular endothelial growth factor (VEGF), a secreted cytokine that regulates endothelial cell proliferation, migration, and survival to coordinate angiogenesis and vascular permeability. VEGF signaling primarily engages VEGFR2 to activate PI3K–AKT, MAPK/ERK, and PLCγ–PKC cascades, integrating hypoxia and metabolic cues with tissue remodeling. Dysregulated VEGF expression is linked to pathological neovascularization, altered perfusion, and inflammatory microenvironment changes that influence tumor biology, wound repair, and retinal and cardiovascular disease models. As a central node in vascular and stromal crosstalk, Vegfa is widely used to probe endothelial–parenchymal signaling and extracellular matrix remodeling.
VEGF CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Vegfa expression without altering the underlying DNA sequence.
VEGF CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Vegfa 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 Vegfa transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous VEGF expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Vegfa locus and enabling the study of VEGF-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of VEGF pathway restoration in tumor cells with silenced or reduced Vegfa expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.