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.
von Willebrand Factor/VWF CRISPR Activation Plasmid (h): sc-400217-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- von Willebrand Factor/VWF CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- von Willebrand Factor/VWF CRISPR Activation Plasmid (h) 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 von Willebrand Factor/VWF CRISPR Activation Plasmid (h) and von Willebrand Factor/VWF CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the VWF 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: von Willebrand Factor/VWF Antibody (C-12): sc-365712
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
von Willebrand Factor/VWF CRISPR Activation Plasmid (h) | sc-400217-ACT | 20 µg | $397.00 | |||
von Willebrand Factor/VWF CRISPR Activation Plasmid (h2) | sc-400217-ACT-2 | 20 µg | $397.00 |
VWF encodes von Willebrand factor, a large multimeric glycoprotein produced by endothelial cells and megakaryocytes that is essential for primary hemostasis. VWF mediates platelet adhesion to exposed subendothelial collagen under high shear stress and stabilizes coagulation factor VIII, linking platelet tethering with the intrinsic coagulation cascade. The protein is stored in Weibel–Palade bodies and platelet α-granules and is regulated by multimer processing and cleavage, influencing thrombosis and vascular integrity. Dysregulation or genetic variation in VWF is associated with bleeding and thrombotic phenotypes and is widely studied in endothelial biology, platelet function, and coagulation pathway research.
von Willebrand Factor/VWF CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous VWF expression without altering the underlying DNA sequence.
von Willebrand Factor/VWF CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the VWF 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 VWF transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous von Willebrand Factor/VWF expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native VWF locus and enabling the study of von Willebrand Factor/VWF-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of von Willebrand Factor/VWF pathway restoration in tumor cells with silenced or reduced VWF expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.