
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Vangl2 CRISPR Activation Plasmid (h) | sc-400805-ACT | 20 µg | $397.00 |
VANGL2 encodes Vangl2, a core planar cell polarity (PCP) component that helps coordinate directional cell behaviors and tissue architecture during development and in adult epithelia. Vangl2 participates in non-canonical WNT/PCP signaling, influencing cytoskeletal remodeling, polarized migration, and oriented cell division through interactions with Dishevelled and downstream RhoA/ROCK and JNK pathways. Altered VANGL2 regulation has been associated with defects in convergent extension and neural tube closure, and dysregulated PCP signaling is frequently linked to epithelial organization changes relevant to cancer biology and neurodevelopmental disorders. As a polarity determinant, Vangl2 is also studied in contexts of ciliogenesis, junctional integrity, and collective cell migration.
Vangl2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous VANGL2 expression without altering the underlying DNA sequence.
Vangl2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the VANGL2 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 VANGL2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Vangl2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native VANGL2 locus and enabling the study of Vangl2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Vangl2 pathway restoration in tumor cells with silenced or reduced VANGL2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.