Dvl-3/Dishevelled 3/DVL3 CRISPR Activation Plasmid (h): sc-401041-ACT

DVL3 encodes Dishevelled 3 (Dvl-3), a cytoplasmic scaffold that relays Wnt ligand signals to downstream effectors to coordinate cell polarity, migration, and fate specification. Through interactions with Frizzled receptors and core Wnt components, Dvl-3 helps balance canonical β-catenin–dependent transcription with non-canonical planar cell polarity and Wnt/Ca²⁺ signaling outputs. DVL3-dependent signaling influences cytoskeletal remodeling, vesicular trafficking, and mitotic spindle orientation, linking it to developmental patterning and tissue homeostasis. Dysregulated Wnt–Dishevelled activity, including altered DVL3 expression or pathway rewiring, is frequently studied in contexts such as tumor biology, invasiveness, and aberrant differentiation programs.

Dvl-3/Dishevelled 3/DVL3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DVL3 expression without altering the underlying DNA sequence.

Dvl-3/Dishevelled 3/DVL3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DVL3 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 DVL3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Dvl-3/Dishevelled 3/DVL3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DVL3 locus and enabling the study of Dvl-3/Dishevelled 3/DVL3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Dvl-3/Dishevelled 3/DVL3 pathway restoration in tumor cells with silenced or reduced DVL3 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.