Dvl-2/Dishevelled 2/DVL2 CRISPR Activation Plasmid (m): sc-420081-ACT

Mouse Dvl2 encodes Dishevelled 2 (DVL2), a cytoplasmic scaffold protein that transduces Wnt signals to downstream effectors in both canonical β-catenin–dependent transcription and non-canonical planar cell polarity and Wnt/Ca2+ pathways. By coupling Frizzled/LRP receptor inputs to pathway components such as Axin, GSK3, and small GTPases, DVL2 influences cell fate specification, polarity, migration, and cytoskeletal organization during development and tissue homeostasis. Dysregulated Wnt–DVL2 signaling is implicated in aberrant proliferation and differentiation programs, making Dvl2 a frequent focus in studies of oncogenic signaling networks and developmental disorders. Its central adapter role also supports investigation of pathway cross-talk with MAPK, PI3K/AKT, and cytoskeletal remodeling processes in disease-relevant cellular phenotypes.

Dvl-2/Dishevelled 2/DVL2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Dvl2 expression without altering the underlying DNA sequence.

Dvl-2/Dishevelled 2/DVL2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Dvl2 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 Dvl2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Dvl-2/Dishevelled 2/DVL2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Dvl2 locus and enabling the study of Dvl-2/Dishevelled 2/DVL2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Dvl-2/Dishevelled 2/DVL2 pathway restoration in tumor cells with silenced or reduced Dvl2 expression.

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