
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
WISP-2 CRISPR Activation Plasmid (h) | sc-402996-ACT | 20 µg | $397.00 |
WISP2 (WISP-2/CCN5) is a secreted matricellular protein in the CCN family that integrates extracellular matrix cues with growth factor signaling to influence cell adhesion, migration, and proliferation. It is regulated downstream of Wnt/β-catenin and intersects with TGF-β, IGF, and integrin-mediated pathways that control cytoskeletal remodeling and stromal–epithelial communication. In human tissues, WISP-2 expression has been linked to programs of tissue remodeling and fibroproliferative responses, and its dysregulation is studied in contexts such as cancer biology, metabolic inflammation, and vascular pathology. These properties make WISP-2 a useful node for investigating ECM-dependent transcriptional control, cell state transitions, and microenvironment-driven phenotypes.
WISP-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous WISP2 expression without altering the underlying DNA sequence.
WISP-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the WISP2 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 WISP2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous WISP-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native WISP2 locus and enabling the study of WISP-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of WISP-2 pathway restoration in tumor cells with silenced or reduced WISP2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.