WBP2 CRISPR Activation Plasmid (h): sc-409856-ACT

WBP2 (WW domain binding protein 2) functions as an adaptor and transcriptional co-regulator that engages WW domain–containing partners and integrates signaling inputs into gene expression programs. It participates in pathways linked to receptor and nuclear signaling, including transcriptional regulation through interactions with coactivator complexes and modulation of proliferation- and differentiation-associated transcriptional outputs. WBP2 activity has been studied in the context of altered signaling states in cancer biology, where changes in co-regulatory networks can influence cell growth and migratory phenotypes. These properties make WBP2 a useful node for investigating transcriptional circuitry, signal-dependent gene regulation, and context-specific pathway remodeling in human cells.

WBP2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous WBP2 expression without altering the underlying DNA sequence.

WBP2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the WBP2 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 WBP2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous WBP2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native WBP2 locus and enabling the study of WBP2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of WBP2 pathway restoration in tumor cells with silenced or reduced WBP2 expression.

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