
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Bcl-9 CRISPR Activation Plasmid (h) | sc-404408-ACT | 20 µg | $397.00 |
BCL9 encodes Bcl-9, a transcriptional co-activator that couples β-catenin to TCF/LEF DNA-binding factors to amplify canonical Wnt signaling output. Through regulation of Wnt-responsive gene programs, Bcl-9 influences cell fate decisions, proliferation, and differentiation, with additional roles in chromatin-associated transcriptional control. Dysregulated BCL9 expression or activity has been linked to aberrant Wnt/β-catenin pathway activation observed in multiple cancers and developmental contexts, making it a useful node for studying pathway dependence and transcriptional rewiring.
Bcl-9 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BCL9 expression without altering the underlying DNA sequence.
Bcl-9 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BCL9 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 BCL9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Bcl-9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BCL9 locus and enabling the study of Bcl-9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Bcl-9 pathway restoration in tumor cells with silenced or reduced BCL9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.