
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APC CRISPR Activation Plasmid (m) | sc-419146-ACT | 20 µg | $397.00 |
Mouse Apc encodes APC, a multifunctional tumor suppressor that scaffolds the β-catenin destruction complex to restrain canonical Wnt signaling and regulate transcriptional programs controlling proliferation and differentiation. APC also contributes to cytoskeletal organization, cell polarity, and microtubule dynamics, linking signaling outputs to directed migration and chromosome segregation. Disruption or altered expression of APC perturbs epithelial homeostasis and stem cell behavior, with broad relevance to studies of intestinal biology, developmental patterning, and oncogenic signaling networks.
APC CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Apc expression without altering the underlying DNA sequence.
APC CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Apc 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 Apc transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous APC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Apc locus and enabling the study of APC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of APC pathway restoration in tumor cells with silenced or reduced Apc expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.